Aging-US: Recent Episodes
Aging (Aging-US) Podcast
A twice-monthly, traditional, peer-reviewed journal with open-access, covering all areas of research on aging, including age-related diseases, such as cancer —and also with a special focus on COVID-19 vulnerability as an age-dependent syndrome.
BUFFALO, NY — August 10, 2026 — A new #essay was #published in Volume 18 of Aging on August 6, 2026, titled “Misha Blagosklonny: a life of ideas.”The article was written by Aging Editorial Board member David Gems from the Institute of Healthy Ageing and Research Department of Genetics, Evolution and Environment, University College London, United Kingdom, along with Aging Editor-in-Chief Marco Demaria from the European Research Institute for the Biology of Ageing (ERIBA), University Medical Center Groningen (UMCG), University of Groningen, the Netherlands. Rather than presenting new experimental findings, the essay examines the life, scientific contributions, and lasting influence of Mikhail (“Misha”) Blagosklonny, whose ideas had a major influence on modern thinking about the biological mechanisms of aging.Dr. Blagosklonny was trained as a physician and experimental scientist before building an influential career in oncology and aging research after moving to the United States. His work combined cancer biology with theoretical biogerontology, leading to the proposal that aging is driven not primarily by the passive accumulation of molecular damage, but by developmental and growth-related programs that continue beyond their beneficial period. Through what he described as conceptual research, Misha synthesized evidence from diverse experimental studies to generate new hypotheses about aging and reinterpret existing biological observations.A central theme of the essay is Dr. Blagosklonny’s development of the hyperfunction theory of aging. Building on observations that persistent activation of the mechanistic target of rapamycin (mTOR) pathway can drive cellular senescence, he proposed that many features of aging arise from the continued activity of biological programs that promote growth and reproduction earlier in life. Rather than viewing aging as an adaptive genetic program, Misha argued that it represents a quasi-program—a genetically determined continuation of normal developmental processes that become harmful later in life. This framework provided a mechanistic explanation linking evolutionary concepts such as antagonistic pleiotropy with molecular pathways that regulate growth, metabolism, and cellular senescence.Full press release - https://www.aging-us.com/news-room/misha-blagosklonnys-scientific-legacy-continues-to-shape-modern-aging-researchDOI - https://doi.org/10.18632/aging.206412Corresponding author - David Gems - david.gems@ucl.ac.ukSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206412Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, hyperfunction, programmatic theory, disposable soma 2, quasi-program, biogerontology, evolutionary physiology, Mikhail BlagosklonnyTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — August 6, 2026 — A new #research perspective was #published in Volume 18 of Aging on July 24, 2026, titled “A brief history of the hyperfunction theory of aging and future directions.”The article was written by João Pedro de Magalhães from the Genomics of Ageing and Rejuvenation Lab, Department of Inflammation and Ageing, College of Medicine and Health, University of Birmingham, United Kingdom.Rather than presenting new experimental findings, the perspective examines the historical development of the hyperfunction theory of aging, reviews evidence supporting programmatic mechanisms of aging, and discusses future directions for understanding why organisms age and how aging might eventually be modified.For decades, most aging research has been dominated by the idea that aging results primarily from the gradual accumulation of molecular damage, including DNA damage, oxidative stress, mitochondrial dysfunction, and protein deterioration. In contrast, the hyperfunction theory proposes that aging is driven largely by developmental and growth programs that continue operating beyond their beneficial period. Rather than being intentionally programmed, aging is viewed as a consequence of biological pathways that promote growth and reproduction early in life but become harmful when they continue later in adulthood.The perspective traces the historical roots of these ideas from early theories proposed in the nineteenth century through Clive McCay’s pioneering caloric restriction experiments and George Williams’ concept of antagonistic pleiotropy. Particular attention is given to the contributions of the late Mikhail Blagosklonny, whose hyperfunction theory proposed that aging results from “quasi-programs”—developmental processes that fail to switch off after their normal biological role has ended. The author argues that this framework provides a mechanistic explanation linking evolutionary theory with many biological features of aging.Full press release - https://www.aging-us.com/news-room/hyperfunction-theory-offers-a-new-perspective-on-why-we-agePaper DOI - https://doi.org/10.18632/aging.206403 Corresponding author - João Pedro de Magalhães - jp@senescence.infoAbstract video - https://www.youtube.com/watch?v=VwC6aJoUUQoSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206403Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, antagonistic pleiotropy, longevity, programmatic aging, quasi-programTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Aging Series - https://www.aging-us.com/longevityAbout Dr. Yuan Zhao - https://www.qmul.ac.uk/sbbs/staff/yuan-zhao.htmlSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206376Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, methylene blue, minoxidil, HFSCs, Wnt/β-catenin, GLP-1 RATo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — August 5, 2026 — A new #research paper was #published in Volume 18 of Aging on July 23, 2026, titled “Adipo-neuroinflammation, cognitive impairment and surrogate markers of cardiovascular risk in patients with Metabolic Dysfunction Associated Steatotic Liver Disease (MASLD).”The study was led by co-first authors Gaetano Pacinella from the University of Palermo, and the Internal Medicine and Stroke Care Ward, Policlinico “P. Giaccone”, Palermo, and Alessandro Del Cuore from the same institutions. Gaetano Pacinella also served as the corresponding author.Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as nonalcoholic fatty liver disease, is increasingly recognized as a systemic condition that extends beyond the liver. People with MASLD have an elevated risk of cardiovascular disease, cognitive decline, and other metabolic complications, yet the biological mechanisms connecting these conditions remain incompletely understood. In this study, researchers investigated whether lipocalin-2 (LCN2), a protein involved in inflammatory and metabolic signaling, is associated with early vascular dysfunction, cognitive impairment, and cardiovascular risk in patients with MASLD.Full press release - https://www.aging-us.com/news-room/fatty-liver-disease-linked-to-early-cardiovascular-and-cognitive-changesDOI - https://doi.org/10.18632/aging.206397Corresponding author - Gaetano Pacinella - gaetano.pacinella@unipa.itAbstract video - https://www.youtube.com/watch?v=CrqTayKl8KISign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206397Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, metabolic dysfunction, cardiovascular risk, lipocalin-2, cognitive impairment, endothelial dysfunctionTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Heart failure remains one of the leading causes of hospitalization among older adults worldwide. During episodes of acute decompensated heart failure (ADHF), excess fluid builds up in the lungs and body, making breathing difficult and increasing the risk of serious complications. Although intravenous loop diuretics such as furosemide are the standard treatment for relieving congestion, many patients continue to experience persistent inflammation, ongoing cardiac remodeling, and worsening heart function despite therapy.A research paper published in Volume 18 of Aging titled “Effects of intravenous furosemide plus small-volume hypertonic saline solutions on inflammatory, remodelling markers and epigenetics signatures of patients with congestive acute decompensated heart failure (ADHF),” investigated whether combining intravenous furosemide with small volumes of hypertonic saline solution (HSS) could improve biological markers associated with heart failure compared with furosemide alone.Full blog post - https://aging-us.org/2026/08/hypertonic-saline-plus-furosemide-improves-heart-failure-biomarkers-in-randomized-trial/DOI - https://doi.org/10.18632/aging.206364Corresponding author - Antonino Tuttolomondo - bruno.tuttolomondo@unipa.itAbstract video - https://www.youtube.com/watch?v=EG65XlcDJ3USign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206364Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, heart failure, acute decompensated heart failure, furosemide, hypertonic saline solutionTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — August 3, 2026 — A new #research paper was #published in Volume 18 of Aging on July 17, 2026, titled “Selective targeting of cancer and senescence via shared metabolic shifts extends lifespan of old mice.”The study was led by first author Zachery R. Robinson, and corresponding author and Aging editorial board member Irina M. Conboy, both from the Department of Bioengineering and QB3 Institute, University of California, Berkeley. The researchers developed a new combination therapy that selectively targets both cancer cells and senescent cells by exploiting metabolic vulnerabilities shared by these two cell types. In laboratory studies and aged mice, the treatment selectively eliminated senescent cells and reduced cancer cell viability while improving physical performance and extending lifespan without significant toxicity to healthy tissues.Cancer and aging are closely linked. As people age, senescent cells accumulate throughout the body. Although these cells no longer divide, they remain metabolically active and release inflammatory molecules known as the senescence-associated secretory phenotype (SASP), which contributes to chronic inflammation, tissue dysfunction, and tumor progression. Existing therapies such as the BCL-2/BCL-xL inhibitor navitoclax (ABT-263) can eliminate both cancer cells and senescent cells but require doses that frequently cause thrombocytopenia, a potentially serious reduction in platelet counts that has limited their clinical use.Full press release - https://www.aging-us.com/news-room/new-drug-combination-targets-cancer-and-senescent-cells-while-extending-lifespan-in-old-miceDOI - https://doi.org/10.18632/aging.206399Corresponding author - Irina M. Conboy - irina@generationlab.coAbstract video - https://www.youtube.com/watch?v=7p5JMvy9TwgSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206399Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, senescence, cancer, metabolic shift, ATPTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 30, 2026 — A new #research perspective was #published in Volume 18 of Aging on July 16, 2026, titled “Towards integration of healthspan strategies into the Italian National Health Service.”The article was led by co-first authors Nicola Marino, affiliated with the AEON Foundation and the Women’s Brain Foundation, and Matteo Fiore from the University of Bologna, with both serving as corresponding authors. Rather than presenting new clinical trial results, the authors propose a prevention-focused framework for the staged, evidence-based evaluation and integration of healthspan strategies into Italy’s National Health Service (Servizio Sanitario Nazionale, SSN) to help address the challenges of an aging population.Italy has one of the oldest populations in the world. Although life expectancy has continued to increase, many older adults spend a substantial portion of those additional years living with chronic disease, disability, or reduced physical and cognitive function. The authors describe this mismatch as the lifespan–healthspan divide and argue that healthcare systems should increasingly focus not only on helping people live longer, but also on extending the years they remain healthy and functionally independent.To address this challenge, the authors outline the concept of longevity medicine, describing it as a prevention-oriented, life-course framework rather than a new medical specialty. The approach integrates principles from geroscience, preventive medicine, and personalized healthcare with the goal of identifying age-related risks earlier and promoting healthy aging before chronic diseases and functional limitations accumulate. At the same time, the paper emphasizes that many emerging tools—including biological-age biomarkers, multi-omic profiling, wearable sensor data, and artificial intelligence-based risk stratification—remain exploratory and should not be adopted routinely until they demonstrate clear clinical utility, cost-effectiveness, and meaningful benefits for patients.Full press release - https://www.aging-us.com/news-room/italy-proposes-a-healthspan-focused-framework-for-healthy-agingDOI - https://doi.org/10.18632/aging.206402Corresponding authors - Nicola Marino - marino@aeonfoundation.eu, and Matteo Fiore - matteo.fiore@auslromagna.itAbstract video - https://www.youtube.com/watch?v=uc1tGVfiHMwSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206402Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, preventive, longevity, national health system, health span, biomarkersTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 27, 2026 — A new #research paper was #published in Volume 18 of Aging on July 13, 2026, titled “Slowing intervertebral disc aging in mice through long-term systemic treatment with the senolytic BCL-2/BCL-xL proteolysis targeting chimera (PROTAC) 753b.”The study was led by first author Peter G. Alexander from the Ferguson Laboratory for Spine Research, Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine, and corresponding author Nam Viet Vo from the same institution. Intervertebral disc degeneration is a leading cause of chronic low back pain and disability. As discs age, they lose important structural components, become less able to absorb mechanical stress, and accumulate senescent cells—dysfunctional cells that stop dividing but continue releasing inflammatory molecules that contribute to tissue degeneration. Senolytic therapies, which selectively eliminate these cells, have emerged as a promising strategy to slow age-related diseases. In this study, researchers evaluated PROTAC 753b, a next-generation senolytic designed to target the anti-apoptotic proteins BCL-2 and BCL-xL while reducing the platelet toxicity associated with earlier drugs in this class.The researchers treated 16-month-old male and female mice with PROTAC 753b for six months and evaluated their intervertebral discs at 22 months of age using histology, molecular analyses, and measurements of inflammatory markers. The treatment significantly improved several measures of intervertebral disc health in aged male mice, preserving the extracellular matrix protein aggrecan and reducing matrix metalloproteinase (MMP)-mediated aggrecan breakdown, a hallmark of disc degeneration. In contrast, female mice showed little overall improvement, revealing a sex-specific response to treatment.Full press release - https://www.aging-us.com/news-room/senolytic-protac-slows-age-related-intervertebral-disc-degeneration-in-male-miceDOI - https://doi.org/10.18632/aging.206394Corresponding author - Nam Viet Vo - nvv1@pitt.eduAbstract video - https://www.youtube.com/watch?v=t0z4MULDr1ASign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206394Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, intervertebral disc aging, cellular senescence, senolytic, anti-apoptosis, PROTAC-753bTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 23, 2026 — A new #research paper was #published in Volume 18 of Aging on July 8, 2026, titled “TM4SF1 is a surface marker of senescent pancreatic β-cells.”The study was led by first author Ana Beathriz Leite Lorente from Joslin Diabetes Center and Harvard Medical School, and São Paulo State University (UNESP), Brazil, and corresponding author Cristina Aguayo-Mazzucato from Joslin Diabetes Center and Harvard Medical School. Type 2 diabetes is characterized by insulin resistance and the progressive loss of pancreatic β-cell function. With aging and metabolic stress, senescent β-cells accumulate within the pancreas, producing less insulin while releasing inflammatory signals that contribute to disease progression. Although eliminating these dysfunctional cells has emerged as a promising therapeutic strategy, a major challenge has been identifying markers that distinguish senescent β-cells from healthy cells with sufficient precision. This study identifies transmembrane 4 L six family member 1 (TM4SF1) as a highly selective surface marker of senescent β-cells, providing a promising candidate for the future development of more selective therapies for type 2 diabetes. In this study, the researchers searched for cell-surface proteins that specifically identify senescent β-cells. Using RNA sequencing, flow cytometry, immunofluorescence, and analyses of both mouse and human pancreatic tissue, they compared TM4SF1 with the previously established senescence marker urokinase-type plasminogen activator receptor (uPAR/PLAUR). Their findings showed that TM4SF1 is expressed predominantly in senescent β-cells while exhibiting much lower expression in non-senescent β-cells and other tissues, making it a more β-cell-specific surface marker than uPAR.Full press release - https://www.aging-us.com/news-room/new-surface-marker-could-advance-precision-therapies-for-type-2-diabetesDOI - https://doi.org/10.18632/aging.206398Corresponding author - Cristina Aguayo-Mazzucato - Cristina.aguayo-mazzucato@joslin.harvard.eduAbstract video - https://www.youtube.com/watch?v=tNbFKdleTJoSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206398Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, senescent β-cell, type 2 diabetes, transmembrane 4 l six family member 1, urokinase-type plasminogen activator receptorTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Coordinating both hands is something most people take for granted. Everyday activities such as buttoning a shirt, preparing a meal, driving, or using a knife and fork all depend on the brain’s ability to precisely control movements on both sides of the body. As people age, however, these tasks often become more difficult, especially when they require both hands to perform different movements at the same time.A research paper published in Volume 18 of Aging titled “Age-specific relationship between the modulation of brain dynamics in response to task demands and bimanual performance,” investigated how aging affects the brain’s ability to adapt to increasingly complex hand-coordination tasks. The study was led by first author Sara Magalhães Ferreira from Hasselt University, with corresponding author Koen Cuypers from Hasselt University and KU Leuven.Full blog - https://aging-us.org/2026/07/brain-flexibility-is-linked-to-hand-coordination-during-aging/DOI - https://doi.org/10.18632/aging.206363Corresponding author - Koen Cuypers - koen.cuypers@uhasselt.beAbstract video - https://www.youtube.com/watch?v=3TbcGFCZV9sSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206363Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, bimanual coordination, Bimanual Tracking Task, BOLD variability, task modulationTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 21, 2026 — A new #research paper was #published in Volume 18 of Aging on July 6, 2026, titled “Inhibition of peroxisomal protein PRX-11 promotes longevity in Caenorhabditis elegans via enhancements to mitochondria.”The study was authored by Yash Flora, Dhriti Shastri, Kathryn R. DeLeo, and K. Adam Bohnert from the Department of Biological Sciences, Louisiana State University.Aging is accompanied by the gradual decline of many cellular structures that help maintain healthy tissues and organs. Among these are peroxisomes, which play essential roles in breaking down toxic molecules and metabolizing lipids, and mitochondria, which generate most of the cell’s energy. Although these organelles work closely together, little has been known about how changes in one influence the aging of the other. This new study reveals that preserving peroxisomes helps maintain healthier mitochondria and extends lifespan in the nematode Caenorhabditis elegans, providing new insight into how communication between cellular organelles influences aging.In this study, the researchers investigated the function of PRX-11, a peroxisomal protein involved in peroxisome division. Previous work from the group showed that reducing PRX-11 activity prevents the age-related degradation of peroxisomes through a process known as pexophagy and increases lifespan. The new study explored why preserving peroxisomes produces these beneficial effects and found that maintaining peroxisomes also preserves mitochondrial health during aging.The researchers found that animals with reduced PRX-11 activity retained long, interconnected mitochondrial networks that resembled those seen in young adults, whereas normal aging was associated with progressive mitochondrial fragmentation. These preserved mitochondria also accumulated less calcium, generated lower levels of oxidative stress, maintained higher ATP-to-ADP ratios, and were associated with improved locomotor function in older animals. Together, these findings indicate that preventing age-related peroxisome loss supports multiple aspects of mitochondrial function during aging.Full press release - https://www.aging-us.com/news-room/preserving-peroxisomes-helps-maintain-mitochondrial-health-and-extend-lifespan-in-c-elegansDOI - https://doi.org/10.18632/aging.206395Corresponding author - K. Adam Bohnert - bohnerta@lsu.eduAbstract video - https://www.youtube.com/watch?v=fbcqBsP90CYSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206395Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, cellular aging, lifespan, pexophagy, mitochondrial tubulation, inter-organelle crosstalkTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Each month, we will highlight a paper published in Aging chosen as the “Editors’ Choice.” These selections are handpicked by our editors and accompanied by a brief summary, showcasing research with significant impact and novel insights in aging and age-related diseases.Cellular senescence is a hallmark of aging and age-related disease, yet the diverse mechanisms that trigger this cellular state remain incompletely understood. The review recently published in Volume 18 of Aging, titled “The multifaceted inducers of cellular senescence,” examines the many intrinsic and extrinsic stimuli that induce senescence, including DNA damage, oxidative and mitochondrial stress, telomere attrition, oncogene activation, cell–cell fusion, and developmental signals. The authors, Hilah Gal and Valery Krizhanovsky, explain how these distinct pathways converge on a stable cell-cycle arrest. By highlighting the complexity and heterogeneity of senescent cells, the authors provide valuable insights that may guide the development of future therapies targeting senescence to promote healthy aging and combat age-related diseases.DOI - https://doi.org/10.18632/aging.206391Corresponding author - Valery Krizhanovsky - valery.krizhanovsky@weizmann.ac.ilAbstract video - https://www.youtube.com/watch?v=5Y7R_8GQ1gkSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206391Keywords - aging, cell senescenceTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 16, 2026 — A new #research paper was #published in Volume 18 of Aging on July 1, 2026, titled “Senescent cells accumulate lipid droplets.”The study was led by first author Noa Rachmian-Cooper and corresponding author Valery Krizhanovsky from the Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel. Cellular senescence is a natural biological process in which damaged or stressed cells permanently stop dividing while remaining metabolically active. Although senescence helps suppress tumor formation and supports normal processes such as tissue repair and development, senescent cells accumulate with age and contribute to chronic inflammation and numerous age-related diseases, including cancer, cardiovascular disease, and Alzheimer’s disease. While many of the biological effects of senescent cells have been linked to inflammatory signaling, much less has been understood about the metabolic changes that accompany senescence.In this study, the researchers investigated how cellular metabolism changes during senescence, with a particular focus on lipid metabolism. Using comprehensive metabolic profiling of human fibroblasts, they discovered that senescent cells accumulate high levels of triacylglycerols—the major precursors of lipid droplets—alongside increased glycolytic activity. Additional laboratory experiments confirmed that senescent cells contain significantly more lipid droplets than actively dividing cells.Full press release - https://www.aging-us.com/news-room/senescent-cells-found-to-accumulate-lipid-droplets-across-aging-and-alzheimers-diseaseDOI - https://doi.org/10.18632/aging.206390Corresponding author - Valery Krizhanovsky - valery.krizhanovsky@weizmann.ac.ilAbstract video - https://www.youtube.com/watch?v=GZbhY3wtGGISign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206390Keywords - aging, senescence, lipid droplets, metabolism, Alzheimer’s diseaseTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 13, 2026 — A new #review was #published in Volume 18 of Aging on June 26, 2026, titled “Hormonal dimorphism in sarcopenia disease.”The review was led by first author Romain Menard and corresponding author Romain Madelaine from the MDI Biological Laboratory, Kathryn W. Davis Center for Regenerative Biology and Aging, Bar Harbor, Maine, USA.Sarcopenia—the progressive loss of skeletal muscle mass, strength, and physical function with aging—is one of the leading causes of frailty and disability in older adults. Although the condition affects millions of people worldwide and has been recognized as a disease by the World Health Organization since 2016, treatment options remain largely limited to exercise and nutritional interventions, with no approved medications specifically targeting the disease. Growing evidence now suggests that one reason for this limited success is that sarcopenia develops through distinct biological mechanisms in women and men.In this comprehensive review, the authors examine how biological sex influences the hormonal mechanisms underlying muscle aging. They focus on three peptide hormones—apelin, insulin, and oxytocin—and describe how age-related changes in these interconnected signaling networks contribute to muscle decline through distinct biological pathways in women and men.According to the review, women often experience an abrupt decline in muscle health during menopause as estrogen levels fall rapidly. This hormonal transition disrupts apelin signaling, accelerates insulin resistance, reduces oxytocin-mediated muscle regeneration, and impairs the function of satellite cells, the muscle stem cells responsible for repair and regeneration. In contrast, men generally undergo a slower, more gradual decline in muscle function that parallels progressive reductions in testosterone, resulting in different patterns of hormonal dysregulation and disease progression.The review also highlights the central roles of apelin, insulin, and oxytocin in maintaining healthy skeletal muscle. Together, these hormones regulate muscle metabolism, glucose utilization, mitochondrial function, protein homeostasis, inflammation, and satellite-cell activity through overlapping signaling pathways. Disruption of this hormonal network during aging is proposed to contribute to impaired muscle repair, reduced metabolic function, chronic inflammation, and progressive muscle loss.Full press release - https://aging-us.net/2026/07/13/sex-specific-hormones-could-hold-the-key-to-better-sarcopenia-treatments/DOI - https://doi.org/10.18632/aging.206392Corresponding author - Romain Madelaine - rmadelaine@mdibl.orgSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206392Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, sarcopenia, hormonal dimorphism, muscle aging, sex-stratified medicine, sexual dimorphismTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Aging Series: https://www.aging-us.com/longevityAbout Dr. Yuan Zhao: https://www.qmul.ac.uk/sbbs/staff/yuan-zhao.htmlSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206372Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, telomeres, telomeraseTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 7, 2026 — A new #review was #published in Volume 18 of Aging on June 22, 2026, titled “The multifaceted inducers of cellular senescence.”The review was led by first author Hilah Gal and corresponding author Valery Krizhanovsky from the Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.Cellular senescence is a fundamental biological process in which damaged or stressed cells permanently stop dividing while remaining metabolically active. This response plays an essential role in suppressing tumor formation, supporting embryonic development, facilitating wound healing, and maintaining tissue integrity. However, as people age, senescent cells accumulate because they are no longer efficiently cleared by the immune system. Their persistence contributes to chronic inflammation, tissue dysfunction, cancer, and many age-related diseases.In this comprehensive review, the authors examine the diverse biological stimuli that trigger cellular senescence and describe how seemingly different stimuli ultimately converge on common molecular pathways that establish stable growth arrest. Rather than viewing senescence as a single process, the review emphasizes its remarkable biological diversity and the importance of understanding how different initiating events shape distinct senescent cell phenotypes.The review discusses several major biological inducers of cellular senescence. One of the best-established mechanisms is telomere attrition, in which repeated cell division gradually shortens chromosome ends until they trigger a persistent DNA damage response. Other important stimuli include direct DNA damage caused by ionizing radiation, ultraviolet light, chemotherapy, and oxidative injury, all of which activate cellular pathways that permanently halt proliferation.Full press release - https://aging-us.net/2026/07/07/multiple-biological-triggers-shape-cellular-senescence-in-aging-and-disease/DOI - https://doi.org/10.18632/aging.206391Corresponding author - Valery Krizhanovsky - valery.krizhanovsky@weizmann.ac.ilAbstract video - https://www.youtube.com/watch?v=5Y7R_8GQ1gkSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206391Keywords - aging, cell senescenceTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
As people live longer, maintaining good health is becoming just as important as extending lifespan. While chronological age simply reflects the number of years a person has lived, biological age measures how well the body is functioning and may better predict future health. Researchers have increasingly focused on lifestyle factors that may slow biological aging, and diet has emerged as one of the most promising.A research paper published in Volume 18 of Aging titled “Plant-based dietary patterns are associated with slower epigenetic aging,” investigated whether diets emphasizing plant foods are associated with slower biological aging as measured by DNA methylation-based epigenetic clocks.Full blog post - https://aging-us.org/2026/07/plant-based-dietary-patterns-are-associated-with-slower-biological-aging/DOI - https://doi.org/10.18632/aging.206362Corresponding author - Hyunju Kim - hyunjuk1@uw.eduAbstract video - https://www.youtube.com/watch?v=FcJ7oEZ-KFkSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206362Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, plant-based diets, DNA methylation, epigenetic aging, all-cause mortality, middle-aged adultsTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 6, 2026 — A new systematic #review was #published in Volume 18 of Aging on June 18, 2026, titled “Life expectancy and causes of death in classical laminopathic progeroid syndromes: systematic review with individual-patient data synthesis.”The study was led by co-first authors Carlos López-Vila, Manuel García-Cordeiro, and Luís Estévez-Martínez from the University of Santiago de Compostela, and corresponding author David Araújo-Vilar from the University of Santiago de Compostela and the University Clinical Hospital of Santiago de Compostela, Spain. Classical laminopathic progeroid syndromes are among the rarest inherited disorders known. Caused by mutations affecting the LMNA gene or the ZMPSTE24 enzyme, these conditions lead to premature aging, severe multisystem disease, and markedly shortened life expectancy. Although Hutchinson-Gilford progeria syndrome (HGPS), mandibuloacral dysplasia (MAD), and restrictive dermopathy (RD) all belong to this group, reliable information about survival and causes of death for each disorder has remained limited because most published reports describe only individual patients or small case series.In this study, researchers performed a comprehensive systematic review and individual-patient data analysis to date of classical laminopathic progeroid syndromes. Following PRISMA guidelines, they analyzed data from 169 published studies together with two additional genetically confirmed institutional cases, creating a cohort of 158 genetically confirmed patients for the primary survival analysis. By examining individual patient records rather than pooled summaries, the investigators were able to compare survival patterns and causes of death across each disease subtype with greater precision.Full press release - https://aging-us.net/2026/07/06/comprehensive-individual-patient-analysis-clarifies-life-expectancy-across-rare-progeria-disorders/DOI - https://doi.org/10.18632/aging.206389Corresponding author - David Araújo-Vilar - david.araujo@usc.esSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206389Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, progeria, Lamin A/C (LMNA), ZMPSTE24, survival, cause of deathTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 1, 2026 — A new #review was #published in Volume 18 of Aging on June 11, 2026, titled “Age-related dysfunctions of the neuroendocrine axes in nonhuman primates with depression-like and anxious behavior.”The review, dedicated to the late Dr. Mikhail (Misha) Blagosklonny, was written by Nadezhda D. Goncharova from the Kurchatov Complex of Medical Primatology, National Research Center “Kurchatov Institute,” Adler, Sochi, Russian Federation.As people grow older, their risk of developing stress-related disorders—including depression, metabolic disease, cardiovascular disease, cognitive decline, and neurodegenerative conditions—increases substantially. However, not everyone ages in the same way. Some individuals appear more resilient to stress, while others develop endocrine and metabolic disturbances that may accelerate aging and disease. Understanding the biological mechanisms behind these differences could help identify people at greater risk and support more personalized approaches to healthy aging.In this review, the author summarizes decades of experimental research investigating how aging affects two major neuroendocrine systems—the hypothalamic-pituitary-adrenal (HPA) axis and the hypothalamic-pituitary-thyroid (HPT) axis—in nonhuman primates displaying either typical adaptive behavior or depression-like and anxiety-like behavior. Because rhesus monkeys closely resemble humans in their physiology, endocrine function, and behavior, they provide a valuable translational model for studying age-related changes that are difficult to examine in people.The research shows that older monkeys with depression-like and anxiety-like behavior develop more pronounced dysfunction of the HPA axis than animals with standard behavior. These animals exhibited impaired negative feedback regulation, higher evening and nighttime cortisol levels, increased responses to acute stress, and greater activation of stress-related hormonal pathways. Together, these findings suggest impaired regulation of stress responses during aging.The review also describes important age-related alterations in thyroid function. Older animals with depression-like and anxiety-like behavior showed lower thyroxine secretion, diminished thyroid responsiveness to hormonal stimulation, and evidence of impaired thyroid gland function. These endocrine changes were accompanied by greater insulin resistance, altered triglyceride metabolism, and reduced insulin secretion in overweight animals, indicating that stress-related neuroendocrine dysfunction may extend well beyond the brain.Importantly, the findings suggest that behavioral characteristics may influence how endocrine systems age. Rather than experiencing identical biological changes over time, individuals with greater vulnerability to stress may develop more severe hormonal disturbances that contribute to age-related disease.Full press - https://aging-us.net/2026/07/01/nonhuman-primate-research-reveals-how-aging-stress-and-behavior-may-interact-to-increase-disease-risk/DOI - https://doi.org/10.18632/aging.206388Corresponding author - Nadezhda D. Goncharova - ndgoncharova@mail.ru (ORCID id: 0000-0002-2720-9846)Abstract video - https://www.youtube.com/watch?v=yj8zvthBiA4To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 29, 2026 — A new #review was #published in Volume 18 of Aging on May 30, 2026, titled “The love and hate relationship between cellular senescence and stemness.”The review was led by first author Angelos Papaspyropoulos and corresponding author Vassilis G. Gorgoulis from the National and Kapodistrian University of Athens and the Biomedical Research Foundation of the Academy of Athens, Greece.Cellular senescence and stemness have traditionally been viewed as biological opposites. Senescent cells permanently stop dividing in response to cellular stress, helping prevent the spread of damaged cells, while stem cells maintain tissue repair by continuously renewing themselves and generating specialized cells. However, growing evidence suggests that the relationship between these two biological processes is far more complex and depends on the tissue type, physiological conditions, and disease context.In this review, the authors summarize recent research examining how senescence and stemness interact across normal tissues, aging, regeneration, and cancer. Rather than always opposing one another, the two processes can either suppress or reinforce each other depending on the biological setting.Under normal physiological conditions, senescence often limits stem cell activity. The review highlights studies showing that excessive senescence can impair the regenerative capacity of mesenchymal stem cells, muscle satellite cells, dental pulp stem cells, and pancreatic β-cell progenitors. In several experimental models, reducing senescence restored stem cell function and improved tissue regeneration.At the molecular level, multiple signaling pathways contribute to this balance, including the p53/p21 and p16INK4A/RB pathways, mTOR signaling, Wnt/β-catenin signaling, and the senescence-associated secretory phenotype (SASP). These pathways help determine whether cells maintain regenerative potential or enter a stable senescent state.The review also emphasizes that the relationship changes dramatically in cancer. In many tumors, senescent cells can promote the emergence of cancer stem cells through inflammatory signals released as part of the SASP or through cells escaping from the senescent state. This interaction has been reported in several malignancies, including B-cell lymphoma, liver cancer, colon cancer, lung cancer, and breast cancer, where stem cell-like properties may contribute to tumor progression, metastasis, and resistance to therapy.Full press release - https://www.aging-us.com/news-room/cellular-senescence-and-stem-cells-share-a-more-complex-relationship-than-previously-recognizedDOI - https://doi.org/10.18632/aging.206387Corresponding author - Vassilis G. Gorgoulis - vgorg@med.uoa.grSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206387Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, senescence, stemnessTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
D Division of Morinaga Milk Industry Co., Ltd., Japan.As researchers continue searching for practical ways to promote healthy aging, increasing attention has focused on interventions that target multiple biological pathways simultaneously. While exercise and healthy eating are widely recognized as important components of healthy aging, scientists are also investigating whether specific dietary components and gut microbes may influence biological aging processes measurable at the molecular level.In this study, researchers evaluated whether a 12-week lifestyle program could affect DNA methylation–based biomarkers of aging in overweight men aged 50 years and older. The intervention combined individualized exercise guidance, dietary counseling, and daily consumption of yogurt containing Bifidobacterium longum BB536, a probiotic strain that has previously been linked to beneficial effects on inflammation and gut health.The randomized controlled trial enrolled 48 participants, who were assigned either to the intervention group or to a control group that maintained their usual lifestyle habits. Participants in the intervention group received dietary counseling focused on reducing overeating, exercise guidance encouraging regular walking or stepper-based activity, and a daily serving of yogurt containing Bifidobacterium longum BB536.To assess biological aging, the investigators measured several DNA methylation–based aging biomarkers before and after the 12-week intervention. Particular attention was given to DunedinPACE, an epigenetic measure designed to estimate the current pace of biological aging rather than biological age itself.Full press release - https://aging-us.net/2026/06/25/lifestyle-intervention-linked-to-slower-biological-aging-markers-in-older-men/DOI - https://doi.org/10.18632/aging.206386Corresponding author - Yukihiro Hishida - yukihiro-hishida639@morinagamilk.co.jpAbstract video - https://www.youtube.com/watch?v=7W5sDpGgZtESign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206386Keywords - aging, DNA methylation clock, DunedinPACE, Multicomponent lifestyle intervention, Bifidobacterium longum BB536To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 23, 2026 — A new #research paper was #published in Volume 18 of Aging on May 28, 2026, titled “p38MAP kinase regulates senescence in human iPS-derived myocytes.”The study was led by first author Hiroki Sato and corresponding author Ryuichiro Sato from The University of Tokyo, along with corresponding author Makoto Shimizu from The University of Tokyo and Ochanomizu University.As people age, skeletal muscle gradually loses strength, mass, and function, contributing to frailty, reduced mobility, and an increased risk of falls. Although cellular senescence is widely recognized as a major driver of aging, the mechanisms that promote aging within mature muscle fibers remain poorly understood. In this study, researchers developed a human cell-based model to investigate how senescence develops in skeletal muscle cells and identified a signaling pathway that appears to play a central role in the process.The research team used human induced pluripotent stem cell (iPSC)-derived myocytes, specialized muscle cells generated from stem cells. To mimic age-related cellular damage, the investigators exposed the cells to low-dose X-ray irradiation, which induced DNA damage without causing extensive cell death.The treated muscle cells developed several characteristics commonly associated with aging. They exhibited muscle fiber atrophy, reduced contractile activity, and increased expression of p21, a well-established marker of cellular senescence. The researchers also observed elevated production of senescence-associated secretory phenotype (SASP) factors, inflammatory and extracellular signaling molecules that are commonly released by senescent cells.To better understand the molecular changes involved, the investigators performed proteomic, transcriptomic, and functional analyses. These studies revealed activation of p38 mitogen-activated protein kinase (p38MAPK), a signaling pathway previously linked to cellular stress responses and aging in other tissues.Further experiments demonstrated that inhibiting p38MAPK partially attenuated several senescence-associated features in the muscle cells. Treatment with p38MAPK inhibitors reduced muscle fiber atrophy, improved contractile function, and suppressed the expression of several senescence-associated factors. Conversely, activating p38MAPK promoted aging-like changes in the cells, further supporting its role in regulating muscle cell senescence.The study also identified activation of an integrin–FAK/SRC–p38MAPK signaling axis following DNA damage. According to the authors, this pathway may help explain how cellular stress is translated into long-term functional decline in skeletal muscle.Importantly, the findings were supported by analyses of human muscle aging datasets, which showed increased activity of MAPK signaling, focal adhesion pathways, and cytokine-related signaling in older skeletal muscle tissue.Full press release - https://aging-us.net/2026/06/23/researchers-identify-key-signaling-pathway-driving-muscle-cell-aging/DOI - https://doi.org/10.18632/aging.206385Corresponding authors - Ryuichiro Sato - roysato@g.ecc.u-tokyo.ac.jp, and Makoto Shimizu - shimizu.makoto@ocha.ac.jpAbstract video - https://www.youtube.com/watch?v=ULm7R74CJx0Website - https://www.Aging-US.com Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
As people live longer, maintaining mental well-being has become an increasingly important part of healthy aging. While regular physical activity is known to support both physical and psychological health, many older adults face barriers that make traditional exercise programs difficult to sustain. Researchers have therefore been exploring new approaches that combine physical activity with enjoyment, social interaction, and cognitive engagement.A review published in Volume 18 of Aging titled “What are the effects of exergames on the mood states of older people? A systematic review of experimental studies, impacts on mental health and recommendations,” examined whether exergames—video games that require physical movement to play—can improve mood and mental health in older adults. The study was led by authors from the Laboratory of Sport and Exercise Psychology, Human Movement Sciences Graduate Program, College of Health and Sport Science of the Santa Catarina State University (UDESC) in Florianópolis, Brazil. Full blog - https://aging-us.org/2026/06/do-exergames-improve-mood-and-mental-well-being-in-older-adults/DOI - https://doi.org/10.18632/aging.206361Corresponding author - Alexandro Andrade - alexandro.andrade.phd@gmail.comAbstract video - https://www.youtube.com/watch?v=mNBh_alqVRISign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206361Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, electronic games, older adults, BRUMS, mental health, physical activityTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 18, 2026 — A new #research paper was #published in Volume 18 of Aging on May 26, 2026, titled “Early-life determinants of cardiometabolic outcomes and accelerated biological ageing in Colombia.”The study was led by first and corresponding author Juan Carlos Rivillas from the Department of Epidemiology and Biostatistics, MRC Centre for Environment and Health, School of Public Health, Imperial College London, United Kingdom. Experiences during childhood can shape health for decades. Adverse childhood experiences (ACEs), such as emotional abuse, domestic violence, food insecurity, poor health, and forced displacement, have long been linked to chronic disease. However, less is known about how these early-life hardships may influence biological aging itself. In this study, researchers examined whether childhood adversity is associated with cardiometabolic disease and accelerated biological aging among older adults in Colombia.The investigators analyzed data from 3,385 adults aged 60 years and older who participated in the nationally representative SABE-Colombia study. Five forms of childhood adversity experienced before age 15 were evaluated: emotional abuse, domestic violence, poor childhood health, food scarcity, and forced migration related to Colombia’s armed conflict. Biological aging was estimated using the Klemera-Doubal Method for Biological Age, a biomarker-based measure that compares biological age with chronological age.Full press release - https://aging-us.net/2026/06/18/childhood-adversity-may-leave-lasting-biological-scars-decades-later/DOI - https://doi.org/10.18632/aging.206384Corresponding author - Juan Carlos Rivillas - j.rivillas-garcia20@imperial.ac.ukAbstract video - https://www.youtube.com/watch?v=5w6vgFzjcNQSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206384Keywords - aging, adverse childhood experiences, forced childhood migration, biological ageing, cardiometabolic outcomes, life course epidemiologyTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Each month, we will highlight a paper published in Aging chosen as the “Editors’ Choice.” These selections are handpicked by our editors and accompanied by a brief summary, showcasing research with significant impact and novel insights in aging and age-related diseases.This exploratory randomized controlled trial, titled “Short-term responsiveness of DNA methylation–based aging biomarkers to a multimodal intervention comprising exercise and dietary guidance involving daily consumption of yogurt containing Bifidobacterium longum BB536: an exploratory randomized controlled trial,” investigated whether a 12-week lifestyle intervention combining exercise, dietary guidance, and daily consumption of yogurt containing Bifidobacterium longum BB536 could influence biological aging.The researchers found a significant slowing of the DNA methylation-based pace of aging measure DunedinPACE in overweight men aged 50 and older, suggesting that feasible lifestyle changes may be associated with short-term improvements in selected epigenetic aging biomarkers.DOI - https://doi.org/10.18632/aging.206386Corresponding author - Yukihiro Hishida - yukihiro-hishida639@morinagamilk.co.jpSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206386Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, DNA methylation clock, DunedinPACE, Multicomponent lifestyle intervention, Bifidobacterium longum BB536To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 16, 2026 — A new #research paper was #published in Volume 18 of Aging on May 22, 2026, titled “Systemic cancer risk profile in neovascular age-related macular degeneration: insights into shared aging-related mechanisms from a nationwide population-based study.”The study was led by first author Hyeong Min Kim and corresponding author Hyewon Chung from Konkuk University College of Medicine and Konkuk University Medical Center in Seoul, Republic of Korea.Neovascular age-related macular degeneration (nAMD) is one of the leading causes of severe vision loss in older adults. Although the disease primarily affects the retina, researchers increasingly recognize that it may reflect broader biological processes associated with aging, including chronic inflammation, vascular dysfunction, and immune dysregulation. These same mechanisms have also been implicated in the development of several cancers, raising questions about whether the two conditions may be biologically connected.To explore this possibility, investigators analyzed data from the Korean National Health Insurance Service, one of the world’s largest population-based healthcare databases. The study included 334,091 individuals aged 50 years and older, including 83,742 patients with nAMD and 250,349 matched controls without the disease. Participants were followed for up to 10 years, allowing researchers to evaluate both overall cancer incidence and risks for specific cancer types.The analysis revealed that individuals with nAMD had a modest but statistically significant increase in overall cancer risk compared with matched controls. However, the increased risk was not observed across all cancers. Instead, patients with nAMD showed elevated risks for several specific malignancies, including thyroid, kidney, pancreatic, lung, bladder, and prostate cancers, while no significant associations were found for many other cancer types.Full press release - https://aging-us.net/2026/06/16/common-aging-mechanisms-may-link-vision-loss-disorder-to-increased-risk-of-certain-cancers/DOI - https://doi.org/10.18632/aging.206383Corresponding author - Hyewon Chung - hchung@kuh.ac.krAbstract video - https://www.youtube.com/watch?v=hViOqGLYr1YSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206383Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, neovascular age-related macular degeneration, cancer, population cohort, polygenic risk, shared susceptibilityTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 11, 2026 — A new #meetingreport was #published in Volume 18 of Aging on May 14, 2026, titled “Foundations of Gerophysics.”The report was led by corresponding authors Maximilian Unfried and Brian K. Kennedy from the National University of Singapore. Aging is often studied through biology, genetics, and medicine. Yet despite tremendous advances, many fundamental questions remain unanswered: Why do organisms age at different rates? Why does resilience decline over time? And can the trajectory of aging be predicted before disease develops? Researchers participating in the inaugural Global Conference on Gerophysics explored whether answering these questions may require integrating biology with the quantitative principles of physics.Held in Singapore on March 5–6, 2025, the conference brought together 160 researchers from physics, biology, computation, and medicine and featured 31 speakers from institutions around the world. The meeting focused on developing a predictive and testable science of aging by applying concepts from dynamical systems, thermodynamics, network theory, stochastic processes, and artificial intelligence to biological aging.Full press release - https://aging-us.net/2026/06/11/physics-meets-aging-researchers-lay-the-foundations-of-gerophysics/DOI - https://doi.org/10.18632/aging.206378Corresponding authors - Maximilian Unfried - unfried@nus.edu.sg, and Brian K. Kennedy - bkennedy@nus.edu.sgAbstract video - https://www.youtube.com/watch?v=hgsA8EhjF0USign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206378Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - gerophysics, geroscience, aging biology, longevity, complex systems, theoretical physicsTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 10, 2026 — A new #research paper was #published in Volume 18 of Aging on May 18, 2026, titled “Transcriptional programs diverge in aging mouse and human skeletal muscle.”The study was led by co-first authors Charles D. Hwang and Siti Rahmayanti and corresponding author Indranil Sinha from Brigham and Women’s Hospital, Harvard University. Aging is widely associated with the gradual loss of muscle mass, strength, and physical function. Much of what scientists know about these changes comes from studies in laboratory mice, which are frequently used to investigate the biological mechanisms of aging and to identify potential therapeutic targets. However, an important question remains: how closely do aging-related changes in mouse muscle reflect what actually occurs in humans?To address this question, researchers performed a detailed comparison of gene expression patterns in skeletal muscle from young and old mice and humans. The team analyzed RNA sequencing data from mouse gastrocnemius muscle and compared it with transcriptomic data from healthy young and older adults obtained through the National Institute on Aging’s GESTALT study.The results revealed substantial differences between the two species. Despite both mice and humans experiencing age-related muscle decline, fewer than 5% of significantly altered biological pathways were shared between them. Many of the genetic programs that changed with aging in mice showed little resemblance to those observed in human skeletal muscle.Full press release - https://aging-us.net/2026/06/10/aging-muscle-follows-different-genetic-programs-in-mice-and-humans/DOI - https://doi.org/10.18632/aging.206382Corresponding author - Indranil Sinha - isinha@bwh.harvard.eduAbstract video - https://www.youtube.com/watch?v=CYKh4X1w8H0Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206382Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - hypoxia, angiogenesis, aging, skeletal muscle, regenerationTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Why do some people appear to age faster than others, even when they are the same age? Researchers increasingly believe that chronological age tells only part of the story. Biological age attempts to capture how well the body’s systems are functioning and may provide a more meaningful picture of overall health.A research paper on this topic was published in Volume 18 of Aging titled “Blood biochemical and gut microbiotic neural network models forecasting human biological age.” In the study, Russian researchers explored whether information from routine blood tests and the gut microbiome could be used to estimate biological age.Full blog - https://aging-us.org/2026/06/blood-tests-and-gut-bacteria-may-help-reveal-your-biological-age/DOI - https://doi.org/10.18632/aging.206360Corresponding author - Alexey Moskalev - amoskalev@med.ruAbstract video - https://www.youtube.com/watch?v=wg3YEwXMKWYSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206360Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, biological age, blood biochemistry, gut microbiome, neural networkTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 5, 2026 — A new #review was #published in Volume 18 of Aging on May 15, 2026, titled “Blue period – features of senescence 30 years after beta-galactosidase.”The review was led by first author Chisaka Kuehnemann and corresponding author Christopher D. Wiley from Tufts University.Cellular senescence has emerged as one of the most important biological processes linked to aging and age-related disease. Senescent cells stop dividing in response to stress or damage, yet they remain metabolically active and release a variety of signaling molecules that can influence surrounding tissues. Over the past three decades, evidence has increasingly shown that the accumulation of these cells contributes to chronic inflammation, tissue dysfunction, and many degenerative conditions associated with aging.In this review, the authors examine how the field has evolved since the landmark discovery of senescence-associated beta-galactosidase (SA-β-gal) in 1995. That finding provided one of the first practical methods for identifying senescent cells and helped establish that these cells accumulate in aging tissues. Since then, researchers have identified numerous additional characteristics of senescence and developed new approaches to study their role in health and disease.The review highlights several major features now recognized as hallmarks of senescent cells. These include stable proliferative arrest, increased lysosomal activity, secretion of inflammatory and signaling molecules collectively known as the senescence-associated secretory phenotype (SASP), mitochondrial dysfunction, alterations in nuclear architecture, accumulation of metals and lipofuscin, and enhanced survival despite exposure to cellular stress.Full press release - https://aging-us.net/2026/06/05/thirty-years-after-the-discovery-of-sa-%ce%b2-gal-researchers-revisit-the-hallmarks-of-cellular-senescence/DOI - https://doi.org/10.18632/aging.206380Corresponding author - Christopher D. Wiley - christopher.wiley@tufts.eduAbstract video - https://www.youtube.com/watch?v=lfMPJF6No7MSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206380Keywords - aging, senescence, biomarkers, SASP, cell deathTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 3, 2026 — A new #research paper was #published in Volume 18 of Aging-US on May 15, 2026, titled “Extracellular vesicles released by senescent myoblasts affect recipient cells via miRNA-target interactions.”The study was led by first author Michael Kamal from the Department of Kinesiology at McMaster University and corresponding author Gianni Parise from the same university.As people age, skeletal muscle gradually loses strength, size, and regenerative capacity. Scientists have increasingly linked these changes to cellular senescence—a state in which damaged cells permanently stop dividing but remain metabolically active. These senescent cells release a complex mixture of signaling molecules known as the senescence-associated secretory phenotype (SASP), which can influence neighboring cells and contribute to tissue dysfunction.In this study, the researchers investigated whether extracellular vesicles (EVs)—tiny membrane-bound particles released by cells—play a role in this process. Specifically, they examined EVs released by senescent muscle precursor cells, known as myoblasts, and analyzed the microRNAs (miRNAs) carried within these vesicles.The team found that senescent myoblasts released factors that impaired normal muscle cell development. When healthy muscle cells were exposed to signals from senescent cells, the resulting muscle fibers became significantly smaller and displayed increased expression of genes associated with cellular stress and senescence.Further analysis revealed that EVs released by senescent myoblasts carried a distinct set of miRNAs. The researchers identified 22 significantly altered miRNAs, including several previously linked to cellular senescence, such as miR-34a, miR-34b, miR-34c, and miR-22. The study also identified miR-301a-3p as a potentially novel senescence-associated miRNA.Full press release - https://aging-us.net/2026/06/03/senescent-muscle-cells-send-molecular-messages-that-may-contribute-to-age-related-muscle-decline/DOI - https://doi.org/10.18632/aging.206379Corresponding author - Gianni Parise - pariseg@mcmaster.ca Abstract video - https://www.youtube.com/watch?v=HKBbraYg8ewSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206379Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, cellular senescence, extracellular vesicles, myoblasts, miRNA, multi-omicsTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — May 27, 2026 — A new #research paper was #published in Volume 18 of Aging-US on May 8, 2026, titled “The mediating role of DNA methylation clocks in associations of race, ethnicity, education, income, and occupation with mortality: findings from NHANES 1999-2002.”The study was led by first and corresponding author Hanyang Shen from the Department of Epidemiology and Population Health at Stanford University. In this study, the authors investigated whether DNA methylation aging biomarkers—often called epigenetic aging clocks—may help explain how social inequalities become biologically embedded and contribute to differences in mortality risk. Social factors such as race, ethnicity, educational attainment, household income, and occupation have long been associated with disparities in health outcomes and life expectancy. However, the biological mechanisms linking these social exposures to long-term disease risk and mortality remain incompletely understood.Using nationally representative data from 2,402 adults in the U.S. National Health and Nutrition Examination Survey (NHANES) 1999–2002 linked to mortality follow-up data through 2019, the researchers examined thirteen different DNA methylation biomarkers alongside traditional clinical and behavioral risk factors. The study evaluated whether these epigenetic aging measures mediated associations between social stratification factors and all-cause mortality.The findings showed that several DNA methylation clocks significantly mediated the relationship between social disadvantage and mortality risk. Among all biomarkers examined, GrimAge2 consistently demonstrated the strongest mediation effects, accounting for up to 52% of mortality disparities in some occupational comparisons. DunedinPoAm, a pace-of-aging biomarker, also demonstrated substantial mediation effects across multiple socioeconomic categories.Importantly, the mediation effects observed for several DNA methylation biomarkers frequently exceeded those of traditional clinical risk factors measured in the study, including C-reactive protein and cholesterol-related markers. The results suggest that epigenetic aging measures may capture the cumulative biological effects of multiple social, environmental, behavioral, and physiological stressors simultaneously.“Among all the 13 DNA methylation biomarkers available in NHANES, GrimAge2 consistently exhibited the strongest positive mediation capturing the social disparities on mortality up to 52% (95%CI: 26%-128%), followed by the DunedinPoAm.”Full press release - https://aging-us.net/2026/05/27/dna-methylation-clocks-may-help-explain-how-social-inequality-influences-mortality/DOI - https://doi.org/10.18632/aging.206377Corresponding author - Hanyang Shen - hyshen@stanford.eduAbstract video - https://www.youtube.com/watch?v=XObIyirTJokSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206377Keywords - aging, race and ethnicity, social position, epigenetic aging, mediation analysis, mortality disparitiesTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — May 20, 2026 — A new #editorial was #published in Volume 18 of Aging-US on May 18, 2026, titled “Public health in the age of longevity interventions: from prevention to system-wide resilience.”The editorial was authored by Jochen Mierau from the University of Groningen and Aging-US Editor-in-Chief Marco Demaria from the University of Groningen and European Research Institute for the Biology of Ageing (ERIBA). In this editorial, the authors examine how modern public health systems may need to evolve as aging populations increasingly face chronic disease, frailty, multimorbidity, and progressive loss of function rather than the acute infectious diseases that shaped 20th-century medicine.The authors argue that many of the greatest gains in human lifespan historically came not from advanced medical technologies, but from broad public health interventions such as sanitation, vaccination, improved nutrition, occupational safety, safer housing, and access to education. While these measures remain essential, they suggest that modern aging societies now face a different challenge: extending healthspan alongside lifespan.The editorial highlights how today’s health risks accumulate gradually across the life course through environmental, metabolic, social, and behavioral exposures. Ultra-processed foods, pollution, tobacco, alcohol, sedentary lifestyles, climate-related stressors, and social isolation are described as contributors to accelerated biological aging and increased vulnerability to chronic disease. The authors emphasize that these interconnected exposures cannot be fully addressed through disease-specific treatment alone.“Rather than representing separate or competing domains, these approaches should be viewed as complementary components of a unified strategy to improve population health across aging societies.”A major focus of the article is the growing scientific interest in longevity-directed interventions that target core biological mechanisms of aging. The authors discuss pathways including cellular senescence, chronic inflammation, metabolic dysfunction, and impaired proteostasis, noting that interventions directed at these processes may help delay or modify multiple age-related diseases simultaneously rather than treating each condition individually after it emerges.Importantly, the editorial emphasizes that longevity interventions should not replace either public health or conventional clinical medicine. Instead, the authors propose a coordinated framework operating across the life course. In this model, public health strategies reduce baseline risk and environmental damage, clinical medicine treats established disease, and longevity-focused therapies may help slow biological decline before major pathology becomes clinically apparent. Figure 1 of the paper (page 2) illustrates this proposed multi-layered framework integrating public health, longevity interventions, and disease-specific care across different stages of life.Full press release - https://www.aging-us.com/news-room/extending-healthspan-through-public-health-and-longevity-medicineDOI - https://doi.org/10.18632/aging.206381Corresponding author - Marco Demaria - m.demaria@umcg.nlPaper Preview Video - https://www.youtube.com/watch?v=KSjfmxpHer8To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — May 19, 2026 — A new #research paper was #published in Volume 18 of Aging-US on May 5, 2026, titled “Methylene blue protects hair follicle stem cells from oxidative and metabolic stress to enhance hair regeneration.”The study was led by first author Kavitha Sadashivaiah and corresponding author Kan Cao from the Department of Cell Biology and Molecular Genetics at the University of Maryland, College Park. In this study, the authors investigated how methylene blue (MB), a long-established mitochondrial-targeted antioxidant, affects human hair follicle stem cells (HFSCs) under conditions of oxidative and metabolic stress. Hair follicle stem cells are essential for maintaining hair growth and regeneration, but aging, ultraviolet radiation, oxidative stress, and metabolic dysfunction can impair their regenerative capacity and contribute to hair thinning and scalp aging.Using cultured human HFSCs, the researchers found that methylene blue significantly enhanced stem cell proliferation and viability while reducing intracellular reactive oxygen species (ROS). Importantly, MB also increased activation of β-catenin signaling, a central pathway involved in hair follicle regeneration, stem cell maintenance, and wound repair. Functional scratch-assay experiments further demonstrated that MB accelerated wound closure and regenerative activity in HFSC cultures.The study also explored how methylene blue interacts with other compounds commonly associated with scalp or hair health. While antioxidant vitamins A and C improved oxidative stress scavenging, they unexpectedly reduced MB-induced β-catenin activation when used in combination. In contrast, minoxidil—the widely used hair growth stimulant—worked synergistically with MB to further enhance β-catenin signaling and improve HFSC viability.“Overall, these findings identify methylene blue as a multifunctional therapeutic candidate that reduces oxidative and metabolic stress while supporting HFSC–mediated hair regeneration.”Another major focus of the paper involved glucagon-like peptide-1 receptor agonists (GLP-1 RAs), medications increasingly used for diabetes and weight management. Recent clinical observations have suggested that some patients receiving GLP-1 RA therapy may experience hair thinning or hair loss. The authors demonstrated that increasing GLP-1 RA concentrations caused dose-dependent reductions in HFSC viability in vitro. However, pretreatment with methylene blue substantially protected the stem cells from GLP-1 RA–associated metabolic stress and premature cell death.Beyond stem cell protection, the paper discusses methylene blue’s broader potential role in scalp health. Because MB absorbs ultraviolet radiation and has previously demonstrated protective effects against UV-induced DNA damage in skin cells, the authors propose that it may help shield the scalp microenvironment from oxidative injury while supporting regenerative signaling pathways important for hair maintenance. The study also highlights MB’s possible antimicrobial properties and its potential influence on scalp microbiome balance.Importantly, the authors emphasize that the findings are based on in vitro cellular models and that further in vivo studies will be necessary before clinical applications can be established. Additional research will be required to define appropriate dosing, pharmacokinetics, long-term safety, and therapeutic efficacy in living systems.Overall, this study identifies methylene blue as a potentially multifunctional therapeutic candidate for supporting hair follicle stem cell health under conditions of oxidative, metabolic, and pharmacologic stress. By combining antioxidant activity with activation of regenerative β-catenin signaling, MB may represent a promising future strategy for protecting scalp health, enhancing hair regeneration, and improving the resilience of aging hair follicle stem cells.DOI - https://doi.org/10.18632/aging.206376
Each month, we will highlight a paper published in Aging-US chosen as the “Editors’ Choice.” These selections are handpicked by our editors and accompanied by a brief summary, showcasing research with significant impact and novel insights in aging and age-related diseases.__________In the research paper, titled “Association of epigenetic age acceleration with MRI biomarkers of aging and Alzheimer’s disease neurodegeneration,” researchers investigated whether epigenetic clocks of biological aging are associated with MRI markers of brain aging and Alzheimer’s disease-related neurodegeneration in 1,196 older women. While none of the five epigenetic clocks examined were linked to accelerated overall brain aging, one measure (AgeAccelGrim2) was associated with MRI patterns related to neurodegeneration.The findings suggest this relationship was largely driven by DNA methylation markers linked to smoking history and changes in frontal and temporal brain regions rather than areas typically affected early in Alzheimer’s disease.Overall, the study indicates that epigenetic aging and brain aging may reflect different aspects of the aging process, while highlighting the potential role of smoking-related biological aging in increasing dementia risk.DOI - https://doi.org/10.18632/aging.206369Corresponding author - Linda K. McEvoy - linda.k.mcevoy@kp.orgAbstract video - https://www.youtube.com/watch?v=kZiRjlKnnsISign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206369Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, epigenetic clocks, brain age, biological aging, smoking, frontal lobeTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — May 15, 2026 — A new #review was #published in Volume 18 of Aging-US on May 4, 2026, titled “Cellular senescence: from pathogenic mechanisms to precision anti-aging interventions.”The study was led by first author Jian Deng and corresponding author Dong Yang from the Department of Targeting Therapy and Immunology, Cancer Center, West China Hospital, Sichuan University, Chengdu, Sichuan, China. In this comprehensive review, the authors examine how cellular senescence contributes to aging and age-related disease across multiple organ systems, while also highlighting the emerging complexity and functional diversity of senescent cell populations. Traditionally, senescent cells have been viewed primarily as harmful byproducts of aging, characterized by irreversible cell-cycle arrest and chronic inflammatory signaling. However, growing evidence suggests that some senescent cells also play beneficial physiological roles in tissue repair, embryonic development, and maintenance of tissue homeostasis.The review outlines how senescence develops in major tissues including the liver, lungs, kidneys, heart, adipose tissue, brain, and skin. Across these organs, aging-related cellular dysfunction is driven by a combination of oxidative stress, mitochondrial dysfunction, DNA damage, chronic inflammation, metabolic stress, telomere shortening, and environmental insults such as ultraviolet radiation and pollution. The authors describe how senescent cells accumulate in highly specialized cell populations—including hepatocytes, endothelial cells, fibroblasts, macrophages, astrocytes, and epithelial cells—where they can disrupt normal tissue architecture and promote chronic disease progression.Importantly, the article emphasizes that senescent cells are highly heterogeneous and should not be treated as a uniform population. Depending on the tissue context and biological environment, senescent cells may exert either protective or harmful effects. For example, certain senescent cells may help limit fibrosis or support wound healing, whereas others drive chronic inflammation, metabolic dysfunction, tissue degeneration, and cancer progression. This growing recognition of functional heterogeneity has prompted a major shift in anti-aging research away from indiscriminate elimination of senescent cells toward more selective and precision-based therapeutic strategies.“Based on these insights, this review summarizes the induction mechanisms of cellular senescence and the subsequent evolution of their functional phenotypes across diverse tissues.”Full press release - https://www.aging-us.com/news-room/precision-anti-aging-strategies-aim-to-target-harmful-senescent-cells-while-preserving-beneficial-onesPaper DOI - https://doi.org/10.18632/aging.206375 Corresponding author - Dong Yang – yangdong@wchscu.cnAbstract video - https://www.youtube.com/watch?v=HkJRwF8mp4AKeywords - cellular senescence, aging mechanisms, functional heterogeneity, precision anti-agingTo learn more about the journal, please visit www.Aging-US.com and connect with us on social media at:Bluesky - bsky.app/profile/aging-us.bsky.socialResearchGate - www.researchgate.net/journal/Aging-1945-4589X - twitter.com/AgingJrnlFacebook - www.facebook.com/AgingUS/Instagram - www.instagram.com/agingjrnl/LinkedIn - www.linkedin.com/company/aging/Reddit - www.reddit.com/user/AgingUS/Pinterest - www.pinterest.com/AgingUS/YouTube - www.youtube.com/@Aging-USSpotify - open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Efforts to improve metabolic health through dietary interventions often come with trade-offs. Some approaches that reduce obesity or extend lifespan in laboratory models can also negatively affect other tissues, including bone.One example is sulfur amino acid restriction (SAAR), a diet low in methionine and lacking cysteine that has repeatedly shown strong anti-obesity effects in animal studies. However, despite these promising metabolic benefits, SAAR has also been associated with reduced bone mineral density, weaker bones, and increased marrow fat accumulation.This has led researchers to ask whether the metabolic benefits of SAAR can be separated from its harmful skeletal effects.A new research paper was published in Volume 18 of Aging-US, titled “D, L-Buthionine-(S, R)-sulfoximine recapitulates the anti-obesity effects of sulfur amino acid restriction without the associated deleterious effects on bone in male mice.” The researchers investigated whether those metabolic benefits could be achieved without the same harmful effects on bone. The study was led by first author Naidu B. Ommi and corresponding author Sailendra N. Nichenametla from the Orentreich Foundation for the Advancement of Science Inc., in collaboration with Dwight A. L. Mattocks from the same institution and Mark C. Horowitz from the Yale University School of Medicine.Full blog - https://aging-us.org/2026/05/glutathione-pathway-may-hold-the-key-to-safer-anti-obesity-interventions/Paper DOI - https://doi.org/10.18632/aging.206358Corresponding author - Sailendra N. Nichenametla - snichenametla@orentreich.orgAbstract video - https://www.youtube.com/watch?v=0adFA_b-q1QSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206358Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - bone, aging, methionine, glutathione, redoxTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — May 12, 2026 — A new #research paper was #published in Volume 18 of Aging-US on May 4, 2026, titled “Host immunosenescence compromises Mycobacterium tuberculosis clearance.”The study was led by first author Falak Pahwa and corresponding author Ranjan Kumar Nanda from the International Centre for Genetic Engineering and Biotechnology (ICGEB), New Delhi, India. In this study, the authors investigated how aging alters immune responses during tuberculosis infection and treatment. Tuberculosis remains one of the world’s deadliest infectious diseases, and older adults are particularly vulnerable due to immunosenescence, the gradual decline of immune function that occurs with aging. Despite the growing burden of tuberculosis in aging populations worldwide, most experimental models continue to rely on young adult animals that do not accurately reflect immune aging.Using multiple age groups of C57BL/6 mice, the researchers examined how aging affects the body’s ability to control Mycobacterium tuberculosis during treatment with rifampicin and isoniazid (RIF-INH), two cornerstone anti-tuberculosis drugs. While young and older mice initially showed similar bacterial burden following infection, older mice demonstrated significantly delayed bacterial clearance in the lungs during the early phase of treatment.Importantly, the study identified several age-associated immune abnormalities linked to impaired bacterial clearance. Older mice exhibited chronic inflammatory signaling, altered T cell responses, accumulation of T-follicular cytotoxic (TFC)-like cells, and evidence of mitochondrial dysfunction within immune cells. Proteomic analysis of splenic CD4+CD44+ T cells further revealed dysregulation of mitochondrial proteins involved in cellular metabolism and immune function.“Collectively, these findings suggest that age-associated immune alterations may disrupt immunometabolic pathways, thereby contributing to the delayed Mtb clearance.”The researchers also observed that older mice maintained elevated inflammatory cytokine levels and developed persistent lung inflammation even after treatment had begun. At the same time, key protective immune responses appeared functionally impaired, suggesting that aging may disrupt the balance between inflammation and effective pathogen control. Together, these findings suggest that age-related immunometabolic dysfunction may play a major role in the reduced treatment response observed in older hosts.Notably, the study found that delayed bacterial clearance in older mice did not appear to result primarily from liver toxicity or impaired drug metabolism. Instead, the evidence suggested that age-related immune dysfunction itself was the dominant factor limiting effective bacterial elimination during therapy.The paper further highlights the emerging importance of mitochondrial health in immune cell function during aging. The authors propose that targeting age-associated immunometabolic defects and mitochondrial dysfunction may represent a promising strategy for improving tuberculosis treatment outcomes in elderly populations.Overall, this study provides new insight into why older adults experience poorer tuberculosis outcomes despite receiving standard therapy. As global populations continue to age, understanding how immunosenescence alters infectious disease responses may become increasingly important for the development of more effective treatment strategies and age-adapted therapeutic interventions.DOI - https://doi.org/10.18632/aging.206374Corresponding author - Ranjan Kumar Nanda - ranjan@icgeb.res.inAbstract video - https://www.youtube.com/watch?v=isPD8ZmUjv8Website - https://www.Aging-US.comMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — May 7, 2026 — A new #research paper was #published in Volume 18 of Aging-US on April 24, 2026, titled “The BHARAT study: a multi-modal, multi-omics investigation of aging signatures in the Indian population.”The study was led by first author Suramya Asthana and corresponding author Deepak Kumar Saini from the Indian Institute of Science (IISc). The authors introduce the BHARAT Study (Biomarkers of Healthy Aging, Resilience, Adversity, and Transitions), India’s first large-scale, discovery-driven multi-omics cohort focused on understanding biological aging in the Indian population. The initiative was developed to address a major gap in aging research, as most existing biological age models and aging datasets have been derived primarily from Western populations.The BHARAT study is a multi-center, cross-sectional observational cohort that integrates clinical, molecular, lifestyle, and environmental data from participants across diverse demographic groups in India. The initiative aims to enroll healthy volunteers spanning multiple age groups, with balanced rural-urban and sex representation. Biological samples—including blood, urine, stool, cheek swabs, and hair—will undergo extensive multi-omics profiling, including epigenomics, proteomics, metabolomics, lipidomics, metagenomics, and immune phenotyping.“By generating interoperable, high-resolution data suited for mechanistic modelling and machine learning, BHARAT contributes a resource of global relevance that would be capable of refining universal models of aging biology while revealing novel, population-specific pathways that inform prevention and intervention strategies.”The initiative uses a hub-and-spoke framework centered at the Indian Institute of Science, which serves as the central hub for biobanking, multi-omics analysis, computational integration, and AI-driven modeling. Clinical and community partners across India contribute participant recruitment, clinical assessments, and biological sampling, enabling the study to capture the country’s extraordinary genetic, environmental, dietary, and socioeconomic diversity.A major focus of the study is the development of population-specific biological aging signatures and predictive models tailored to Indian populations. Researchers aim to identify biomarkers associated with resilience, frailty, and age-related decline while also recalibrating biological clocks that may not accurately reflect aging trajectories in non-Western populations. The study further seeks to establish standardized reference datasets and create scalable infrastructure for future longitudinal aging research in India.Importantly, the BHARAT study combines untargeted discovery-based omics technologies with advanced artificial intelligence and machine learning approaches. By integrating molecular data with clinical and lifestyle information, the initiative aims to improve understanding of how biological aging is shaped by genetics, environment, nutrition, infection burden, and social determinants of health.Overall, this study establishes a comprehensive framework for aging research in one of the world’s most diverse populations. By generating large-scale, population-specific biological datasets, the BHARAT initiative may help advance precision aging research, improve risk prediction models, and support the development of more personalized approaches to healthy aging and disease prevention.DOI - https://doi.org/10.18632/aging.206373Corresponding author - Deepak Kumar Saini - deepaksaini@iisc.ac.inAbstract video - https://www.youtube.com/watch?v=qH2AbitDURQWebsite - https://www.Aging-US.comMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — May 5, 2026 — A new #research paper was #published in Volume 18 of Aging-US on April 13, 2026, titled “Cross species activity of TERT human telomerase component.”The study was led by co–first authors Raúl Sánchez-Vázquez and Paula Martínez, with María A. Blasco serving as corresponding author, from the Spanish National Cancer Centre (CNIO), Madrid, Spain. In this study, the researchers explored a key question in aging and regenerative medicine: can the human telomerase protein function effectively in other species commonly used in preclinical research? Telomerase plays a central role in maintaining chromosome integrity by preventing telomere shortening—a process closely linked to cellular aging and disease.To investigate this, the team introduced the human telomerase catalytic subunit (TERT) into primary lung fibroblasts from several mammalian species, including monkey, pig, rabbit, rat, dog, and mouse. They then assessed both biochemical activity and the ability of telomerase to extend telomeres over time.The results revealed a clear distinction between biochemical compatibility and true biological function. In vitro, human TERT was able to form active complexes with telomerase RNA from several species, including monkey, pig, rabbit, and rat. However, this activity did not always translate into effective telomere maintenance in living cells.Notably, only human and non-human primate cells showed progressive telomere lengthening over time. In contrast, other species—even those showing initial enzymatic activity—failed to sustain telomere extension during long-term culture. In some cases, telomeres continued to shorten, suggesting that functional integration of telomerase depends on additional species-specific factors.The study also uncovered important limitations in commonly used animal models. Mouse and canine cells did not support human TERT activity, and in some cases, expression of the human enzyme led to reduced cell viability and signs of cellular stress.“These results reveal that only non-human primate cells support full functional activity of the human telomerase protein in a cellular context, underscoring their suitability as preclinical models for telomerase-based therapeutic strategies.”Importantly, the findings highlight that successful telomerase activity in a test tube does not necessarily reflect what happens inside a living cell. The recruitment, regulation, and function of telomerase depend on a complex network of interacting proteins and cellular processes, many of which differ across species.Overall, this study provides important insight into the challenges of translating telomerase-based therapies from preclinical models to humans. By identifying non-human primates as the most compatible system, the work offers a clearer path forward for developing therapies aimed at treating telomere-related diseases and age-associated conditions.DOI - https://doi.org/10.18632/aging.206372Corresponding author - Maria A. Blasco - mblasco@cnio.esAbstract video - https://www.youtube.com/watch?v=XxjjId5i_WwSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, telomeres, telomeraseTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
On April 25, 2026, the NOVA (Neuroscience of Vitality and Aging) Conference brought together a dynamic and interdisciplinary audience in Boston, MA. With over 600 attendees spanning students, researchers, clinicians, investors, and patient advocates, the event highlighted both the complexity of brain aging and the growing momentum behind efforts to better understand and treat neurodegenerative diseases.In the opening keynote, Dr. Joanne Smikle of the American Brain Foundation emphasized the need to remember the “why” behind this research. She highlighted the power of intentional collaboration and the belief that breakthroughs in one neurological disease may translate to others. Even small monthly contributions as little as $10.00 can collectively drive meaningful progress.Full recap - https://aging-us.org/2026/04/aging-us-supports-the-nova-conference-2026/Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — April 29, 2026 — A new #research paper was #published in Volume 18 of Aging-US on April 10, 2026, titled “Stage-dependent transcriptomic changes in human dermal fibroblast senescence model.”The study was led by first author Michiko Kudo from the University of Tokyo and DHC Corporation Laboratories and corresponding author Shuichi Asakawa from the University of Tokyo. In this work, the researchers took a closer look at how gene expression changes as cells age, focusing on human dermal fibroblasts—a widely used model for studying aging in skin and connective tissues. While cellular senescence is known to play a central role in aging, the timing and progression of molecular changes during this process have remained difficult to define.To explore this, the team developed a stepwise model of replicative senescence, categorizing cells into three stages—young, middle, and old—based on their cumulative number of divisions. This approach allowed them to capture the gradual nature of aging, rather than relying on acute stress models that may overlook early-stage transitions.One of the more interesting findings was that the “middle” stage—often overlooked—is not just a simple midpoint, but a biologically active transition phase. Although gene expression profiles in young and middle cells appeared similar at first glance, a closer look showed that important molecular changes had already begun during this phase.In particular, genes involved in immune and inflammatory responses were activated early, even before cells reached full senescence. This suggests that aging-related inflammation may begin much earlier than previously appreciated, gradually intensifying as cells progress toward the late stage.At the same time, genes responsible for maintaining basic cellular functions—such as protein synthesis, cell structure, and adhesion—showed a progressive decline as aging advanced. Together, these changes suggest a shift in cellular priorities, where stress and inflammatory signals increase while maintenance and repair functions gradually decline.To better understand these patterns, the researchers combined transcriptomic analysis with network and matrix factorization approaches. These methods revealed distinct gene expression programs associated with different stages of aging, including early immune activation, mid-stage extracellular remodeling, and late-stage functional decline.“These findings suggest that immune–inflammatory responses are engaged from early senescence, whereas cell adhesion and maintenance pathways decline progressively.”Importantly, the results point to the middle stage of senescence as a potential window for intervention. Unlike fully senescent cells, which exhibit more stable and potentially irreversible changes, cells in this transitional phase may retain some degree of plasticity, making them more responsive to therapeutic strategies.Overall, this study offers a clearer picture of how aging unfolds at the molecular level. By identifying stage-specific changes in gene expression, the authors provide new insight into the early drivers of cellular senescence and highlight potential targets for delaying or modifying age-related decline.DOI - https://doi.org/10.18632/aging.206371Corresponding author - Shuichi Asakawa - asakawa@g.ecc.u-tokyo.ac.jpAbstract video - https://www.youtube.com/watch?v=DZNfYmj4DW8Website - https://www.Aging-US.comBluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Joan Brock Virginia Health Sciences at Old Dominion University), in collaboration with Jennifer Q. Zhou, Kan Wang, and Ming-lei Guo from the same institution.Full blog - https://aging-us.org/2026/04/p38-mapk-driven-epigenetic-regulation-identified-as-a-key-mechanism-in-lung-fibrosis/Paper DOI - https://doi.org/10.18632/aging.206357Corresponding author - Yan Y Sanders - sandery@odu.eduAbstract video - https://www.youtube.com/watch?v=yP0CwWMUhnYSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206357Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, senescence, fibroblast activation, p38 MAPK, lung fibrosis, H4K16AcTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — April 27, 2026 — A new #hypothesis paper was #published in Volume 18 of Aging-US on April 8, 2026, titled “From Hydra to rotifer and beyond: implications for human aging and delayed senescence.”The study was led by first and corresponding author Michael Bordonaro from the Geisinger College of Health Sciences. In this work, the author explores a bold and testable hypothesis centered on two very different invertebrate models of aging: the freshwater cnidarian Hydra and the rotifer Brachionus manjavacas. Hydra are well known for their remarkable ability to maintain tissue integrity over time through continuous stem cell renewal, effectively avoiding many of the hallmarks of aging under laboratory conditions. In contrast, rotifers represent the opposite end of the biological spectrum, with short lifespans, fixed somatic cell numbers, and a predictable pattern of age-related decline.Building on these contrasts, the paper proposes that introducing Hydra-like gene expression patterns into rotifers could delay senescence and extend healthspan. The hypothesis focuses in particular on conserved molecular pathways, including the transcription factor FoxO, which plays a central role in maintaining stem cell function and cellular resilience. Rather than attempting to recreate full stem cell renewal in rotifers—an organism with a fixed adult cell number—the proposed strategy emphasizes improving cellular maintenance, stress resistance, and proteostasis within existing cells.The paper outlines an iterative experimental framework, beginning with targeted genetic manipulation in rotifers and extending to more complex organisms such as Daphnia and mouse models. This stepwise approach is designed to identify which elements of the Hydra genetic program are truly responsible for its resistance to aging, while also allowing researchers to monitor potential trade-offs, including increased risk of uncontrolled cell growth.“We hypothesize that delayed senescence at the organismal level is possible through recapitulation of Hydra-like patterns of gene expression in rotifers, and that data obtained may help generate hypotheses for somatic interventions and prioritize pathways for mammalian validation in future studies.”Importantly, the author emphasizes that complete elimination of aging is unlikely in complex organisms due to evolutionary and biological constraints. Instead, the goal is more realistic: extending healthspan and delaying the onset of age-related decline. The paper also highlights the importance of balancing potential benefits with risks, particularly the possibility that enhancing cellular renewal pathways could increase susceptibility to neoplasia.Overall, this study presents a conceptual and experimental roadmap for translating insights from simple organisms into strategies that may eventually inform human aging research. By bridging the gap between negligible senescence and rapid aging models, the work provides a fresh perspective on how conserved biological mechanisms might be harnessed to improve health across the lifespan.DOI - https://doi.org/10.18632/aging.206370Corresponding author - Michael Bordonaro - mbordonaro1@geisinger.eduAbstract video - https://www.youtube.com/watch?v=YGzYf3W5jNATo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — April 23, 2026 — A new #research paper was #published in Volume 18 of Aging-US on April 7, 2026, titled “Association of epigenetic age acceleration with MRI biomarkers of aging and Alzheimer’s disease neurodegeneration.”The study was led by first and corresponding author Linda K. McEvoy from the Kaiser Permanente Washington Health Research Institute, in collaboration with a multidisciplinary team of researchers across leading institutions in the United States and Europe.In this study, the researchers examined whether epigenetic measures of biological aging are associated with structural brain changes linked to aging and Alzheimer’s disease. Using data from 1,196 older women enrolled in the Women’s Health Initiative Memory Study, they analyzed five widely used epigenetic clocks and compared them with MRI-derived measures obtained approximately eight years later.The findings revealed a clear distinction between different aspects of aging. None of the epigenetic clocks were associated with accelerated brain aging as measured by the SPARE-BA index, a composite MRI marker of brain age. However, one specific clock—AgeAccelGrim2—was significantly associated with the Alzheimer’s Disease Pattern Similarity Score (AD-PS), a validated imaging biomarker linked to increased risk of dementia.Further analyses suggested that this association was largely driven by epigenetic signatures related to smoking exposure. In particular, a DNA methylation marker reflecting cumulative smoking history was linked to reduced frontal and temporal lobe volumes—regions commonly affected in age-related neurodegeneration. Notably, no significant associations were observed with hippocampal or entorhinal cortex volumes, areas more directly implicated in early Alzheimer’s pathology.“Taken together with prior findings, these results suggest that measures of epigenetic and brain age acceleration capture different aspects of biological aging, and that AgeAccelGrim2 is predictive of neurodegenerative changes associated with smoking that increase risk of dementia.”The study highlights the complexity of biological aging and underscores that not all aging biomarkers reflect the same underlying processes. While epigenetic clocks are increasingly used to estimate biological age, their relationship with brain structure appears to depend on the specific pathways they capture—particularly those influenced by environmental exposures such as smoking.Overall, these findings provide important insight into how molecular measures of aging relate to neuroimaging markers of brain health. By distinguishing between general brain aging and disease-related neurodegeneration, this work helps refine the use of epigenetic biomarkers in aging research and may support future efforts to identify individuals at risk for cognitive decline.DOI - https://doi.org/10.18632/aging.206369Corresponding author - Linda K. McEvoy - linda.k.mcevoy@kp.orgAbstract video - https://www.youtube.com/watch?v=kZiRjlKnnsISign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206369Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, epigenetic clocks, brain age, biological aging, smoking, frontal lobeTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — April 21, 2026 — A new meeting report was published in Volume 18 of Aging-US on April 6, 2026, titled “Toward actionable interventions in human aging (12th ARDD meeting, 2025).”The report was led by corresponding authors Aleksandr Dekan and Daniela Bakula from the University of Copenhagen, Denmark, in collaboration with an international group of researchers spanning academia, industry, and biotechnology.Bringing together experts from across the global aging research community, the 12th ARDD meeting focused on one central goal: moving beyond descriptive studies of aging toward interventions that can actively improve human healthspan. The discussions reflected a clear shift in the field—from understanding the hallmarks of aging to identifying the molecular mechanisms that can be targeted to modify them.Key presentations explored whether biological age can be reversed, highlighting the epigenome as a central regulator of cellular identity. Emerging evidence suggests that partial cellular reprogramming may restore youthful function, while systemic effects observed in preclinical models point to the possibility of organ-wide or even whole-body rejuvenation.The meeting also emphasized the importance of maintaining genomic integrity, with accumulating DNA damage linked to widespread transcriptional stress and age-associated functional decline. At the same time, chronic inflammation, metabolic dysfunction, and cellular senescence were consistently identified as major drivers of aging, reinforcing the need for integrated, multi-targeted therapeutic strategies.Advances in biomarker development were another major focus. Researchers presented new generations of biological aging clocks—ranging from organ-specific proteomic signatures to single-cell and imaging-based approaches—capable of predicting disease risk and monitoring intervention outcomes with increasing precision.In parallel, the integration of artificial intelligence into drug discovery is accelerating the development of novel therapeutics. From generative AI-designed proteins to platform-based identification of new drug targets, these approaches are helping bridge the gap between basic research and clinical application.“This focus is predicated on the hypothesis that aging is not solely a result of stochastic damage accumulation but may be a tractable, modifiable, and potentially reversible biological process amenable to intervention.”Beyond laboratory science, the meeting highlighted the growing importance of translational strategies, regulatory pathways, and investment models in bringing anti-aging therapies to market. A consensus emerged around a “disease-first” approach, in which targeting specific age-related conditions may provide a practical pathway for validating interventions that also influence underlying aging biology.Overall, the ARDD 2025 meeting underscored a major turning point in the field. Aging research is no longer confined to observation—it is increasingly positioned to deliver actionable interventions that could reshape how age-related diseases are prevented and treated.DOI - https://doi.org/10.18632/aging.206368Corresponding authors - Aleksandr Dekan - adekan@sund.ku.dk, and Daniela Bakula - bakula@sund.ku.dkVideo abstract - https://www.youtube.com/watch?v=LntAWVQMKqETo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — April 17, 2026 — A new #research paper was #published in Volume 18 of Aging-US on April 3, 2026, titled “Modeling premature aging in yeast via the expression of Progerin.”The study was led by first author Zachery R. Belak from the University of Saskatchewan, and corresponding author Troy A.A. Harkness from the University of Saskatchewan and the University of Alberta. The team developed a yeast-based model to study premature aging by expressing Progerin, the toxic protein responsible for Hutchinson–Gilford Progeria Syndrome. Using genetically engineered yeast cells, they compared the effects of Progerin with its normal counterpart, Lamin A, to better understand how protein accumulation impacts cellular aging.Their findings show that Progerin expression leads to slower cell growth, increased genome instability, and a significant reduction in chronological lifespan. In contrast, Lamin A did not produce the same harmful effects, highlighting the specific role of Progerin in driving premature aging phenotypes.The study also demonstrates that Progerin accumulates in aging mother cells and remains more stable than Lamin A, suggesting a mechanism by which damaged or toxic proteins are retained during the aging process. These observations mirror what has been reported in human cells, reinforcing the relevance of this model system.“Taken together, expression of Progerin in yeast cells mimics what is observed in human cells, establishing yeast as a powerful model to discover genetic mechanisms driving premature and normal aging.”Overall, the researchers present a practical and efficient model for studying the biological mechanisms underlying premature aging. Their work provides a valuable platform for testing new strategies aimed at reducing toxic protein accumulation and improving cellular health during aging.DOI - https://doi.org/10.18632/aging.206367Corresponding author - Troy AA. Harkness - taharkne@ualberta.caAbstract video - https://www.youtube.com/watch?v=VYQKAJjgIb8Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206367Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, Hutchinson-Gilford Progeria Syndrome, yeast, Progerin, Lamin A, premature agingTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — April 15, 2026 — A new #research paper was #published in Volume 18 of Aging-US on March 30, 2026, titled “A manually curated gene–phenotype catalogue for progeroid syndromes and premature aging.”The study was led by Nuša Likar and Tanja Kunej from the University of Ljubljana, Slovenia. The researchers developed a comprehensive, manually curated catalogue integrating data from 84 scientific publications and the OMIM database. The resulting resource systematically organizes genetic and clinical information on progeroid syndromes, linking 144 genes to 56 syndromes and 160 distinct clinical entities, making it one of the most extensive datasets in this field to date.Using genome–phenome association analysis and protein–protein interaction networks, the study reveals the complex genetic and phenotypic heterogeneity underlying premature aging disorders. The findings highlight strong enrichment in genome maintenance and DNA repair pathways, reinforcing their central role in aging biology.The catalogue also demonstrates how single genes, such as LMNA, can be associated with multiple syndromes, illustrating the pleiotropic nature of genetic variants in progeroid conditions and their broader relevance to human aging mechanisms.“Overall, this study provides a reference resource and framework to support future research into premature aging syndromes and their broader implications for understanding physiological aging.”Overall, the authors present a valuable framework for improving the classification, diagnosis, and study of rare premature aging disorders. Their work not only advances understanding of progeroid syndromes but also offers important insights into the biological processes that drive normal human aging.DOI - https://doi.org/10.18632/aging.206366Corresponding author - Tanja Kunej - tanja.kunej@bf.uni-lj.siAbstract video - https://www.youtube.com/watch?v=Ov6Saz34ZpESign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206366Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, premature aging, progeroid syndromes, DNA repair, LMNA geneTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
0.001) in 509 individuals from the TwinsUK cohort, and both signals replicated in 1,160 individuals from the KORA cohort (p = 7.2e-08 and p = 0.007, respectively). Sensitivity analyses including covariates of other cocoa and coffee metabolites suggest that the effect is specific to theobromine. Our findings indicate that the reported beneficial links between theobromine intake on health and ageing extend to the molecular epigenetic level in humans.Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206344Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, theobromine, epigenetic aging, DNA methylation, metabolomics, nutritionTo learn more about the journal, visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Aging has long been attributed to a range of biological processes, including DNA damage, telomere shortening, and mitochondrial dysfunction. Yet, these frameworks often describe downstream consequences rather than a single unifying cause. Despite decades of research, a central question remains unresolved: what ultimately determines lifespan across species? Increasing attention has turned to cellular energy metabolism—particularly pathways responsible for rapid ATP generation—as a potential key driver. Understanding how these metabolic changes unfold over time, and how they influence survival, regeneration, and disease, remains a major challenge in aging biology.A new research perspective published in Volume 18 of Aging-US introduces a unifying concept in aging biology, titled “A decline in glycolytic ATP production is the fundamental mechanism limiting lifespan; species with an optimal rate of decline over time survived.”Full blog - https://aging-us.org/2026/04/decline-in-glycolytic-atp-production-proposed-as-a-fundamental-mechanism-limiting-lifespan/Paper DOI - https://doi.org/10.18632/aging.206356Corresponding author - Akihiko Taguchi - taguchi@fbri.orgAbstract video - https://www.youtube.com/watch?v=rA23radaoqISign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206356Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - hypothesis, aging, glycolytic ATP production, lifespan, Heterocephalus glaberTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Each month, we will highlight a paper published in Aging-US chosen as the “Editors’ Choice.” These selections are handpicked by our editors and accompanied by a brief summary, showcasing research with significant impact and novel insights in aging and age-related diseases._____In this study, titled “Plant-based dietary patterns are associated with slower epigenetic aging,” the researchers examined whether plant-based dietary patterns are linked to biological aging in large, diverse U.S. populations. Using data from the Atherosclerosis Risk in Communities (ARIC) Study and National Health and Nutrition Examination Survey (NHANES), they analyzed several versions of plant-based diet scores that reflect higher intake of plant foods and lower intake of animal products, as well as distinctions between healthy and less healthy plant-based foods. They then compared these dietary patterns with DNA methylation-based “epigenetic clocks,” which estimate biological age, including GrimAge2, PhenoAge, and HannumAge.The results showed that greater adherence to overall plant-based diets, provegetarian diets, and especially healthy plant-based diets was consistently associated with slower epigenetic aging, meaning participants appeared biologically younger than their chronological age. In contrast, diets higher in less healthy plant-based foods did not show the same benefits.The findings suggest that diets emphasizing whole plant foods and limiting animal products may help slow biological aging at the molecular level.DOI - https://doi.org/10.18632/aging.206362Corresponding author - Hyunju Kim - hyunjuk1@uw.eduAbstract video - https://www.youtube.com/watch?v=FcJ7oEZ-KFkSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206362Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, plant-based diets, DNA methylation, epigenetic aging, all-cause mortality, middle-aged adultsTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — April 9, 2026 — A new #research paper was #published in Volume 18 of Aging-US on March 27, 2026, titled “ATF5 is required for the maintenance of mitochondrial homeostasis and skeletal muscle health during aging.”Led by first author Victoria C. Sanfrancesco and corresponding author David A. Hood, both from the Muscle Health Research Centre, School of Kinesiology and Health Science, York University, Toronto, Ontario, Canada, the study investigated the role of activating transcription factor 5 (ATF5) in regulating mitochondrial quality control and skeletal muscle function during aging.Using young and aged mouse models with and without ATF5 expression, the researchers examined how this transcription factor contributes to mitochondrial homeostasis, protein turnover, and stress response pathways. The analysis focused on key mechanisms such as the integrated stress response (ISR) and mitochondrial unfolded protein response (UPRmt), which are essential for maintaining mitochondrial integrity.The authors found that ATF5 plays a critical role in coordinating mitochondrial quality control and adaptive stress signaling in skeletal muscle. Notably, the absence of ATF5 prevented the typical age-related decline in muscle mass but resulted in increased muscle fatigability and elevated mitochondrial reactive oxygen species (ROS) production. Additionally, the loss of ATF5 disrupted normal stress-response signaling and altered protein degradation pathways, highlighting its importance in maintaining muscle function with age.“Collectively, these results suggest that ATF5 functions to maintain mitochondrial quality control and muscle endurance at the expense of muscle mass, and its absence attenuates the normal compensatory stress response to contractile activity with age.”The authors conclude that while ATF5 contributes to preserving mitochondrial function and endurance capacity, its role in regulating muscle mass and stress adaptation is complex. Further studies are needed to clarify how modulation of ATF5 and related pathways could be leveraged to improve muscle health and mitigate age-related decline in mitochondrial function and physical performance.DOI - https://doi.org/10.18632/aging.206365Corresponding author - David A. Hood - dhood@yorku.caAbstract video - https://www.youtube.com/watch?v=u2OeppqIPN4Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206365Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, skeletal muscle, ATF5, mitochondria, stress responseTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — April 7, 2026 — A new #research paper was #published in Volume 18 of Aging-US on March 26, 2026, titled “Effects of intravenous furosemide plus small-volume hypertonic saline solutions on inflammatory, remodelling markers and epigenetics signatures of patients with congestive acute decompensated heart failure (ADHF).”Led by first author Mario Daidone from University Hospital, Policlinico, Paolo Giaccone, and the University of Palermo, with corresponding author Antonino Tuttolomondo from University Hospital, Policlinico, Paolo Giaccone, and University of Palermo, the randomized trial compared i.v. furosemide plus small-volume hypertonic saline solution (HSS) with i.v. furosemide alone in patients with acute decompensated heart failure due to reduced ejection fraction. The study enrolled 200 subjects, randomly assigning 107 to furosemide plus HSS and 93 to furosemide alone.The authors found that patients treated with i.v. furosemide plus HSS showed lower increases in inflammatory and remodeling biomarkers after saline load, including IL-6, hsTnT, sST2, galectin-3, and NT-proBNP, and the intervention was associated with reduced miR181b expression compared with furosemide alone. These findings suggest that adding small-volume hypertonic saline to loop diuretic therapy may influence both circulating biomarkers and miRNA-related epigenetic signatures in acute heart failure.“Nevertheless, the possible effects of the i.v. furosemide + HSS treatment on natriuretic and inflammatory markers of heart failure deserve further confirmation, whereas the effects of this type of treatment on epigenetic signatures of pathologic mechanisms involved in the left ventricular dysfunction involved in AHF pathogenesis seem to be still not studied.”The authors note that this was a randomized trial in a specific ADHF population, so additional studies will be needed to confirm the durability of the biomarker changes, define the optimal patient groups, and determine whether these molecular effects translate into improved clinical outcomes. Future work may also clarify how the saline strategy interacts with cardiac remodeling and miRNA regulation in larger and more diverse heart failure cohorts.DOI - https://doi.org/10.18632/aging.206364Corresponding author - Antonino Tuttolomondo - bruno.tuttolomondo@unipa.itAbstract video - https://www.youtube.com/watch?v=EG65XlcDJ3USign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206364Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, heart failure, acute decompensated heart failure, furosemide, hypertonic saline solutionTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — April 2, 2026 — A new #research paper was #published in Volume 18 of Aging-US on March 24, 2026, titled “Age-specific relationship between the modulation of brain dynamics in response to task demands and bimanual performance.”Led by first author Sara Magalhães Ferreira from Hasselt University, with corresponding author Koen Cuypers from Hasselt University and KU Leuven, the study examined how age affects BOLD variability and its modulation with task demands during a bimanual task. The authors used fMRI in 22 younger and 23 older healthy adults who performed three increasingly complex task conditions.The authors found that older adults showed higher BOLD variability in cerebellar lobule VIIIb and greater modulation across task conditions in sensorimotor and cerebellar regions. Modulation of BOLD variability predicted performance in an age- and region-dependent manner: in younger adults, reduced modulation in sensorimotor and visuospatial areas correlated with better performance, whereas in older adults, increased modulation in the inferior and superior parietal lobules was linked to higher performance. Across groups, better outcomes were associated with greater modulation in the middle occipital gyrus but lower modulation in cerebellar Crus I. “In sum, this study highlights the potential role of BOLD variability modulation in shaping bimanual performance during aging.”The authors note that, while the age-related differences in BOLD dynamics were clear, they did not find robust evidence supporting a brain-behavior relationship in bimanual performance, which limits how directly the neural findings can be interpreted behaviorally. They recommend future work using multimodal imaging, longitudinal designs, and studies that examine both cognitive and motor domains within the same participants to determine whether variability modulation reflects aging, experience, intervention, or broader cross-functional signatures of aging.DOI - https://doi.org/10.18632/aging.206363Corresponding author - Koen Cuypers - koen.cuypers@uhasselt.beAbstract video - https://www.youtube.com/watch?v=3TbcGFCZV9sSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206363Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, bimanual coordination, Bimanual Tracking Task, BOLD variability, task modulationTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Inflammation is a double-edged sword. It defends the body against infection and injury, yet when it becomes chronic, it can accelerate aging and fuel the very diseases that shorten human life. For decades, scientists have observed that people with higher levels of inflammatory markers like interleukin-6 (IL6) and C-reactive protein (CRP) tend to have shorter lifespans. But the critical question has always been: does inflammation cause mortality, or does it merely reflect underlying disease?A research paper, titled “Causal effects of inflammation on long-term mortality: A mendelian randomization study” was published in Volume 18 of Aging-US by an international team of researchers, provides a definitive answer by using a powerful genetic technique to untangle cause from effect.The team’s investigation demonstrates that the IL6 inflammatory pathway has a direct causal impact on human survival—but with a surprising twist: two components of the same pathway pull in opposite directions.Full blog - https://aging-us.org/2026/04/il6-and-il6r-opposing-forces-of-inflammation-that-shape-human-survival/DOI - https://doi.org/10.18632/aging.206352Corresponding author - Eliano P. Navarese - elianonavarese@gmail.comAbstract video - https://www.youtube.com/watch?v=Br1A0jgU-4MSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206352Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, mendelian randomization, inflammatory biomarkers, mortality, cardiovascular diseaseTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — March 31, 2026 — A new #research paper was #published in Volume 18 of Aging-US on March 20, 2026, titled “Plant-based dietary patterns are associated with slower epigenetic aging.”Led by first and corresponding author Hyunju Kim from the Department of Epidemiology and the Cardiovascular Health Research Unit, Department of Medicine, University of Washington, the study examined whether four plant-based diet indices — overall PDI, provegetarian diet, healthy PDI, and unhealthy PDI — were associated with DNA methylation-based measures of epigenetic aging. The authors analyzed data from the Atherosclerosis Risk in Communities (ARIC) Study (n = 2,810) and the National Health and Nutrition Examination Survey (NHANES, n = 2,056), and assessed associations with GrimAge2, HannumAge, and PhenoAge. The researchers found that each standard deviation higher in the overall PDI, provegetarian diet, and healthy PDI was associated with decelerated GrimAge2, while higher overall PDI and provegetarian diet were also associated with decelerated PhenoAge and HannumAge. By contrast, unhealthy PDI was not significantly associated with epigenetic aging. The findings suggest that plant-rich dietary patterns, especially those emphasizing healthier plant foods, may be linked to slower biological aging in largely non-vegetarian populations.“No significant association was observed for unhealthy PDI and any of the DNA methylation-based aging.”The authors note that these are observational data and do not establish causality. They call for longitudinal and interventional studies to determine whether sustained adherence to healthy plant-based dietary patterns can directly influence epigenetic aging and related health outcomes over time.DOI - https://doi.org/10.18632/aging.206362Corresponding author - Hyunju Kim - hyunjuk1@uw.eduAbstract video - https://www.youtube.com/watch?v=FcJ7oEZ-KFkSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206362Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, plant-based diets, DNA methylation, epigenetic aging, all-cause mortality, middle-aged adultsTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — March 25, 2026 — A new #review was #published in Volume 18 of Aging-US on March 18, 2026, titled “What are the effects of exergames on the mood states of older people? A systematic review of experimental studies, impacts on mental health and recommendations.”Led by Camile de Bem Gaspar and Whyllerton Mayron da Cruz, with corresponding author Alexandro Andrade, all from the Laboratory of Sport and Exercise Psychology, Human Movement Sciences Graduate Program, College of Health and Sport Science of the Santa Catarina State University (UDESC) in Florianópolis, Brazil, the review examined whether exergames can influence mood in older adults. The authors followed systematic review and meta-analysis methods, screened 651 studies, and found nine that met the inclusion criteria, representing 325 participants aged 61 to 78.9 years.The review found that exergames were associated with better mood outcomes, including reductions in tension, anger, fatigue, confusion, and depressive symptoms, while also promoting engagement, immersion, and socialization. In the studies that measured mood more broadly, participants described exergames as improving well-being and emotional state, and no included study reported worsened mood after participation.“The results indicate that the practice of exergames had a positive effect on the mood of older adults.”The authors note, however, that the evidence base remains small and heterogeneous, with only nine eligible trials and several different mood measures used across studies. They call for longer-term interventions, larger and more diverse samples, and additional home-based or low-cost exergame studies to determine how durable the benefits are and how best to recommend them for older adults in real-world settings.DOI - https://doi.org/10.18632/aging.206361Corresponding author - Alexandro Andrade - alexandro.andrade.phd@gmail.comAbstract video - https://www.youtube.com/watch?v=mNBh_alqVRISign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206361Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, electronic games, older adults, BRUMS, mental health, physical activityTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — March 23, 2026 — A new #research paper was #published in Volume 18 of Aging-US on March 12, 2026, titled “Blood biochemical and gut microbiotic neural network models forecasting human biological age.”Led by Anastasia A. Kobelyatskaya from the Russian Clinical Research Center for Gerontology, Pirogov Russian National Research Medical University, and the Institute of Biology of Aging and Healthy Longevity Medicine with Preventive Medicine Clinic, Petrovsky Russian Research Centre of Surgery — with corresponding author Alexey Moskalev from the Institute of Biology of Aging and Healthy Longevity Medicine with Preventive Medicine Clinic, Petrovsky Russian Research Centre of Surgery — the study builds a gender-specific biochemical model (seven routine clinical markers, e.g., cystatin-C, IGF-1, DHEAS, plus sex-specific sets) and a microbiota model (45 species measured by full-length 16S sequencing). Both models were trained and tested on the same 637-person dataset and achieved mean absolute errors of around six years and R² values above 0.8.The team emphasised interpretability: they applied SHapley Additive exPlanations (SHAP) to convert each model from a “black box” into a more interpretable tool, showing how individual predictors (for example, DHEAS, cystatin-C, NT-proBNP in the blood model, and species such as Blautia obeum in the microbiota model) shift predicted age in years for a given individual. The biochemical clock yielded a small (clinically accessible) predictor set (7 markers) to ease clinical translation, while the microbiota clock used a 45-species signature and highlighted microbiome taxa whose abundance gradients correlate with predicted microbiotic age.“As the proposed models possess both global and local explainability, they hold future potential for application in monitoring the effectiveness of various interventions in clinical trials.”The authors note limitations and next steps: the cohort was restricted to a Caucasian population, and the microbiota model requires sequencing resources that may limit immediate clinical rollout. They call for external validation in larger, ethnically diverse cohorts, prospective testing to link model predictions to health outcomes, and application of the explainable models to monitor responses in intervention trials (for example, lifestyle, diet, or drug studies) where a change in predicted biological age would be an early, interpretable signal of benefit.DOI - https://doi.org/10.18632/aging.206360Corresponding author - Alexey Moskalev - amoskalev@med.ruAbstract video - https://www.youtube.com/watch?v=wg3YEwXMKWYSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206360Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, biological age, blood biochemistry, gut microbiome, neural networkTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Aging Series - https://www.aging-us.com/longevityAbout Dr. Yuan Zhao - https://www.qmul.ac.uk/sbbs/staff/yuan-zhao.htmlAbstract video - https://www.youtube.com/watch?v=d4TSI4Ot3yMAbstractAging (senescence) is characterized by development of diverse senescent pathologies and diseases, leading eventually to death. The major diseases of aging, including cardiovascular disease, cancer and chronic obstructive pulmonary disease (COPD), are multifactorial disorders, resulting from complex interactions between multiple etiologies. Here we propose a general account of how different determinants of aging can interact to generate late-life disease. This account, initially drawn from studies of the nematode Caenorhabditis elegans, depicts senescence as the product of a two-stage process. The first stage involves the diverse causes of disease prior to aging, that cause disruption of normal biological function. These include infection, mechanical injury and mutation (somatic and inherited). Second, etiologies largely confined to aging: deleterious, late-life consequences of evolved wild-type gene action, including antagonistic pleiotropy. Prior to aging, diverse insults lead to accumulation of various forms of injury that is largely contained, preventing progression to major pathology. In later life, wild-type gene action causes loss of containment of latent disruptions, which form foci for pathology development. Pathologies discussed here include osteoarthritis, cancer, late-life recrudescence of infection, and consequences of late-acting deleterious mutations. Such latent injury foci are analogous to seeds which in later life, in the context of programmatic senescent changes, germinate and develop into disease.Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206339Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, C. elegans, disease, hyperfunction, multifactorial modelTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — March 18, 2026 — A new #editorial was #published in Volume 18 of Aging-US on March 10, 2026, titled “Healthy life extension: Geroscience’s north star.”Led by David A. Barzilai — who is affiliated with Geneva College of Longevity Science, Healthspan Coaching LLC (Barzilai Longevity Consulting), and Harvard Medical School — the editorial pays tribute to the late Mikhail Blagosklonny and states that geroscience should adopt healthy life extension (measured as health-adjusted survival such as HALE and QALYs) as its primary objective rather than treating lifespan and healthspan as competing goals. Dr. Barzilai urges clearer outcome priorities, disciplined evidence in mammals, and coordinated investment that matches the field’s potential to delay multimorbidity and extend high-quality years of life.The piece reviews data showing that increases in life expectancy have outpaced gains in healthy life expectancy and summarizes calls to measure success by health-adjusted longevity rather than biomarkers alone. It highlights examples where targeting conserved aging pathways produced replicable lifespan gains in mammals (for example, rapamycin in mice) and notes early human-facing signals (for example, mTOR inhibition improving influenza vaccine responses in older adults) that illustrate how aging-biology interventions can be clinically legible on shorter timelines. The editorial also frames the practical challenge: while lifespan evidence is ideal, human trials must use rigorous, meaningful endpoints that map to delayed multimorbidity, preserved function, and resilience. “Geroscience is for healthy life extension. We should stop pretending that lifespan and healthspan compete.”Dr. Barzilai calls for a “moonshot”-level commitment to aging biology that includes larger, better-funded basic programs, clinical trials with health-adjusted survival endpoints, and translational pipelines able to move robust mammalian lifespan findings toward human studies. He stresses the need for replicable mammalian lifespan data paired with human endpoints that reflect quality of life and independence. The editorial closes with a direct pledge in honor of Dr. Blagosklonny’s legacy, in part to make healthy life extension the field’s north star and measure success in years worth living.DOI - https://doi.org/10.18632/aging.206359Corresponding author - David A. Barzilai - d.barzilai@gcls.studyIntro video - https://www.youtube.com/watch?v=_MwFvDg7EjwSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206359Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, geroscience, longevity, healthspan, longevity medicine, healthy life extensionTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
The aging of an organism is reflected not only in the function of its organs but also in the molecular signatures written into its cells. For years, scientists have cataloged the changes in protein-coding genes and various non-coding RNAs that occur as we grow older. However, one class of molecules—circular RNAs originating from the genome of our cellular power plants, the mitochondria—has remained largely unexplored.A new research paper, titled “Aging-associated mitochondrial circular RNAs” published in Volume 18 of Aging-US by a multi-institutional team of researchers, provides the first detailed profile of these molecules and reveals a surprising link to cellular energy metabolism. The team’s investigation demonstrates that a specific mitochondrial circular RNA, circMT-RNR2, is depleted in older individuals and plays a direct role in regulating the TCA cycle, the engine of cellular energy production.Full blog - https://aging-us.org/2026/03/mitochondrial-circular-rnas-new-players-in-human-aging/Paper DOI - https://doi.org/10.18632/aging.206354Corresponding authors - Je-Hyun Yoon - jehyun-yoon@ou.edu, and Young-Kook Kim - ykk@jnu.ac.krAbstract video - https://www.youtube.com/watch?v=f8uZ6_tcOHwSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206354Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, circular RNA, MT-RNR2, GRSF1, TCA cycleTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Cancer), is pleased to announce its participation as an exhibitor at the American Association for Cancer Research (AACR) Annual Meeting 2026. The meeting will take place April 17–22, 2026, at the San Diego Convention Center in San Diego, CA.Conference attendees are warmly invited to visit Booth 3641 to meet members of the Impact Journals team, discover notable recent publications, and discuss opportunities for collaboration.The mission of Impact Journals is to maximize research impact through insightful peer review, eliminate borders between specialties by linking different fields of oncology and biomedical science, and foster the application of both basic and clinical science. This mission is grounded in a strong commitment to ethical standards and scientific integrity. At Impact Journals, evolving digital technologies, tools, and ideas are continually integrated into a robust scientific integrity process.The AACR Annual Meeting serves as a focal point for the global cancer research community, bringing together scientists, clinicians, healthcare professionals, survivors, patients, and advocates to share the latest advances in cancer science and medicine. From population science and prevention to cancer biology, translational and clinical studies, survivorship, and advocacy, the AACR Annual Meeting highlights the work of leading researchers from institutions around the world.To learn more about Impact Journals, please visit impactjournals.com.For media inquiries, email media@impactjournals.com.
BUFFALO, NY — March 13, 2026 — A new #research paper was #published in Volume 18 of Aging-US on March 2, 2026, titled “D, L-Buthionine-(S, R)-sulfoximine recapitulates the anti-obesity effects of sulfur amino acid restriction without the associated deleterious effects on bone in male mice.”Led by Naidu B. Ommi from the Orentreich Foundation for the Advancement of Science — with corresponding author Sailendra N. Nichenametla from the same institution — the study tests whether the glutathione (GSH)-lowering compound D, L-buthionine-(S, R)-sulfoximine (BSO) reproduces the anti-obesity effects of sulfur amino acid restriction (SAAR) without causing the bone loss seen with SAAR diets. Using diet-induced obese male C57BL6/NTac mice fed high-fat diets, the authors compared: a control methionine-replete diet, a SAAR diet (low methionine, no cysteine), SAAR plus the GSH precursor N-acetylcysteine (NAC), and control diet plus BSO in drinking water. Using body-composition, micro-CT, histomorphometry, and biomechanical testing, the team confirmed prior work that SAAR reduces body fat but also lowers trabecular and cortical bone mineral density, increases marrow adiposity, reduces osteoblast numbers, and weakens bone biomechanical strength. Crucially, while NAC supplementation reversed the bone defects of SAAR (implicating cysteine/glutathione restriction in bone loss), BSO reproduced the lean, anti-obesity phenotype without producing the deleterious bone effects observed in SAAR mice. In short, BSO recapitulated the anti-obesity benefits of SAAR without causing the same bone loss — a finding with potential relevance to developing anti-obesity strategies that avoid skeletal harm.“Despite its anti-obesity effects, BSO did not exert any detrimental effects on bones.”The authors emphasize next steps and caveats. They call for mechanistic studies to define how GSH lowering drives fat loss yet spares bone under BSO treatment, investigations of age-at-onset, tissue-specific, and sex-specific effects, and long-term safety studies to assess off-target or delayed adverse effects of BSO before any clinical development. The paper frames BSO as a promising tool compound to dissect the beneficial versus deleterious axes of sulfur amino acid biology, but not yet as a human therapy without further preclinical evaluation.DOI - https://doi.org/10.18632/aging.206358Corresponding author - Sailendra N. Nichenametla - snichenametla@orentreich.orgAbstract video - https://www.youtube.com/watch?v=0adFA_b-q1QSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206358Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - bone, aging, methionine, glutathione, redoxTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Joan Brock Virginia Health Sciences at Old Dominion University) — the study examines how the stress-activated kinase p38 MAPK contributes to persistent profibrotic gene expression in replicative (passage-driven) senescence of human lung fibroblasts and in primary fibroblasts from patients with idiopathic pulmonary fibrosis (IPF). Using IMR90 lung fibroblasts at low and high population-doubling levels and primary IPF fibroblasts, the authors show that TGF-β1 upregulates profibrotic genes (α-SMA and Col3A1) in both young and near-senescent cells, but that high-PDL (near-senescent/senescent) fibroblasts exhibit a delayed but sustained p38 MAPK response to TGF-β1. Pharmacological inhibition of p38 MAPK (SB202190) blunted profibrotic transcription and reduced H4K16 acetylation (H4K16ac) enrichment at α-SMA and Col3A1 promoters, indicating an epigenetic mechanism linking p38 signaling to fibrotic gene activation. “These findings suggest that a p38 MAPK–dependent epigenetic mechanism is involved in fibroblast activation, supporting the therapeutic potential of p38 MAPK inhibition for treating age-related fibrotic diseases such as IPF.”The authors place these molecular results in a clinical context: persistent fibroblast activation and senescence are features of IPF and other age-associated fibrotic disorders, and the data here support targeting p38 MAPK to interrupt an epigenetically reinforced profibrotic program. The study used multiple readouts (western blot, RT-qPCR, ChIP for H4K16ac) and included primary IPF cells to strengthen translational relevance, while also noting that further work is required to test safety and efficacy in vivo.The paper outlines clear next steps: determine the upstream triggers that sustain p38 signaling in near-senescent fibroblasts, map the chromatin-level events downstream of p38 that maintain H4K16ac at profibrotic promoters, and evaluate p38 inhibition in animal models of age-related pulmonary fibrosis. The authors also recommend exploring whether epigenetic modulators that reverse H4K16ac enrichment can synergize with kinase inhibition to restore repair capacity without impairing normal tissue healing.DOI - https://doi.org/10.18632/aging.206357Corresponding author - Yan Y Sanders - sandery@odu.eduAbstract video - https://www.youtube.com/watch?v=yP0CwWMUhnYSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206357Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, senescence, fibroblast activation, p38 MAPK, lung fibrosis, H4K16AcTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Biomarkers of aging help researchers understand how diseases influence the body over time. However, most current biomarkers rely on measurements from mixed cell populations, making it difficult to distinguish between changes caused by shifts in cell types and aging processes occurring within individual cells.In this study, titled “Single-cell transcriptomics reveal intrinsic and systemic T cell aging in COVID-19 and HIV” and published in Volume 18 of Aging-US, researchers used single-cell RNA sequencing to analyze aging-related changes in human T cells. They developed Tictock, a single-cell transcriptomic clock that predicts both cellular age and T cell type across six human T cell subsets.Applying this tool, the researchers found that acute COVID-19 was associated with increased proportions of CD8⁺ cytotoxic T cells, while T cell composition remained relatively stable in individuals with HIV receiving antiretroviral therapy (HIV+ART). Despite these differences, both conditions showed signs of accelerated transcriptomic aging, particularly in naïve CD8⁺ T cells.Further analysis identified shared aging-related genes and biological pathways linked to ribosomal components and TNF receptor binding. These findings demonstrate how single-cell transcriptomic biomarkers can help separate systemic immune changes from cell-intrinsic aging processes, providing new tools to measure immune aging in disease.DOI - https://doi.org/10.18632/aging.206353Corresponding author - Eric Verdin - EVerdin@buckinstitute.orgAbstract video - https://www.youtube.com/watch?v=_r3AF7OrgKYSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206353Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, transcriptomic clock, aging biomarkers, systemic aging, intrinsic agingTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Aging reshapes the immune system in two fundamental ways: it alters the proportions of different immune cell types circulating in the blood, and it induces molecular changes within each individual cell. For years, researchers have struggled to disentangle these two intertwined processes using standard “bulk” measurements, which average signals across millions of cells and obscure what is happening at the single-cell level.A new research paper, titled “Single-cell transcriptomics reveal intrinsic and systemic T cell aging in COVID-19 and HIV” published in Volume 18 of Aging-US by researchers at the Buck Institute for Research on Aging in California, the University of Southern California, and the University of Copenhagen, introduces an innovative solution. The team of Alan Tomusiak, Sierra Lore, Morten Scheibye-Knudsen, and corresponding author Eric Verdin, developed a novel tool called Tictock (T immune cell transcriptomic clock) that uses single-cell RNA sequencing to separately measure systemic and cell-intrinsic components of immune aging, and then applied it to understand how COVID-19 and HIV affect T cells.Full blog - https://aging-us.org/2026/03/tictock-a-single-cell-clock-measures-immune-aging-in-viral-infections/Paper DOI - https://doi.org/10.18632/aging.206353Corresponding author - Eric Verdin - EVerdin@buckinstitute.orgAbstract video - https://www.youtube.com/watch?v=_r3AF7OrgKYSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206353Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, transcriptomic clock, aging biomarkers, systemic aging, intrinsic agingTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — March 3, 2026 — A new #research perspective was #published in Volume 18 of Aging-US on February 24, 2026, titled “A decline in glycolytic ATP production is the fundamental mechanism limiting lifespan; species with an optimal rate of decline over time survived.”Led by Akihiko Taguchi — who is also the corresponding author and is affiliated with the Department of Regenerative Medicine Research, Foundation for Biomedical Research and Innovation at Kobe — the perspective advances a unifying conceptual framework in which a programmed or selected decline in glycolytic ATP production over the lifespan underlies aging phenotypes across species. The authors argue that glycolysis supplies the rapid ATP required for cell division and DNA/mitochondrial repair, and that a progressive reduction in glycolytic ATP with age can explain reduced cell proliferation, impaired repair, and other hallmark features of aging. “The simple explanation is that only species that happened to have an optimal rate of reduction in glycolytic ATP production over time were selected and survived through generational changes.”The perspective synthesizes evidence from comparative biology, cellular metabolism, and translational studies to link glycolytic decline with lifespan variation among species — for example, contrasting short-lived rodents with long-lived species such as the naked mole rat, which maintain high glycolytic flux in low-oxygen niches. The authors also highlight mechanisms connecting glycolysis to mitophagy, telomere dynamics, and proteostasis, arguing that maintaining glycolytic ATP supports repair processes while a shift toward oxidative metabolism improves energy efficiency under resource limitation but reduces rapid-repair capacity.The authors propose several concrete next steps to test the hypothesis. These include in vivo and in vitro interventions that modulate glycolysis (for example, gene transfer of glycolysis-related enzymes or pharmacologic activators such as terazosin), longitudinal measurements of glycolytic ATP production across aging cohorts, and comparative studies across species with differing lifespans to define the “optimal rate” of decline. They also suggest mechanistic studies of gap-junction–mediated metabolic coupling (for example, between hematopoietic stem cells and endothelium) and experiments to determine whether restoring glycolytic flux can rescue age-related deficits in DNA repair and tissue regeneration.While the perspective offers a coherent conceptual model, the authors are explicit about limitations and caution: the idea is currently a hypothesis that requires experimental validation, and the evolutionary rationale (selection for an optimal rate of glycolytic decline) must be tested by comparative and mechanistic work. Translation to human rejuvenation therapies — whether via stem-cell approaches, metabolic activators, or gene transfer — will require careful preclinical studies to evaluate efficacy, safety, and long-term consequences.DOI - https://doi.org/10.18632/aging.206356Corresponding author - Akihiko Taguchi - taguchi@fbri.orgAbstract video - https://www.youtube.com/watch?v=rA23radaoqISubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — February 27, 2026 — A new #research paper was #published in Volume 18 of Aging-US on February 6, 2026, titled “Causal effects of inflammation on long-term mortality: a Mendelian randomization study.”Led by Eliano P. Navarese from Department of Life and Health Sciences, Link Campus University and SIRIO MEDICINE Research Network, Nicolaus Copernicus University, who is also the corresponding author — the study used large-scale Mendelian randomization (MR) to test whether genetically proxied levels of inflammatory biomarkers causally influence long-term all-cause mortality. The analysis combined genome-wide association instruments from more than 750,000 individuals and used FinnGen mortality data (median follow-up 11.7 years) to assess effects on overall survival and major cardiovascular endpoints. Using robust MR methods and multiple sensitivity analyses, the authors report that genetically higher IL6R (soluble IL-6 receptor) levels were associated with reduced all-cause mortality (odds ratio per 1-SD increase: 0.95; 95% CI: 0.91–0.98), and with lower risk of atrial fibrillation, coronary artery disease, stroke, and lung cancer. By contrast, genetically higher IL6 levels were associated with increased mortality (OR 1.05; 95% CI: 1.02–1.08). No significant causal effects were observed for CRP or GDF15, suggesting those markers more likely reflect disease burden than drive it.“These results support IL6R antagonism as a potential strategy for cardiovascular disease prevention.”The authors emphasize that the opposing directions for IL6 and IL6R point to distinct biological mechanisms: IL6 likely promotes chronic pro-inflammatory states that increase cardiovascular risk, while higher circulating IL6R (reflecting altered receptor shedding and signaling) appears to dampen harmful IL6 activity at the vessel wall and myocardium, yielding cardiovascular protection. Sensitivity and cis-MR analyses reinforced the IL6R protective signal and showed minimal evidence of directional pleiotropy. Together, the genetic evidence aligns with clinical trial data for IL6R antagonists in other settings and supports further evaluation of IL6R-targeted strategies for cardiovascular prevention.The paper also notes important limitations and next steps. Analyses were restricted to individuals of European ancestry, so results require replication in other ancestries. Translating genetic evidence into preventive therapies will need careful clinical evaluation, long-term safety assessment, and trials designed for primary prevention in high-risk populations. The authors also call for additional mechanistic work to map how IL6/IL6R modulation alters vascular inflammation and downstream disease processes.DOI - https://doi.org/10.18632/aging.206352Corresponding author - Eliano P. Navarese - elianonavarese@gmail.comAbstract video - https://www.youtube.com/watch?v=Br1A0jgU-4MSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206352Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, mendelian randomization, inflammatory biomarkers, mortality, cardiovascular diseaseTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Aging-US sincerely thanks all reviewers who contributed their expertise and time during 2025.Rigorous and constructive peer review is essential to scientific progress. Through their careful evaluations, our reviewers played a central role in maintaining the scientific quality, integrity, and credibility of the journal.Their efforts also directly support one of the core missions of Aging-US, which is to increase the visibility and impact of high-quality research in the biology of aging and age-related disease.We are deeply grateful for this commitment to excellence and to the aging research community, and we look forward to continued collaboration in the coming year.–Marco DemariaEditor-in-Chief, Aging-US____________To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — February 24, 2026 — A new #research paper was #published in Volume 18 of Aging-US on February 10, 2026, titled “Aging-associated mitochondrial circular RNAs.”Led by first author Hyejin Mun from the University of Oklahoma — with corresponding authors Je-Hyun Yoon from the University of Oklahoma and Young-Kook Kim from Chonnam National University Medical School — the study profiles mitochondrial circular RNAs in Peripheral Blood Mononuclear Cells (PBMCs) from young and old human cohorts and probes how mitochondrial circRNAs and the mitochondrial RNA-binding protein GRSF1 relate to mitochondrial metabolism and cellular senescence.Using total RNA sequencing of PBMCs from young and old donors and complementary cell-based experiments, the authors report that a large fraction of circular RNA junctions originates from the mitochondrial genome, with MT-RNR2 producing the most abundant circular junctions. They show that circMT-RNR2 levels are depleted in older cohorts and in replicative senescence of human fibroblasts, and that the mitochondria-localized RNA-binding protein GRSF1 interacts with both linear and circular MT-RNR2. Loss of GRSF1 reduced circMT-RNR2 levels, decreased mitochondrial TCA intermediates (fumarate and succinate), and accelerated cellular senescence and mitochondrial dysfunction — findings that link mitochondrial circRNAs to mitochondrial energetics and proliferative status in younger cells. “Taken together, our findings demonstrate the existence and possible function of circular MT-RNR2 during human aging and senescence, implicating its role in promoting the TCA cycle.”The authors note key limitations and outline next steps: clarifying the biogenesis mechanism of mitochondrial circular RNAs (including whether trans-splicing contributes), mapping direct interactions between mitochondrial transcripts and metabolic enzymes, and performing mechanistic studies (in vivo and in additional human cohorts) to test how circMT-RNR2 and GRSF1 influence mitochondrial energetics and organismal aging. These follow-ups will determine whether mitochondrial circular RNAs are actionable targets for modulating mitochondrial metabolism or delaying aspects of cellular aging.DOI - https://doi.org/10.18632/aging.206354Corresponding authors - Je-Hyun Yoon - jehyun-yoon@ou.edu, and Young-Kook Kim - ykk@jnu.ac.krAbstract video - https://www.youtube.com/watch?v=f8uZ6_tcOHwSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206354Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, circular RNA, MT-RNR2, GRSF1, TCA cycleTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — February 19, 2026 — A new #research paper was #published in Volume 18 of Aging-US on February 8, 2026, titled “Single-cell transcriptomics reveal intrinsic and systemic T cell aging in COVID-19 and HIV.”In this study, co-first authors Alan Tomusiak from the Buck Institute for Research on Aging and the University of Southern California, and Sierra Lore from the Buck Institute for Research on Aging and the University of Copenhagen, together with corresponding author Eric Verdin from the Buck Institute for Research on Aging, developed a new single-cell transcriptomic clock called T immune cell transcriptomic clock (Tictock) to measure aging in specific immune cells. Immune aging increases susceptibility to infection, cancer, and chronic inflammatory disease. Most aging clocks, used to measure it, rely on bulk measurements from mixed cell populations. As a result, they cannot determine whether age-related signals reflect shifts in cell proportions or true molecular aging within defined immune cells.To address this limitation, the research team used single-cell RNA sequencing, a method that measures gene expression in individual cells. They analyzed nearly two million immune cells from the blood of healthy adults to develop Tictock. This tool integrates automated classification of six canonical T cell subsets with cell-type specific age prediction models. This design enables the separation of systemic aging, reflected by changes in cell proportions, from intrinsic aging, which occurs within individual cells.When the team applied Tictock to patients with acute COVID-19, they found two clear effects. First, COVID-19 altered T cell composition, including significant reductions in naïve CD8 and naïve CD4 T cells. Second, the infection increased the biological age of naïve CD8 T cells. In people living with HIV who were receiving long-term antiretroviral therapy, T cell proportions remained largely stable. However, naïve CD8 T cells still showed signs of accelerated aging.The study also uncovered shared biological pathways linked to immune aging. Many of the genes that predicted age were involved in ribosomes, the structures that help cells produce proteins. The researchers also observed that older immune cells often had shorter average transcript lengths, a feature previously linked to aging. These findings suggest that changes in protein production and gene regulation play an important role in immune decline.“Gene Ontology enrichment of 209 genes shared across six clock models identified common pathways including the cytosolic small ribosomal subunit, TNF receptor binding, and cytosolic ribosome components.”Overall, Tictock was designed to measure relative aging within defined T cell populations rather than overall biological aging. By distinguishing systemic from cell-intrinsic immune aging, it provides a clearer understanding of how viral infections such as COVID-19 and HIV reshape immune function. This approach enables the study of immune aging at single-cell resolution and may support improved immune risk assessment in clinical and research settings.DOI - https://doi.org/10.18632/aging.206353Corresponding author - Eric Verdin - EVerdin@buckinstitute.orgAbstract video - https://www.youtube.com/watch?v=_r3AF7OrgKYSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsTo learn more about the journal, please visit https://www.Aging-US.com.MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — February 18, 2026 — A new #editorial was #published in Volume 18 of Aging-US on February 8, 2026, titled “Polyploidy-induced senescence: Linking development, differentiation, repair, and (possibly) cancer?”In this editorial, Iman M. Al-Naggar of the University of Connecticut School of Medicine, UConn Health, and the University of Connecticut Center on Aging, with George A. Kuchel of the University of Connecticut Center on Aging, examines the biological and clinical significance of polyploidy-induced senescence. The authors discuss how this process may contribute to normal tissue development and long-term repair, while also influencing cancer risk. Their perspective centers on the bladder and outlines how aging-related cellular changes may shape tumor initiation.Aging remains the strongest risk factor for bladder cancer, which is predominantly of urothelial origin. Cellular senescence is defined as a stable growth arrest in which cells remain metabolically active but no longer divide. Polyploidy refers to cells that contain extra copies of their genome. Although polyploidy is frequently associated with cancer, it also occurs in several healthy tissues as part of normal development and adaptation to stress. The editorial highlights increasing evidence that polyploidy and senescence can function together as a coordinated biological program.The authors focus on bladder umbrella cells, which form the barrier between urine and the bloodstream. In mice, these cells naturally become polyploid early in life and display markers of senescence across the lifespan. Rather than representing dysfunction, this state may help maintain tissue architecture, reinforce barrier integrity, and support resistance to environmental stress. In this context, polyploidy-induced senescence may act as a differentiation program that preserves organ structure.“Polyploidization and senescence may be interrelated stress responses, yet they have been studied mostly in isolation.”However, this protective mechanism may become unstable. Polyploidy-induced senescence depends on intact tumor suppressor pathways, including regulators such as p16. If these safeguards are lost through mutation, deletion, or epigenetic silencing, polyploid senescent cells may escape growth arrest. Re-entry into the cell cycle under these conditions may promote chromosomal instability and aneuploidy, increasing the likelihood of malignant transformation. The authors propose that a subset of bladder cancers may arise from polyploid umbrella cells that have bypassed this senescent barrier.The editorial also discusses implications for cancer therapy. Many anticancer treatments induce senescence and polyploidization in tumor cells. Although this approach can initially suppress proliferation, some polyploid cancer cells may later adapt, reduce their ploidy, and resume division, contributing to relapse and treatment resistance. Understanding how polyploidy and senescence interact may therefore inform therapeutic strategies.Overall, the authors emphasize the need to study polyploidy and senescence together rather than in isolation. Integrating ploidy assessment into large-scale mapping efforts of senescent cells may improve insight into aging biology, tumor initiation, and resistance to therapy.DOI: https://doi.org/10.18632/aging.206355Corresponding author: Iman M. Al-Naggar - alnaggar@uchc.eduIntroduction video - https://www.youtube.com/watch?v=3Cl-JoV-j0ohttps://www.Aging-US.com MEDIA@IMPACTJOURNALS.COM
Aging has long been explained in different ways. One traditional view is that it results from the gradual accumulation of molecular damage over time. Another perspective, based on evolutionary theory, suggests that natural selection strongly protects health during youth and reproductive years but becomes less effective later in life. As a result, biological effects that appear in older age may persist because they have little impact on reproduction. Over the past two decades, researchers have also explored the idea that biological programs beneficial early in life may continue operating later in ways that become harmful. Processes that once supported growth, repair, and reproduction may, with time, contribute to chronic disease.A recent review article, titled “Aging as a multifactorial disorder with two stages,” published in Aging-US by researchers at University College London and Queen Mary University of London, brings these different perspectives together into a unified model, to propose a broader explanation of how aging-related diseases develop. The review appears in a special issue honoring the late scientist Misha Blagosklonny, whose theoretical work on programmatic aging significantly influenced the field. Full blog - https://aging-us.org/2026/02/how-aging-leads-to-chronic-disease-a-two-stage-model/Paper DOI - https://doi.org/10.18632/aging.206339Corresponding author - David Gems - david.gems@ucl.ac.ukAbstract video - https://www.youtube.com/watch?v=d4TSI4Ot3yMSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206339Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, C. elegans, disease, hyperfunction, multifactorial modelTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
While maternal health has traditionally been central to research on pregnancy and child development, there is growing recognition that paternal factors also play a role, particularly the father’s age. Several studies have found a modest increase in risk of neurodevelopmental conditions, including autism spectrum disorder, among children born to older fathers. However, the biological mechanisms underlying this association are still not fully understood.One emerging explanation involves epigenetics, chemical modifications that influence how genes are expressed without altering the underlying DNA sequence. Among these is DNA methylation. Earlier studies have suggested that sperm from older men may carry age-related changes in DNA methylation, but few have explored these patterns on a genome-wide scale or focused specifically on regions that are most likely to influence offspring development.The Study: Exploring Age-Dependent Methylation at Imprint Control Regions in Human SpermIn a study, titled “Age-specific DNA methylation alterations in sperm at imprint control regions may contribute to the risk of autism spectrum disorder in offspring,” published in Aging-US and selected as the Editors’ Choice for January, 2026, researchers investigated how DNA methylation patterns in sperm change with age. The study was led by first authors Eugenia Casella and Jana Depovere, with corresponding author Adelheid Soubry from the University of Leuven.Full blog - https://aging-us.org/2026/02/epigenetic-changes-in-sperm-may-explain-association-between-paternal-age-and-autism-risk/Paper DOI - https://doi.org/10.18632/aging.206348Corresponding author - Adelheid Soubry - adelheid.soubry@kuleuven.beVideo abstract - https://www.youtube.com/watch?v=XC3p49Uw49wSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206348Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, epigenome, sperm, 450K, imprinting, autismTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Aging Series - https://www.aging-us.com/longevityAbstractIdiopathic pulmonary fibrosis (IPF) is a condition predominantly affecting the elderly and leading to a decline in lung function. Our study investigates the aging-related mechanisms in IPF using artificial intelligence (AI) approaches. We developed a pathway-aware proteomic aging clock using UK Biobank data and applied it alongside a specialized version of Precious3GPT (ipf-P3GPT) to demonstrate an AI-driven mode of IPF research. The aging clock shows great performance in cross-validation (R2=0.84) and its utility is validated in an independent dataset to show that severe cases of COVID-19 are associated with an increased aging rate. Computational analysis using ipf-P3GPT revealed distinct but overlapping molecular signatures between aging and IPF, suggesting that IPF represents a dysregulation rather than mere acceleration of normal aging processes. Our findings establish novel connections between aging biology and IPF pathogenesis while demonstrating the potential of AI-guided approaches in therapeutic development for age-related diseases.Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206295Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, IPF, generative AI, transformer, proteomicsTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/YouTube - https://www.youtube.com/@Aging-USReddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
When we think of aging, we often picture wrinkles or gray hair. But aging also occurs deep within our cells. One key area of research focuses on “epigenetic aging,” the gradual changes in how DNA is regulated over time. These changes are tracked using tools called epigenetic clocks, which estimate a person’s biological age based on specific molecular markers in the blood. Unlike chronological age, biological age reflects the body’s functional state and can be influenced by health, lifestyle, and environmental factors.While chocolate and coffee have been associated with better health outcomes, pinpointing the responsible specific compounds has been difficult. These foods contain multiple bioactive substances that are often consumed together, and few studies have explored their individual effects on the human epigenome, the system of chemical modifications that control gene activity and change with age.A recent study provides new insight, suggesting that theobromine, a compound naturally found in cocoa, may be associated with slower biological aging in humans.The Study: Investigating Theobromine and Epigenetic Aging in TwinsUK and KORA CohortsThe research titled “Theobromine is associated with slower epigenetic ageing,” was led by Ramy Saad from King’s College London and Great Ormond Street Hospital for Children NHS Foundation Trust, alongside Jordana T. Bell from King’s College London. The study was recently published in Aging-US. Full blog - https://aging-us.org/2026/01/chocolate-compound-linked-to-slower-biological-aging/Paper DOI - https://doi.org/10.18632/aging.206344Corresponding authors - Ramy Saad - ramy.saad@kcl.ac.uk, and Jordana T. Bell - jordana.bell@kcl.ac.ukAbstract video - https://www.youtube.com/watch?v=S0P1USM8L6ESign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206344Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, theobromine, epigenetic aging, DNA methylation, metabolomics, nutritionTo learn more about the journal, visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — January 20, 2026 — A new #review was #published in Volume 17, Issue 12 of Aging-US on December 30, 2025, titled “Aging as a multifactorial disorder with two stages.”“This article is a contribution to the special issue of Aging celebrating the life and work of Misha Blagosklonny (more formally, Mikhail Vladimirovich Blagosklonny), who died in October 2024.”In this review, David Gems and Alexander Carver from University College London, together with Yuan Zhao from Queen Mary University of London, present a new theoretical model to explain how aging leads to the development of chronic diseases. Drawing on evolutionary theory and biological research, the authors propose that aging is driven by a combination of early-life damage and harmful genetic activity in later life. This framework helps explain why diseases such as cancer, arthritis, and infections often appear in old age and offers insight into how they might be prevented.Aging is the biggest risk factor for most chronic diseases, but the biological reasons for this association are still debated. The authors address this by introducing a two-stage model. In the first stage, individuals experience disruptions early in life, such as infections, injuries, or genetic mutations. Although the body can often contain or repair this damage, it does not fully eliminate it. In the second stage, which begins in later life, normal genetic processes begin to act in ways that are no longer beneficial. These late-life changes weaken the body’s ability to contain earlier damage, allowing it to develop into disease.The review emphasizes that aging is a multifactorial process, shaped by many interacting causes rather than a single underlying mechanism. The model suggests that early-life disruptions and later-life genetic activity work together to drive age-related diseases. For example, dormant viruses can re-emerge as infections like shingles due to weakened immunity in older adults. Similarly, injuries to joints in youth can lead to osteoarthritis as tissues change with age. Inherited mutations may also remain silent for decades before contributing to conditions such as cancer or fibrosis later in life.This two-stage model builds on long-standing ideas from evolutionary biology, particularly the theory that aging occurs because natural selection has less influence in later life. The authors also draw on studies in the roundworm Caenorhabditis elegans, where early mechanical damage can lead to fatal infections in old age, suggesting similar patterns may occur in humans.Overall, this review presents a new framework for understanding how different causes of aging interact over time. By identifying two key stages, early-life damage and late-life genetic activity, it highlights potential strategies for promoting healthier aging through prevention and targeted intervention.DOI - https://doi.org/10.18632/aging.206339Corresponding author - David Gems - david.gems@ucl.ac.ukAbstract video - https://www.youtube.com/watch?v=d4TSI4Ot3yMSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206339Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, C. elegans, disease, hyperfunction, multifactorial modelTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — January 16, 2026 — A new #research paper was #published in Volume 17, Issue 12 of Aging-US on December 29, 2025, titled “Age-specific DNA methylation alterations in sperm at imprint control regions may contribute to the risk of autism spectrum disorder in offspring.”The study – selected as our Editors’ Choice for January, 2026 – was led by first authors Eugenia Casella and Jana Depovere, with corresponding author Adelheid Soubry from the University of Leuven. The research shows that a man’s age is linked to specific changes in sperm DNA that may influence early development in children. These findings are relevant as autism diagnoses have increased while many men are becoming fathers later in life.Autism spectrum disorder is a growing public health concern affecting millions of families worldwide. The study focused on DNA methylation, a natural process that helps regulate how genes function without changing the DNA sequence itself. DNA methylation plays a key role during early development and can be sensitive to age-related biological changes.Researchers analyzed sperm samples from 63 healthy, non-smoking men between the ages of 18 and 35. DNA methylation was measured at hundreds of thousands of locations across the genome. The analysis identified more than 14,000 DNA sites where methylation levels changed with age, with most showing a gradual decrease as men got older.“To identify sperm-specific marks, we conducted an epigenome-wide association study in sperm from 63 men, using the Illumina 450K array.”While individual changes were small, their location within the genome was important. Many age-related changes occurred near imprint control regions, which help ensure that certain genes are active only from one parent. These regions are established during sperm development and are usually maintained after fertilization. Disruptions in these regions may affect how genes are regulated in offspring.Researchers found that several genes affected by age-related DNA changes have previously been linked to autism. These genes are involved in brain development, nerve communication, and early growth. Changes in their regulation may increase vulnerability to neurodevelopmental differences.Overall, the findings provide new biological insight into earlier evidence linking paternal age to child health. However, the authors note that autism is a complex condition shaped by many genetic and non-genetic factors, and no single cause has been identified. The study results suggest that age-related changes in sperm DNA may be one contributing factor. By clarifying how paternal age influences sperm biology, this research supports future studies in reproductive health as family planning increasingly shifts toward later parenthood.DOI - https://doi.org/10.18632/aging.206348Corresponding author - Adelheid Soubry - adelheid.soubry@kuleuven.beAbstract video - https://www.youtube.com/watch?v=XC3p49Uw49wSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206348Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, epigenome, sperm, 450K, imprinting, autismTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — January 15, 2026 — A new #research paper was #published in Volume 17, Issue 12 of Aging-US on December 1, 2025, titled “CD47 antisense oligonucleotide treatment improves glucose homeostasis and alleviates dyslipidemia in aged male mice.”Led by Taesik Gwag and Shuxia Wang from the University of Kentucky and the Lexington Veterans Affairs Medical Center, the research shows that reducing CD47 levels improves blood sugar regulation and lipid balance in older mice. These findings are significant because metabolic disorders linked to aging increase the risk of diabetes, cardiovascular disease, and other chronic conditions. The results suggest that CD47 may be a promising target for improving metabolic health during aging.As people age, metabolic problems such as insulin resistance, high cholesterol, and increased abdominal fat become more common, even without significant weight gain. CD47 is known to play roles in immune signaling and aging-related inflammation, and earlier studies have linked it to metabolic dysfunction. This study examined whether lowering CD47 activity could reverse age-related metabolic decline.Researchers treated aged male mice with an antisense oligonucleotide (ASO) designed to reduce CD47 for ten weeks. The treatment led to lower fasting blood glucose, improved glucose tolerance, and enhanced insulin sensitivity. Circulating lipid levels, including cholesterol and free fatty acids, were also reduced. Importantly, these benefits occurred without changes in overall body weight, indicating improved metabolic efficiency rather than weight loss.“Twenty-month-old male mice were treated with control ASO or CD47 ASO (25 μg/g) for 10 weeks.”One of the most notable findings was a selective reduction in visceral fat, the deep abdominal fat closely associated with metabolic disease. Fat cells in this tissue were smaller, reflecting reduced fat production within the cells rather than increased fat breakdown. This change helps explain why metabolic health improved without weight loss.Treatment also improved brown fat tissue function. Brown fat plays a key role in energy use and metabolism. Treated mice showed increased activity of genes involved in energy burning and hormone-like signaling, supporting improved whole-body glucose and lipid balance. Moreover, the liver showed improved glucose metabolism. While liver fat content was unchanged, genes involved in glucose uptake and processing were more active, further contributing to better blood sugar control.Together, these findings identify CD47 as a key regulator of age-related metabolic dysfunction. By improving glucose control, lipid balance, and fat tissue function in aged male mice, CD47 antisense therapy offers a promising path for future strategies aimed at reducing metabolic disease risk in aging populations.DOI: https://doi.org/10.18632/aging.206343Corresponding authors: Taesik Gwag - Taesik.gwag@uky.edu and Shuxia Wang - swang7@uky.eduAbstract video: https://www.youtube.com/watch?v=U6CiiOIaIWISign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206343Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
The results of studies revealed in the paper #published in Volume 17, Issue 12, titled “Age-specific DNA methylation alterations in sperm at imprint control regions may contribute to the risk of autism spectrum disorder in offspring,” indicate that advanced paternal age increases the risk of autism spectrum disorder (ASD) in children, potentially due to sperm epigenetic changes.To explore this, the authors performed an epigenome-wide association study on sperm from 63 men using the Illumina 450K array, identifying 14,622 age-related differentially methylated CpGs (DMCs), with many linked to imprinted genes and imprint control regions (ICRs). These alterations may disrupt gene expression and contribute to neurodevelopmental disorders like ASD. Several imprinted genes identified—including OTX1, PRDM16, and others—are associated with ASD, warranting further research into their role in paternal age effects on autism.Further genetic research may clarify how paternal age affects autism. Changes in DNA methylation within ICRs before conception could add to ASD’s complexity. Though measured effects were small, even minor sperm epigenetic changes could influence populations as fatherhood is delayed. Preventive and educational programs could benefit public health.DOI - https://doi.org/10.18632/aging.206348Corresponding author - Adelheid SoubrySign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206348Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, epigenome, sperm, 450K, imprinting, autismTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
As we age, every tissue in the body undergoes gradual molecular changes. A long-standing question in aging research is whether these changes follow common patterns across tissues or whether each tissue ages on its own. While DNA-based “epigenetic clocks” can estimate age accurately across different tissues, identifying consistent patterns in gene expression has been much more challenging.One reason for this difficulty is methodology. Most studies focus on whether genes increase or decrease their expression levels with age. However, genes do not function in isolation. They operate within complex networks, coordinating their activity with many others. Changes in these relationships may be important aspects of the aging process. To understand this, researchers from the University of São Paulo performed a study titled “A combination of differential expression and network connectivity analyses identifies a common set of RNA splicing and processing genes altered with age across human tissues.”Full blog - https://aging-us.org/2026/01/a-common-aging-pattern-changes-in-rna-splicing-and-processing-across-human-tissues/Paper DOI - https://doi.org/10.18632/aging.206347Corresponding author - Nadja C. de Souza-Pinto - nadja@iq.usp.brAbstract video - https://www.youtube.com/watch?v=A1slKwaSd6gSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206347Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, gene expression, co-expression network analysis, RNA processingTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@Aging-USLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — January 7, 2026 — A new #meetingreport was #published in Volume 17, Issue 12 of Aging-US on December 23, 2025, titled “Cellular senescence meets infection: highlights from the 10th annual International Cell Senescence Association (ICSA) conference, Rome 2025.”Led by Stefanie Deinhardt-Emmer from Jena University Hospital and Marco De Andrea from the University of Piemonte Orientale and the University of Turin, the report summarizes key discussions from the 10th International Cell Senescence Association conference held in Rome in September 2025. It focuses on how infections can trigger cellular senescence, a state in which cells stop dividing and release inflammatory signals. This link is important since it connects infectious diseases with aging, chronic inflammation, and lasting tissue damage.Although cellular senescence is best known for its role in aging and cancer, the meeting highlighted its emerging importance in infection biology. Researchers described how viruses and bacteria can induce senescence in infected cells and spread its effects to nearby tissues. This process, known as infection-driven senescence (IDS), can help limit pathogen replication but may also prolong inflammation and slow recovery, particularly in older adults and during chronic infections.Several sessions focused on respiratory viruses like influenza and SARS-CoV-2. Researchers showed that these viruses can promote senescence in lung cells, contributing to persistent inflammation and reduced healing. Experimental models suggested that decreasing the amount of senescent cells improved lung repair, even after the virus was cleared, offering insight into why some patients experience long-lasting respiratory symptoms.Chronic viral infections were another major theme. Human cytomegalovirus and HIV were shown to drive senescence in immune and vascular cells. In people with HIV, viral proteins were associated with biological changes resembling accelerated aging, despite effective antiviral therapy. These findings help explain why age-related conditions occur earlier and more frequently in this population.In the meeting, it was also demonstrated that senescence is not limited to viral infections. Researchers reported that the bacterium Mycobacterium abscessus induces senescence in immune cells during chronic infection. These senescent cells increased inflammation and susceptibility to further infection. Removing them reduced bacterial levels in experimental models, suggesting new directions for treating persistent bacterial disease.“Mechanistically, IDS integrates DNA damage responses, inflammatory signaling, and metabolic stress, with consistent activation of p16INK4a, p21, and NF-κB pathways.”Across the conference, speakers discussed therapies that either remove senescent cells or reduce their harmful inflammatory signals. These approaches, known as senolytic and senomorphic strategies, showed promise in preclinical studies as potential tools to limit infection-related tissue damage and chronic inflammation.Overall, the meeting report presents infection-driven senescence as a unifying concept linking infection, immunity, and aging. The discussions at ICSA 2025 highlight a growing field with important implications for understanding chronic disease and the long-term health effects of infections.DOI: https://doi.org/10.18632/aging.206349Abstract video: https://www.youtube.com/watch?v=gOHEBJs7DIcConnect with us on social media:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc
BUFFALO, NY — January 5, 2026 — A new #research paper featured as the #cover of Volume 17, Issue 12 of Aging-US was #published on December 22, 2025, titled “A combination of differential expression and network connectivity analyses identifies a common set of RNA splicing and processing genes altered with age across human tissues.”In this study by Caio M.P.F. Batalha from the University of São Paulo, André Fujita from the University of São Paulo and Kyushu University, and Nadja C. de Souza-Pinto also from the University of São Paulo, researchers investigated how gene activity changes with age across multiple human tissues. They found that many tissues share common aging-related alterations in genes involved in RNA splicing and RNA processing. These findings are important because RNA processing is essential for accurate protein production, and disruptions in this process are linked to aging and disease.Aging affects all tissues, yet identifying molecular changes that are shared across the body has remained challenging. To address this, researchers moved beyond traditional approaches that focus exclusively on changes in gene expression levels. They also analyzed how genes alter their patterns of interaction within regulatory networks, capturing age-related changes that are not evident from expression data alone.“Gene expression data (in TPM – transcripts per million) were obtained from the Genotype-Tissue Expression (GTEx) project.”Using RNA sequencing data from nearly one thousand human donors aged 20 to 70, the research team analyzed eight tissues, including blood, brain, heart, skin, and muscle. The results showed that many aging-related changes become evident only when gene network behavior is considered. When gene expression and network connectivity were analyzed together, a consistent group of genes emerged across tissues, most of which were linked to RNA splicing and RNA processing, key steps in the production of functional proteins.The study also revealed that these RNA-related genes are highly interconnected at the protein level. Many of them form known protein complexes, including components of the spliceosome, which plays a central role in RNA maturation. With age, the interactions among these genes tend to reorganize in similar ways across tissues, pointing to a shared biological response rather than independent, tissue-specific effects.In addition to RNA processing, the researchers observed age-related changes in pathways involved in managing damaged RNAs and proteins, including protein degradation, autophagy, and DNA damage response mechanisms. These pathways support cellular quality control and help limit the accumulation of molecular errors that increase with age.Overall, this study identifies RNA splicing and RNA processing as central, conserved features of human aging across tissues. It also demonstrates that network-based approaches provide a more complete view of the aging transcriptome, offering new insights into age-related biological changes and potential directions for aging research.DOI - https://doi.org/10.18632/aging.206347Corresponding author - Nadja C. de Souza-Pinto - nadja@iq.usp.brAbstract video - https://www.youtube.com/watch?v=A1slKwaSd6gSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@Aging-USLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — December 30, 2025 — A new #research paper was #published in Volume 17, Issue 11 of Aging-US on November 26, 2025, titled “Epigenetic aging signatures and age prediction in human skeletal muscle.”In this study, first author Soo-Bin Yang and corresponding author Hwan Young Lee from Seoul National University College of Medicine investigated how DNA methylation patterns in skeletal muscle change with age. Their findings offer a new and highly accurate method for estimating a person’s age, with potential applications in forensic science and aging research.Skeletal muscle is essential for movement, energy balance, and physical strength, functions that become more important to monitor as people age. This study improves our understanding of how muscle tissue changes over time at the molecular level. Unlike previous research, which mainly analyzed living individuals of European descent, this study used postmortem samples from an Asian population.“We analyzed DNA methylation profiles from 103 pectoralis major muscle samples from autopsies of South Korean individuals (18–85 years) using the Infinium EPIC array.”The researchers analyzed DNA from over 100 pectoralis major muscle samples taken from individuals aged 18 to 85. They identified 20 DNA methylation sites, called CpGs, that were strongly associated with age. These CpGs were found in genes involved in muscle function, stress response, metabolism, and age-related diseases. Using these markers, the team built two machine learning models to predict age: one using Next-Generation Sequencing (NGS) and another using Single Base Extension (SBE). Both models were highly accurate, with average prediction errors between 3.8 and 5.5 years.The new “epigenetic clocks” outperformed existing age-prediction models designed for other tissue types. However, when applied to cardiac and uterine muscle, these models showed much lower accuracy, reinforcing the need for tissue-specific approaches in molecular age estimation.Beyond predicting age, the study also provides insight into how DNA methylation may affect muscle aging. Several of the identified CpGs were located in regions that regulate gene expression, being associated with a reduction of it in older muscle samples. Some of the affected genes are associated with sarcopenia, an age-related loss of muscle mass and strength.Overall, this study introduces two reliable and cost-effective methods to estimate age from skeletal muscle, even when the DNA is partially degraded, making it especially useful in forensic settings. It also offers a path forward for developing future therapies that may slow age-related muscle decline and highlights how skeletal muscle aging can differ depending on population, tissue type, and anatomical location.DOI - https://doi.org/10.18632/aging.206341Corresponding author - Hwan Young Lee - hylee192@snu.ac.krAbstract video - https://www.youtube.com/watch?v=1i6Ua0cceMUSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206341Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, skeletal muscle, age, DNA methylation, next generation sequencing, single base extensionTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — December 23, 2025 — A new #research paper was #published in Volume 17, Issue 11 of Aging-US on November 25, 2025, titled “A natural language processing–driven map of the aging research landscape.”In this study, Jose Perez-Maletzki from Universidad Europea de Valencia and Universitat de València, together with Jorge Sanz-Ros from Stanford University School of Medicine, used artificial intelligence (AI) to analyze a century of global aging research, revealing shifts in focus and highlighting underexplored areas.The team analyzed over 460,000 scientific abstracts published between 1925 and 2023 to identify key themes, trends, and research gaps in the study of aging. Their goal was to provide a comprehensive, unbiased view of how the field has evolved and where future research could have the greatest impact.The study found that aging research has moved from basic cellular studies and animal models to a growing focus on clinical topics, particularly age-related diseases such as Alzheimer’s and dementia. Using natural language processing and machine learning, the researchers grouped publications into thematic clusters and tracked how interest in each topic changed over time.“By integrating Latent Dirichlet Allocation (LDA), term frequency-inverse document frequency (TF-IDF) analysis, dimensionality reduction and clustering, we delineate a comprehensive thematic landscape of aging research.”One key finding was the growing separation between basic biological studies and clinical research. While both areas have grown significantly, they often progress independently with limited overlap. Clinical studies tend to focus on geriatrics, healthcare, and neurodegenerative diseases, while basic science emphasizes cellular mechanisms such as oxidative stress, telomere shortening, mitochondrial dysfunction, and senescence. The authors note that this lack of integration limits the translation of laboratory discoveries into medical applications.The study also showed that some emerging topics, such as autophagy, RNA biology, and nutrient sensing, are expanding rapidly but remain separated from clinical applications. In contrast, long-established links, such as those between cancer and aging, remain strong. The analysis also highlighted that potentially important associations, such as those between mitochondrial dysfunction and senescence or epigenetics and autophagy, are rarely studied and may be new research opportunities.This AI-driven analysis offers a new way to guide future research by identifying how different areas of aging science are interconnected or isolated. It also highlights how research priorities may be shaped by policy or funding trends, as seen in the heavy focus on Alzheimer’s disease. As the global population continues to age, understanding how biological processes relate to clinical outcomes is critical. This study not only offers a historical map of aging science but also serves as a tool to support more connected, interdisciplinary, and effective future research.DOI - https://doi.org/10.18632/aging.206340Corresponding author - Jorge Sanz-Ros - jsanzros@stanford.eduAbstract video - https://www.youtube.com/watch?v=O4dJUGQ2ZcUSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsTo learn more about the journal, visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — December 19, 2025 — A new #research paper was #published in Volume 17, Issue 11 of Aging-US on November 18, 2025, titled “Epigenetic age predicts depressive symptoms during the COVID-19 pandemic in the Canadian Longitudinal Study on Aging: importance of biological sex.”This study, led by Cindy K. Barha of the University of Calgary and the University of British Columbia, along with Teresa Liu-Ambrose of the University of British Columbia, found that older women with a younger biological age measured years before the COVID-19 pandemic experienced a greater increase in depressive symptoms during the early lockdown period. These findings could help shape future mental health strategies, particularly for women with high emotional or caregiving demands.Epigenetic age is a biological marker that reflects how the body is aging and may differ from a person’s actual age. Using long-term data from the Canadian Longitudinal Study on Aging (CLSA), the researchers investigated whether epigenetic age could predict changes in mental health during a major public health crisis. The study included over 600 adults, with an average baseline age of 63, and used two widely accepted epigenetic clocks, the DNAmAge and the Hannum Age, to estimate biological age. Depressive symptoms were tracked at four time points between 2012 and 2020, including during the height of the pandemic.“The mean participant chronological age at study entry was 63±10 years (46% female).”The analysis showed that in women, a younger biological age predicted a greater rise in depression during the early phase of the COVID-19 pandemic. This was not observed in men or in individuals with older biological ages.The study challenges the common belief that a younger biological age always signals better mental or physical resilience. The researchers suggest that women with younger biological profiles may have been more socially or professionally active before the pandemic. When lockdowns disrupted daily routines and social connections, these individuals may have experienced more emotional distress.Additional factors, such as reduced physical activity, loss of routine, and decreased social interaction, known to affect both mental health and biological aging, may have had a stronger emotional effect on this group. The findings highlight the importance of considering biological sex when studying how aging affects mental well-being during stressful events.Although the study has some limitations, including the time gap between biological age measurement and the pandemic, it gives valuable insights into how biological and social factors interact during periods of crisis. Future research could use epigenetic clocks to better identify individuals at greater risk of mental health challenges during large-scale public health emergencies.Overall, this study adds to the growing field of social epigenetics and suggests that biological age may support more targeted public health planning, especially for older adults.DOI - https://doi.org/10.18632/aging.206337Corresponding author - Teresa Liu-Ambrose - teresa.ambrose@ubc.caAbstract video - https://www.youtube.com/watch?v=DVm78jKsdkYSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY— December 17, 2025 — We are pleased to announce that we have officially joined ResearchGate, the professional network for scientists and researchers. This collaboration enhances the visibility, accessibility, and impact of research published in Aging-US among the global scientific community.By integrating ResearchGate, Aging-US offers authors and readers an additional channel to discover, share, and discuss cutting-edge findings in aging research. The journal’s presence on the platform includes a dedicated profile, article listings, author profiles, and metrics that help track readership and engagement.As the field of aging research continues to grow rapidly, it is essential that high-quality studies are easy to find, access, and share. Joining ResearchGate allows Aging-US authors to connect their work with a wider network of peers, fostering collaboration, advancing understanding of the biology of aging, and helping translate discoveries into better health outcomes.ResearchGate hosts millions of researchers worldwide and provides tools for sharing publications, asking and answering research questions, and discovering new collaborators across institutions and disciplines. Aging-US’s participation on the platform reinforces its commitment to open scientific dialogue and timely dissemination of rigorously reviewed aging research.Authors publishing in Aging-US can now:-Link their publications directly to their ResearchGate profiles.-Track reads, recommendations, and citations through the platform’s analytics.-Engage with other scientists interested in aging, geroscience, and translational research.Readers and researchers can follow Aging-US on ResearchGate to stay updated on newly published articles, special issues, and calls for papers.To learn more about the journal, visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — December 16, 2025 — A new #research paper was #published in Aging-US on December 10, 2025, titled “Theobromine is associated with slower epigenetic ageing.”In this study, led by Ramy Saad from King’s College London and Great Ormond Street Hospital for Children NHS Foundation Trust, alongside Jordana T. Bell from King’s College London, researchers found that higher levels of theobromine, a natural compound found in cocoa, are associated with slower biological aging in humans. The findings suggest that theobromine may support healthy aging.Epigenetic aging refers to biological changes that affect how genes function over time. It is measured using blood-based markers such as DNA methylation and telomere length, which together provide a more accurate picture of aging than chronological age.In this work, researchers analyzed data from two large European studies. In 509 women from the TwinsUK cohort, they found that higher blood levels of theobromine were associated with slower aging, especially based on GrimAge, an epigenetic clock that predicts the risk of age-related disease and early death. The results were confirmed in 1,160 men and women from the German KORA study.“We initially tested for the association between six metabolites found in coffee and cocoa, and epigenetic measures of ageing in blood samples from 509 healthy females from the TwinsUK cohort (median age = 59.8, IQR = 12.81, BMI = 25.35).“Importantly, theobromine’s effects were independent of related compounds such as caffeine. Even after adjusting for these other substances and different lifestyle factors, the association with slower aging remained strong. The study also associated higher theobromine levels with longer telomeres, another marker of healthy aging.While theobromine is commonly found in cocoa and chocolate, the study does not suggest increasing chocolate intake. However, it highlights the potential of everyday dietary components such as theobromine to influence aging. These findings support growing evidence that certain plant-based compounds may play a role in promoting long-term health. By identifying a connection between theobromine and slower biological aging, the study opens new directions for research into nutritional strategies for healthy aging.DOI - https://doi.org/10.18632/aging.206344Corresponding authors - Ramy Saad - ramy.saad@kcl.ac.uk, and Jordana T. Bell - jordana.bell@kcl.ac.ukAbstract video - https://www.youtube.com/watch?v=S0P1USM8L6ESign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206344Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, theobromine, epigenetic aging, DNA methylation, metabolomics, nutritionTo learn more about the journal, visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — December 12, 2025 — A new #research paper was #published in Volume 17, Issue 11 of Aging-US on November 14, 2025, titled “Methylglyoxal-induced glycation stress promotes aortic stiffening: putative mechanistic roles of oxidative stress and cellular senescence.”The study was led by first authors Parminder Singh of the Buck Institute for Research on Aging and Ravinandan Venkatasubramanian of the University of Colorado Boulder, with senior contributions from corresponding authors Pankaj Kapahi (Buck Institute for Research on Aging) and Zachary S. Clayton (University of Colorado Boulder and University of Colorado Anschutz Medical Campus). The researchers investigated how methylglyoxal (MGO), a toxic byproduct that builds up in blood vessels with age or metabolic dysfunction like diabetes, contributes to artery stiffening. Their findings are especially important to aging and diabetes-related cardiovascular risk.Aortic stiffening, which reduces the flexibility of the body’s largest artery, is a key predictor of cardiovascular disease in older adults. The research team used young and aged mice to study how MGO affects vascular health. In young mice, chronic exposure to MGO increased aortic stiffness by 21%. However, when treated with Gly-Low, a supplement containing natural compounds such as nicotinamide and alpha-lipoic acid, this stiffening was completely prevented. Gly-Low also reduced the buildup of MGO and its harmful byproducts, particularly MGH-1, in both blood and tissue.“Aortic stiffness was assessed in vivo via pulse wave velocity (PWV) and ex vivo through elastic modulus.”The research showed that MGO’s damage goes beyond structural changes. It also caused the endothelial cells that line blood vessels to enter senescence, a state in which cells stop dividing and begin releasing inflammatory signals. This led to lower levels of nitric oxide, a molecule essential for blood vessel relaxation. In human vascular cells in lab culture, Gly-Low reversed these aging-like changes and restored nitric oxide production.In older mice, which naturally develop stiffer arteries, Gly-Low treatment during four months significantly reduced stiffness and lowered MGO and MGH-1 levels. This suggests that Gly-Low may help slow or even reverse vascular aging by reducing glycation stress.The study also identified the glyoxalase-1 pathway as a critical mechanism. This is a natural detox system that helps clear harmful molecules like MGO. Gly-Low appeared to boost this pathway. When the pathway was chemically blocked, Gly-Low’s protective effects disappeared, confirming its role in the process.Overall, the findings highlight glycation stress as a modifiable contributor to vascular aging. The results suggest that natural compound-based therapies, like Gly-Low, may offer a potential strategy to protect arteries from age- and diabetes-related damage.DOI - https://doi.org/10.18632/aging.206335Corresponding authors: Pankaj Kapahi - pkapahi@buckinstitute.org; Zachary S. Clayton - Zachary.Clayton@cuanschutz.eduAbstract video: https://www.youtube.com/watch?v=i_rtq8eIb8cSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589X - https://twitter.com/AgingJrnlFacebook - https://www.facebook.com/AgingUS/Instagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Pinterest - https://www.pinterest.com/AgingUS/YouTube - https://www.youtube.com/@Aging-USSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Treating aggressive cancers that do not respond to standard therapies remains one of the most significant challenges in oncology. Among these are basal-like breast cancers (BLBC), which lack hormone receptors and HER2 amplification. This makes them unsuitable for many existing targeted treatments. As a result, therapeutic options are limited, and patient outcomes are often poor.One emerging strategy is to induce senescence, a state in which cancer cells permanently stop dividing but remain metabolically active. This approach aims to slow or stop tumor growth without killing the cells directly. Although promising, the clinical application of senescence-based therapies has been limited by several challenges.Senescence is typically identified using biomarkers such as p16, p21, and beta-galactosidase activity. However, these markers are often already present in aggressive cancers like BLBC (Sen‑Mark+ tumors), making it difficult to determine whether a treatment is truly inducing senescence or merely reflecting the tumor’s existing biology. Moreover, conventional screening methods may mistake reduced cell growth for senescence, cell death, or temporary growth arrest, leading to inaccurate assessments. This is especially problematic in large-scale drug screening, where thousands of compounds must be evaluated quickly and reliably.To overcome these issues, researchers from Queen Mary University of London and the University of Dundee have developed a new machine learning–based method to improve the detection of senescence in cancer cells. Their findings were recently published in Aging-US.The Study: Developing the SAMP-ScoreThe study, titled “SAMP-Score: a morphology-based machine learning classification method for screening pro-senescence compounds in p16-positive cancer cells,” was led by Ryan Wallis and corresponding author Cleo L. Bishop from Queen Mary University of London. This paper was featured on the cover of Aging-US Volume 17, Issue 11, and highlighted as our Editors’ Choice.Full blog - https://aging-us.org/2025/12/using-machine-learning-to-identify-senescence-inducing-drugs-for-resistant-cancers/Paper DOI - https://doi.org/10.18632/aging.206333Corresponding author - Cleo L. Bishop - c.l.bishop@qmul.ac.ukAbstract video - https://www.youtube.com/watch?v=qXI_KI3EgHESign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206333Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, SAMP-Score, senescence, senescent marker positive cancer cells, Sen-Mark+, machine learning, pro-senescence, high-throughput compound screeningTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@Aging-USLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
The paper featured on the cover of this issue of Aging-US, published on October 30, 2025, entitled “SAMP-Score: a morphology-based machine learning classification method for screening pro-senescence compounds in p16-positive cancer cells,” represents an important methodological and conceptual advance at the interface of senescence biology, imaging and drug discovery.In this study, led by first author Ryan Wallis and corresponding author Cleo L. Bishop (Queen Mary University of London), the authors introduce SAMP-Score, a machine-learning–based framework designed to identify bona fide senescence induction in cancer cells where canonical markers fail. This is a timely and much-needed contribution to the field.Therapy-induced senescence has emerged as a powerful strategy to restrain tumor growth, yet its reliable detection in cancer cells remains a major bottleneckIn these contexts, cells often already display features associated with cellular aging, rendering conventional senescence markers ambiguous or misleading. Distinguishing true senescence from toxicity, stress responses or baseline “aged” phenotypes is therefore a critical unmet need.Rather than relying on predefined molecular readouts, the authors take a different approach and train a machine-learning model to recognize senescence-associated morphological profiles (SAMPs) which are subtle but reproducible changes in cellular architecture captured through high-content microscopy. By learning directly from image-based phenotypes, SAMP-Score is able to identify senescence with a level of precision that is difficult to achieve using marker-based strategies alone.The strength of the platform demonstrated through a large-scale screen of over 10,000 novel chemical entities in p16-positive basal-like breast cancer cells. From this screen, the compound QM5928 emerged as a robust inducer of senescence across multiple cancer models, notably without inducing cytotoxicity. Importantly, QM5928 retains activity in cellular contexts that are resistant to CDK4/6 inhibition, including palbociclib-refractory, p16-high tumors.Mechanistically, the authors show that QM5928 promotes nuclear relocalization of p16, consistent with a functional engagement of cell-cycle arrest pathways. These nuanced phenotypic changes would likely have gone undetected without the resolution and discrimination provided by SAMP-Score, underscoring the platform’s ability to separate true senescence from confounding cellular states.This work exemplifies how machine learning and quantitative imaging can be harnessed to solve long-standing problems in senescence research, moving the field beyond binary marker expression toward phenotype-driven classification. Beyond its immediate relevance for cancer therapy, SAMP-Score offers a broadly applicable framework for senescence-based screening efforts across biological contexts.DOI - https://doi.org/10.18632/aging.206333Corresponding author - Cleo L. Bishop - c.l.bishop@qmul.ac.ukAbstract video - https://www.youtube.com/watch?v=qXI_KI3EgHESign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206333Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Bluesky - https://bsky.app/profile/aging-us.bsky.socialResearchGate - https://www.researchgate.net/journal/Aging-1945-4589Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@Aging-USLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — December 8, 2025 — A new #research paper was #published in Volume 17, Issue 11 of Aging-US on September 12, 2025, titled “Infusion of blood from young and old mice modulates amyloid pathology.”This study was led by co-first authors Matias Pizarro from Universidad Adolfo Ibáñez and Ruben Gomez-Gutierrez from The University of Texas Health Science Center at Houston, alongside corresponding authors Claudia Duran-Aniotz from Universidad Adolfo Ibáñez and Rodrigo Morales from The University of Texas Health Science Center at Houston and Universidad Bernardo O’Higgins. The goal was to investigate how blood from young and old mice influences Alzheimer’s-related changes in a transgenic mouse model. The findings indicate that age-dependent circulating factors can either worsen or mitigate brain changes associated with dementia, highlighting blood and its components as potential therapeutic targets.Alzheimer’s disease is a progressive neurodegenerative disorder characterized by misfolded amyloid proteins, inflammation, and gradual cognitive decline, with aging as its main risk factor. In this work, whole blood from young adult or very old wild-type mice was repeatedly infused into Tg2576 mice, a well-established model of amyloid accumulation and memory impairment. Over several months, recipient mice received 30 weekly blood infusions, followed by behavioral testing and detailed neuropathological analyses.“Tg2576 mice express the human APP harboring the Swedish mutation.”Mice that received blood from old donors performed worse in both short- and long-term spatial memory tasks than mice infused with young blood, suggesting that aged blood contains factors that impair cognition. When the team examined brain tissue, they found more cortical amyloid deposits detected by a specific antibody in mice treated with old blood, while overall amyloid levels measured biochemically did not change, suggesting differences in plaque type or compactness rather than total amount. The expression of amyloid precursor protein in the brain was also higher after old-blood infusion, which may partly explain the shift in amyloid pathology.Despite these changes in plaques and memory, classical markers of astrocyte activation, a sign of brain inflammation, did not differ between groups, pointing to more subtle molecular shifts. A broad proteomic analysis of brain samples revealed dysregulation of proteins involved in synapse formation, calcium signaling, and the endocannabinoid system, pathways important for neuronal communication and plasticity. Among them, the calcium channel–related protein CACNA2D2 and the signaling protein BRAF were increased in mice that received old blood, confirming that aged blood circulation can reshape key signaling networks linked to neuronal function and degeneration.Overall, this study supports the idea that blood is not just a passive carrier but a powerful modulator of brain health during aging and disease. While young blood has been associated in previous work with improved synaptic function and reduced amyloid and tau changes, this study emphasizes the harmful impact of old blood, particularly on cortical amyloid patterns and memory. The identification of CACNA2D2 and BRAF as potential mediators of these effects suggests new avenues for targeting blood-borne factors or downstream brain pathways to slow or modify Alzheimer’s-related decline.DOI - https://doi.org/10.18632/aging.206319Corresponding authors - Claudia Duran-Aniotz - Claudia.Duran@uai.cl, and Rodrigo Morales - Rodrigo.MoralesLoyola@uth.tmc.eduAbstract video - https://www.youtube.com/watch?v=zsBDSAipH3wTo learn more about the journal, visit https://www.Aging-US.com.MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — December 3, 2025 — A new #essay was #published in Volume 17, Issue 11 of Aging-US on November 19, 2025, titled “On the intergenerational transfer of ideas in aging and cancer research: from the hypothalamus according to V.M. Dilman to the mTOR protein complex according to M.V. Blagosklonny.”In this work, Aleksei G. Golubev from the N.N. Petrov National Medical Research Center of Oncology reflects on the legacy of two influential Russian scientists, Vladimir M. Dilman and his son Mikhail V. Blagosklonny, who each introduced groundbreaking ideas about aging and cancer. Drawing from his own experience working in Dilman’s lab, Golubev explores how their ideas remain deeply relevant to today’s scientific understanding.The essay connects Dilman’s “elevation theory” with Blagosklonny’s “hyperfunction theory,” two frameworks that challenge the conventional view of aging as a process of decline. Instead, both propose that aging results from continued biological processes that once supported growth but eventually become harmful when left unchecked.Dilman believed that aging begins with reduced sensitivity in the hypothalamus, a brain region that regulates the body’s balance. This desensitization disrupts metabolism and hormone levels, setting the stage for many chronic illnesses. Decades later, Blagosklonny expanded on this idea at the molecular level. Central to his theory is the mTOR protein complex, which regulates growth and metabolism and is now a major focus in aging research.Golubev also explores the historical and personal connections between the two scientists. Dilman, an endocrinologist trained in the Soviet Union, and Blagosklonny, a molecular biologist educated during the post-Soviet period, represent two generations shaped by a shared scientific tradition. “Dilman’s scientific legacy is not as well recognized as it should be, partly due to bias in citation practices.”The essay also draws attention to a troubling trend in science: the tendency to overlook early contributions, especially from non-Western scholars. Many of Dilman’s insights, such as the connection between high blood sugar, insulin resistance, and cancer, have since been validated by modern tools, yet his work is rarely cited. Golubev points out how citation practices, language barriers, and historical isolation have contributed to this lack of recognition.Finally, Golubev encourages the scientific community to look back and acknowledge the foundational work that shaped modern aging science. It also highlights the importance of cross-generational knowledge in moving science forward. By tracing the intellectual journey from hormonal regulation in the brain to molecular pathways in cells, this essay demonstrated the relevance of old ideas in a new biological era.DOI - https://doi.org/10.18632/aging.206338Corresponding author - Aleksei G. Golubev - lxglbv@rambler.ruAbstract video - https://www.youtube.com/watch?v=LvrdghTKGwsSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206338Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, gerontology, history of science, hyperfunction, mTOR, hypothalamus, cancer, metabolism, immunityTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@Aging-USLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — December 1, 2025 — A new #research paper featured on the #cover of Volume 17, Issue 11 of Aging-US was #published on October 30, 2025, titled “SAMP-Score: a morphology-based machine learning classification method for screening pro-senescence compounds in p16 positive cancer cells.”In this study led by first author Ryan Wallis along with corresponding author Cleo L. Bishop, from Queen Mary University of London, researchers developed a machine learning tool to identify compounds that induce cancer cells into senescence. The tool, called SAMP-Score, offers a new strategy for drug discovery in cancers with poor treatment options like basal-like breast cancer.Senescence is a process where damaged or aged cells stop dividing. In cancer therapy, inducing senescence is an approach to control tumor growth. However, it is difficult to detect true senescence in cancer cells that already appear aged. These cancers, often called Sen-Mark+ cancers, include basal-like breast cancer and typically lack reliable markers to confirm senescence. SAMP-Score was designed to address this problem.Instead of relying on traditional markers, the researchers built a machine learning model trained to recognize patterns based on senescent cells’ shape and structure under a microscope. These visual patterns, known as senescence-associated morphological profiles (SAMPs), allowed the model to distinguish real signs of aging from other effects such as toxicity or normal variation. By analyzing thousands of cell images, the model learned to classify whether a cell had truly entered senescence.“To demonstrate the potential application of SAMP-Score in p16 positive cancer therapeutic discovery, we assessed a diversity screen of 10,000 novel chemical entities in MB-468 cells (p16 positive BLBC).”The team used SAMP-Score to screen more than 10,000 experimental compounds. One compound, QM5928, consistently triggered senescence in several cancer cell types without killing them, making it a promising candidate for further study. Importantly, it worked in cancers resistant to known drugs like palbociclib, which are often ineffective in cancers with high p16 expression like basal-like breast cancer. Further analysis revealed that QM5928 caused the p16 protein to move into the nucleus of cancer cells, a possible sign that the protein is helping stop cell division. This subtle effect was only detectable using the detailed imaging and analysis made possible by SAMP-Score, highlighting the tool’s ability to distinguish true senescence from toxic responses and making it a powerful resource in cancer drug discovery.By combining machine learning with high-resolution imaging, this study introduces a new way to find and evaluate cancer therapies. SAMP-Score could accelerate efforts to develop treatments that exploit the body’s natural aging processes to fight cancer, especially for patients with resistant tumors. The tool is openly available at GitHub, making it accessible for other researchers exploring senescence-based cancer therapies.DOI - https://doi.org/10.18632/aging.206333Corresponding author - Cleo L. Bishop - c.l.bishop@qmul.ac.ukAbstract video - https://www.youtube.com/watch?v=qXI_KI3EgHESubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@Aging-USLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Interest in healthier, longer lives is rising, supported by recent scientific advances in aging research. But turning those discoveries into everyday healthcare solutions remains a work in progress. In this landscape, longevity clinics have attracted attention as personalized alternatives to traditional medicine.What Are Longevity Clinics?Longevity clinics are private centers offering tailored programs designed to improve long-term health and slow biological aging. Using advanced diagnostics such as genetic sequencing, full-body imaging, and blood tests, they develop personalized plans that may include exercise, nutrition, hormone therapy, or experimental treatments. Frequently found in countries like the United States, Switzerland, and the United Arab Emirates, these clinics reflect a growing global interest in preventive healthcare, though their high costs and scientific credibility remain subjects of debate.The Editorial“Longevity clinics: between promise and peril,” an editorial by Marco Demaria, Editor-in-Chief of Aging-US, from the European Research Institute for the Biology of Ageing (ERIBA), University Medical Center Groningen (UMCG), University of Groningen (RUG), was published in Aging-US (Volume 17, Issue 10). Full blog - https://aging-us.org/2025/11/longevity-clinics-balancing-innovation-with-regulation/Paper DOI - https://doi.org/10.18632/aging.206330Corresponding author - Marco Demaria — m.demaria@umcg.nlAbstract video - https://www.youtube.com/watch?v=Bt84xBdii0sSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206330Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, longevity clinics, biomarkers, frailty, senescenceTo learn more about the journal, visit https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@Aging-USLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — November 25, 2025 — A new #research paper was #published in Volume 17, Issue 10 of Aging-US on October 13, 2025, titled “Hospitalization with infections and risk of Dementia: a systematic review and meta-analysis.”This large-scale meta-analysis, led by first author Wei Yu Chua from the National University of Singapore and corresponding author Eng-King Tan from the National Neuroscience Institute and Duke-NUS Medical School in Singapore, shows that adults hospitalized with infections have a significantly higher risk of developing dementia. The findings are especially important as global populations grow older and hospitalizations for infections increase, highlighting a potential new approach for dementia prevention.“Out of 1900 studies that were screened initially, 16 studies comprising 4,266,276 patients were included for analysis.” The researchers analyzed data from over 4 million individuals across 16 studies, making this study the most comprehensive review to date on the association between infection-related hospital stays and long-term brain health. The results showed that being hospitalized for an infection raised the risk of all-cause dementia by 83%. Among the types of infections studied, sepsis carried the highest risk, followed by pneumonia, urinary tract infections, and skin or soft tissue infections. The risk of developing vascular dementia was notably higher than that of Alzheimer’s disease.One possible explanation for the association between infections and dementia is that infections trigger systemic inflammation that may reach the brain. Inflammatory molecules can cross the blood-brain barrier, potentially leading to the buildup of damaging proteins and the death of brain cells. This process may be more severe in older adults, whose immune systems are often slower to respond and recover. The study also suggests that even a single infection-related hospitalization can speed up cognitive decline, especially in individuals already at higher risk.Importantly, the risk of dementia was greatest within the first year following an infection but remained elevated for many years afterward. In fact, studies with follow-ups longer than a decade showed even stronger associations. These results suggest the need for early cognitive monitoring after hospital discharge, particularly in older adults recovering from infections.These findings have important implications for healthcare systems, particularly those serving aging populations, and underscore the lasting impact that infections can have on the brain. This research highlights the importance of looking beyond genetics and lifestyle for prevention strategies. With over 50 million people affected by dementia worldwide and annual care costs in the U.S. exceeding $300 billion, identifying new and preventable risk factors is critical. Reducing infections, improving hospital care, and monitoring brain health after illness may offer promising ways to protect cognitive function in aging populations.DOI - https://doi.org/10.18632/aging.206329Corresponding author - Eng-King Tan - tan.eng.king@singhealth.com.sgAbstract video - https://www.youtube.com/watch?v=uyv5VHHHIA4Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206329Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsTo learn more about the journal, visit https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@Aging-USLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
0.01) when evaluating all cohorts.”The authors suggest that other factors, such as the health of the egg’s mitochondria or mutations in maternal-effect genes, may explain why some embryos stop developing. These insights could help researchers identify new ways to improve embryo quality, especially for older women undergoing IVF.Importantly, the study focused on embryos that developed far enough to be tested, which helped avoid technical problems that come with analyzing arrested embryos directly. This approach allowed for more reliable comparisons across age groups and embryo quality.Overall, the study highlights the importance of maternal age as a key factor in embryo development, independent of chromosomal results. It also opens new directions for research, aiming to better understand why embryos fail to develop and how this knowledge might lead to improved fertility treatments in the future.DOI - https://doi.org/10.18632/aging.206328Corresponding author - Emre Seli - emre.seli@yale.eduAbstract video - https://www.youtube.com/watch?v=g0oS3HBNmuQSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206328Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, ovarian aging, reproductive aging, embryonic arrest, embryonic aneuploidy, developmental arrestTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@Aging-USLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — November 18, 2025 — A new #research paper was #published in Volume 17, Issue 10 of Aging-US on October 3, 2025, titled “Growth hormone excess drives liver aging via increased glycation stress.”In this study, led by first author Parminder Singh alongside with corresponding authors Pankaj Kapahi from the Buck Institute for Research on Aging and Andrzej Bartke from Southern Illinois University School of Medicine, researchers investigated how elevated growth hormone (GH) levels contribute to liver aging and dysfunction. They found that excess GH disrupts liver metabolism in ways that resemble aging-related liver damage. The study suggests that managing glycation stress may help prevent or treat liver diseases linked to abnormal hormone levels.Excess GH is known to cause different disorders, but its long-term impact on internal organs like the liver has remained unclear. To address this, researchers used a mouse model engineered to overproduce bovine GH and examined how chronic hormone exposure affects liver function over time.“Pathological conditions such as acromegaly or pituitary tumors result in elevated circulating GH levels, which have been implicated in a spectrum of metabolic disorders, potentially by regulating liver metabolism.”The team found that young mice with GH overexpression showed molecular and cellular patterns similar to those in naturally aged livers. In both groups, genes involved in metabolism were suppressed, while those linked to immune and inflammatory responses were activated. On one hand, the metabolic changes were associated with the buildup of advanced glycation end products, harmful compounds formed when sugars attach to proteins or fats without proper regulation. On the other hand, the immune and inflammatory changes reflected a process known as “inflammaging,” a form of chronic, low-grade inflammation commonly associated with aging. By revealing the overlap between hormone-driven and age-related liver dysfunction, the study provides new insight into how GH may accelerate aging processes.Importantly, the team showed that reducing glycation stress can reverse many of these negative effects. Mice treated with a compound that lowers glycation levels demonstrated improved liver health, reduced insulin resistance, and enhanced physical function. This intervention also corrected several abnormal genetic patterns caused by excess GH. The findings point to a potential therapeutic strategy for liver diseases associated with aging and hormonal imbalances.Overall, this research identifies glycation and its byproducts as key contributors to liver damage caused by excess GH. It suggests that targeting glycation could offer broad therapeutic benefits, not only for hormone-related conditions but also for supporting liver health during aging.DOI - https://doi.org/10.18632/aging.206327Corresponding authors - Andrzej Bartke - abartke@siumed.edu and Pankaj Kapahi - pkapahi@buckinstitute.orgAbstract video - https://www.youtube.com/watch?v=6v8xi5muLwASign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206327Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, growth hormone, glycation stress, Gly-LowTo learn more about the journal, visit https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@Aging-USLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Aging Series - www.aging-us.com/longevityAbstractThe study assesses the effectiveness and safety of the Stem Cell Regenera Treatment for oocyte activation in women with ovarian failure, including conditions such as Poor Ovarian Response (POR), Diminished Ovarian Reserve (DOR), and Premature Ovarian Insufficiency (POI). This retrospective observational study was conducted from January 2023 to December 2024 at the IVIRMA Alicante Clinics in Spain.Women diagnosed with ovarian failure participated in the study, which involved mobilizing Hematopoietic Stem Cells from bone marrow into peripheral blood using granulocyte colony- stimulating factor (G-CSF). This was followed by an intraovarian injection of Stem Cell Factor- enriched Platelet Rich Plasma (SCFE-PRP).The primary outcome measures were the rate of oocyte activation, leukocytes and stem cell count, and pregnancy rates. Oocyte activation was defined as an increase in total Antral Follicle Count of three or more follicles after treatment and/or at least a 20% rise in Anti-Müllerian Hormone levels. Safety was assessed based on adverse effects. Pregnancy rates were evaluated for both spontaneous gestation and following in vitro fertilization (IVF) treatment.A total of 145 women participated: the overall activation rate was 68.28%, with 7.07% achieving spontaneous gestation and 14.14% achieving pregnancy following IVF. Mobilization of CD34+ cells was successful in all participants, with an average collection of 32.96 CD34+ cells/μl. No severe adverse effects were observed. The study concluded that the Stem Cell Regenera Treatment is effective and safe for oocyte activation in women with ovarian failure in real-world practice.Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206274Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, Stem Cell Regenera, oocyte activation, ovarian regeneration, G-CSF, SCFE-PRP, ovarian failureTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@Aging-USLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — November 13, 2025 — A new #research paper was #published in Volume 17, Issue 10 of Aging-US on October 3, 2025, titled “The role of phenylalanine and tyrosine in longevity: a cohort and Mendelian randomization study.”In this study led by Jie V. Zhao, Yitang Sun, Junmeng Zhang, and Kaixiong Ye from the University of Hong Kong and the University of Georgia, researchers investigated whether two amino acids, phenylalanine and tyrosine, affect how long people live (lifespan). The results suggest that higher levels of tyrosine are linked to shorter life expectancy in men, pointing to potential sex-specific approaches to promoting longevity.Phenylalanine and tyrosine are amino acids involved in metabolism and brain function. Both are found in protein-rich foods and dietary supplements, but their long-term effects on aging are not well understood. Tyrosine, in particular, is a building block of neurotransmitters such as dopamine, which regulate mood and cognitive function, making it a molecule of interest in aging research.The study analyzed data from more than 270,000 individuals in the UK Biobank. Using both observational and genetic methods, the researchers examined the associations between blood levels of phenylalanine and tyrosine with overall mortality and predicted lifespan. Although both amino acids were initially linked to higher mortality risk, only tyrosine showed a consistent and potentially causal association with reduced life expectancy in men. Genetic analyses estimated that elevated tyrosine levels could shorten men’s lifespan by nearly one year. No significant effect was observed in women.These findings remained consistent even after adjusting for related factors, including the role of phenylalanine. This suggests that tyrosine may independently influence aging. The researchers also observed that men tend to have higher tyrosine levels than women, which could partly explain the gender gap in lifespan.“Phenylalanine showed no association with lifespan in either men or women after controlling for tyrosine.”The exact mechanisms behind this effect are still under investigation. However, tyrosine’s involvement in insulin resistance and the production of stress-related neurotransmitters may be contributing factors. Insulin resistance is associated with many age-related diseases, and hormone-related pathways influenced by tyrosine may differ between men and women, potentially explaining the sex-specific outcomes.Although tyrosine is commonly marketed as a supplement for enhancing focus and mental performance, the study raises concerns about its long-term impact on lifespan. While the researchers did not directly study tyrosine supplementation, their findings suggest that people with high tyrosine levels may benefit from dietary adjustments. Strategies such as protein restriction could help reduce tyrosine levels and support healthier aging.Further studies are needed to confirm these findings and explore whether diet and lifestyle changes can safely lower tyrosine levels to promote longevity.DOI - https://doi.org/10.18632/aging.206326Corresponding author - Jie V. Zhao - janezhao@hku.hkAbstract video - https://www.youtube.com/watch?v=rr0G44TD36MSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@Aging-USLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Aging-US proudly sponsored the Future of Aging Research (FAR) Mixer 2025, hosted by the Aging Initiative on November 7 in Cambridge, MA, uniting students, researchers, and biotechnology leaders to advance aging research and shape a healthier, longer-lived future.Highlights from the FAR Mixer 2025The 2025 FAR Mixer featured keynote speaker Dr. Kristen Fortney, Co-Founder and CEO of BioAge Labs, who shared insights into how translational research and clinical pipelines have evolved over the past decade. Dr. Fortney highlighted how obesity-targeting drugs are opening new avenues for metabolic and aging research. She explained that while obesity and osteoporosis are currently major therapeutic priorities, the next wave of reimbursable diseases will likely focus on muscle loss and chronic inflammation, reflecting their growing recognition as key factors in healthy aging. She also emphasized the importance of human databases in target discovery, cross-sector partnerships between pharma and biotech, and the increasing focus on small-molecule interventions to address age-related diseases.Focus talks showcased the diversity and depth of modern aging research.Full recap - https://aging-us.org/2025/11/aging-us-supports-the-future-of-aging-research-mixer-2025/To learn more about the journal, please visit www.Aging-US.com and connect with us on social media at:Facebook - www.facebook.com/AgingUS/X - twitter.com/AgingJrnlInstagram - www.instagram.com/agingjrnl/YouTube - www.youtube.com/@Aging-USLinkedIn - www.linkedin.com/company/aging/Bluesky - bsky.app/profile/aging-us.bsky.socialPinterest - www.pinterest.com/AgingUS/Spotify - open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Synucleinopathies are a group of age-related neurological disorders, including Parkinson’s disease, dementia with Lewy bodies, and multiple system atrophy. Most individuals are not diagnosed until these diseases have significantly progressed, as early symptoms, such as a reduced sense of smell, subtle cognitive or motor changes are too vague to serve as reliable indicators. To uncover specific biological signs that appear earlier and clearly point to the disease process, researchers from Saarland University developed a study titled “Brain region-specific and systemic transcriptomic alterations in a human alpha-synuclein overexpressing rat model,” featured as the cover Aging-US, Volume 17, Issue 10.Full blog - https://aging-us.org/2025/11/alpha-synuclein-overexpression-in-rats-reveals-early-clues-to-synucleinopathies/Paper DOI - https://doi.org/10.18632/aging.206331Corresponding author - Thomas Hentrich - thomas.hentrich@uni-saarland.deAbstract video - https://www.youtube.com/watch?v=Yl6AfVchkb0Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206331Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, alpha-synuclein, transgenic rat model, different brain regions, transcriptome analysisTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@Aging-USLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — November 11, 2025 — A new #research paper was #published in Volume 17, Issue 10 of Aging-US on October 1, 2025, titled “L-β-aminoisobutyric acid (L-BAIBA) in combination with voluntary wheel running exercise enhances musculoskeletal properties in middle-age male mice.”In this study led by first author Julian A. Vallejo and corresponding author Michael J. Wacker from the University of Missouri, Kansas City, researchers investigated how L-β-aminoisobutyric acid (L-BAIBA), a natural compound released during exercise, works together with regular physical activity to improve muscle and bone health in middle-aged male mice. The findings may support new strategies to maintain musculoskeletal health in aging populations, especially those at risk for mobility loss or osteoporosis.Muscle and bone strength naturally decline with age, increasing the risk of falls, fractures, and reduced quality of life. While exercise remains the most effective way to counteract this deterioration, it is often difficult for older individuals to maintain sufficient activity levels to see results. L-BAIBA, a molecule naturally produced during physical activity, is known to promote energy metabolism and support muscle and bone cells. This study explored its potential to work in synergy with endurance exercise to maximize health benefits in aging bodies.Researchers studied 12-month-old male mice that were split into different groups. Some remained sedentary, while others exercised freely on running wheels. Half of each group received daily L-BAIBA supplementation. After three months, the mice that received both the supplement and exercise showed greater improvements than those receiving either one alone. The soleus, a slow-twitch muscle essential for endurance and balance, grew larger and stronger only in the combined treatment group. These muscles also shifted to a more fatigue-resistant fiber type and had a larger number of oxidative fibers.“To investigate this hypothesis, we subjected 12-month-old (as a model of middle-age) male C57BL6 mice to voluntary wheel running (VWR) with L-BAIBA (100mg/kg/day) (VWR+L-BAIBA), VWR alone, L-BAIBA alone, or none (CTRL) for three months.”The study also showed significant improvements in bone health. Mice that received both exercise and L-BAIBA developed thicker and denser trabecular bone, along with reduced fat levels in the bone marrow, indicators of stronger, healthier bones. These changes were not observed in the groups that only exercised or only received L-BAIBA. Although the compound caused minor changes in heart electrical activity, it did not affect heart size or overall function, suggesting it is safe in this setting.These findings suggest that L-BAIBA may enhance the benefits of physical activity by supporting muscle strength and bone structure, particularly in slow-twitch muscle fibers. This combination could serve as a therapeutic strategy to help older adults, including those unable to engage in regular exercise, maintain musculoskeletal health.As the aging population grows, there is a growing need for solutions that support muscle and bone health without requiring strenuous activity. This research highlights the potential of natural, exercise-related molecules like L-BAIBA to help maintain mobility and strength throughout aging.DOI - https://doi.org/10.18632/aging.206325Corresponding author - Michael J. Wacker — wackerm@umkc.eduAbstract video - https://www.youtube.com/watch?v=A-zfrLUikfQVisit https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@Aging-USLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — November 5, 2025 — A new #research paper was #published in Volume 17, Issue 10 of Aging-US on September 10, 2025, titled “Longitudinal associations of epigenetic aging with cognitive aging in Hispanic/Latino adults from the Hispanic Community Health Study/Study of Latinos.”In this study led by Myriam Fornage, from The University of Texas Health Science Center at Houston, researchers found that faster biological aging, measured by DNA-based epigenetic clocks, is associated with greater cognitive decline and higher risk of mild cognitive impairment (MCI) in Hispanic/Latino adults. The results highlight the potential of epigenetic clocks to track changes in brain health over time, helping improve early detection and monitoring of age-related cognitive problems.Cognitive decline and dementia are major public health concerns, especially among aging populations. In this study, researchers followed 2671 Hispanic/Latino adults (average age 57; 66% women) over a seven-year period. They measured each participant’s biological age using epigenetic clocks and assessed their cognitive performance at two time points.“We evaluated the associations of 5 epigenetic clocks and their between-visit change with multiple measures of cognitive aging that included a global and domain-specific cognitive function score at each visit, between-visit change in global and domain-specific cognitive function score, and MCI diagnosis at visit 2 (V2).”Epigenetic clocks estimate biological age based on DNA chemical modifications, called methylation, that accumulate with age. The study evaluated five different clocks, including newer models like GrimAge and DunedinPACE, which are designed to more accurately reflect health-related aging.The researchers found that individuals with faster biological aging showed lower cognitive function and higher probability of developing MCI over time. Among the five clocks studied, newer models such as GrimAge and DunedinPACE showed the strongest associations with memory, processing speed, and overall brain health. These findings suggest that tracking changes in biological age over time may be more effective than relying on a single measurement to identify those at risk for cognitive impairment.Importantly, the associations between biological aging and cognitive decline remained significant even after accounting for other known risk factors such as education, language preference, and cardiovascular health. This supports the idea that epigenetic clocks capture unique biological processes that influence brain aging. The study also found that the impact of changes in biological age over time was comparable to that of APOE4, a well-established genetic risk factor for Alzheimer’s disease.Overall, this is the first large-scale study to examine these associations in a Hispanic/Latino population, a group that is underrepresented in aging research. By identifying early biological signs of brain aging, this work highlights the potential of epigenetic clocks as tools for routine health assessments. Monitoring changes in these biological markers could help detect individuals at risk for cognitive decline and guide timely interventions to preserve brain health.DOI - https://doi.org/10.18632/aging.206317Corresponding author - Myriam Fornage - Myriam.Fornage@uth.tmc.eduAbstract video - https://www.youtube.com/watch?v=kG0Y-F_sodsTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@Aging-USLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — November 3, 2025 — A new #research paper featured on the #cover of Volume 17, Issue 10 of Aging-US was #published on October 20, 2025, titled “Brain region-specific and systemic transcriptomic alterations in a human alpha-synuclein overexpressing rat model.”In this study, led by first author Vivien Hoof and corresponding author Thomas Hentrich from Saarland University, Germany, researchers investigated how excess alpha-synuclein—a protein linked to Parkinson’s disease—affects gene activity in different brain regions and the gut. They found that early, region-specific gene disruptions may contribute to the appearance of disease, with some effects also detected in the gut. These early molecular changes could serve as biomarkers for Parkinson’s and point to new directions for treatment.Alpha-synuclein accumulates in the brains of individuals with Parkinson’s disease and other age-related neurological conditions known as synucleinopathies. To better understand this process, the research team used a genetically modified rat model that overexpresses human alpha-synuclein. They studied gene expression in the striatum, cortex, and cerebellum—three key brain regions involved in movement and cognition—and analyzed how these changes evolved with age. “Transcriptomic analyses were performed on gene and transcript level of striatal, frontocortical, and cerebellar tissue in 5- and 12-month-old transgenic (BAC SNCA) and wild type rats […]”The results showed that gene alterations appeared earlier and were more pronounced in young rats, particularly in the striatum and cortex, before any visible signs of disease manifested. This early disruption challenges the common belief that gene alterations gradually increase with age and suggests that early-life molecular changes may be critical in disease development.The researchers also found that many gene expression changes were unique to individual brain regions. However, they identified a set of genes that were consistently affected across all brain regions and the gut. This suggests that the disease may begin to affect the entire body—not just the brain—long before symptoms become noticeable.Several of the shared genes are involved in synaptic signaling and inflammation—processes known to be altered in Parkinson’s. Others are linked to dopamine production and neuronal plasticity, indicating potential early efforts by the brain to compensate for the harmful effects of the alpha-synuclein buildup.Overall, this study provides a detailed view of how alpha-synuclein affects gene networks early in the disease process. Understanding these changes may help identify biomarkers and develop targeted therapies before irreversible brain damage occurs.DOI - https://doi.org/10.18632/aging.206331Corresponding author - Thomas Hentrich - thomas.hentrich@uni-saarland.deAbstract video - https://www.youtube.com/watch?v=Yl6AfVchkb0Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206331Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, alpha-synuclein, transgenic rat model, different brain regions, transcriptome analysisTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@Aging-USLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — October 27, 2025 — A new #research paper was #published in Volume 17, Issue 9 of Aging-US on September 17, 2025, titled “Depletion of the TRF1 telomere-binding protein leads to leaner mice with altered metabolic profiles.”In this study led by first author Jessica Louzame Ruano and corresponding author Maria A. Blasco from the Spanish National Cancer Centre (CNIO), researchers investigated the role of TRF1, a protein known for protecting telomeres, in regulating whole-body metabolism. The results suggest that TRF1 influences metabolic health through mechanisms unrelated to its known function in telomere maintenance.Obesity and metabolic disorders are major health concerns, especially as people age. To explore TRF1’s role beyond telomere protection, the research team studied both normal mice and genetically modified mice that lacked TRF1. Mice without TRF1 remained leaner over time, resisted fat accumulation, and showed healthier blood sugar and insulin levels compared to normal mice. Importantly, these benefits occurred without any detectable shortening of telomeres.The leaner body composition in TRF1-deficient mice was not due to reduced food intake or increased physical activity. Instead, the fat loss appeared to result from biological changes in how energy was processed and stored. Male mice without TRF1 gained less weight and had lower LDL cholesterol levels, even on a high-fat diet. Female mice showed milder effects, reflecting known sex-based differences in susceptibility to diet-induced obesity. This highlights the importance of including both sexes in metabolic research.“Major metabolic pathways related with energy production and regulation of metabolism homeostasis were also found downregulated in Trf1-deficient mice.”Gene expression analysis in the liver revealed shifts in several key pathways. Genes related to fat production, energy generation, and muscle growth were downregulated, while genes linked to inflammation and cholesterol synthesis were upregulated. The mice also showed signs of higher energy expenditure and a shift from using fat to protein as an energy source, possibly due to their reduced fat reserves. However, some older mice developed mild liver stress, including fibrosis and DNA damage, suggesting a possible long-term trade-off.Overall, this study expands the understanding of how telomere-related proteins influence more than just cellular aging. By identifying a connection between TRF1 and metabolism, the research opens new possibilities for targeting TRF1 or its pathways to address obesity and related conditions. Still, further studies are needed to clarify how TRF1 affects fat development and whether similar effects occur in humans.DOI - https://doi.org/10.18632/aging.206320Corresponding author - Maria A. Blasco — mblasco@cnio.esAbstract video - https://www.youtube.com/watch?v=7AG3TBgDZIwSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206320Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, Trf1, metabolism, leaner, fat, telomeresTo learn more about the journal, visit https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — October 23, 2025 — A new #research paper was #published in Volume 17, Issue 9 of Aging-US on September 11, 2025, titled “Roles of plasminogen activator inhibitor-1 in aging-related muscle and bone loss in mice.”In this study led by first author Takashi Ohira and corresponding author Hiroshi Kaji from Kindai University Faculty of Medicine, researchers found that female mice lacking the gene for plasminogen activator inhibitor-1 (PAI-1) were protected from age-related muscle weakness and bone thinning. This suggests that PAI-1 could be a potential target for future treatments to reduce frailty in aging populations.As the global population continues to age, more people are affected by conditions such as sarcopenia and osteoporosis. These disorders involve the progressive loss of skeletal muscle mass and bone density, leading to reduced mobility, a greater risk of falls, and a lower quality of life.To investigate the role of PAI-1 in aging, researchers compared young (6-month-old) and aged (24-month-old) male and female mice, with and without the PAI-1 gene. They found that PAI-1 levels increased with age in both sexes. However, only female mice lacking the PAI-1 gene experienced a significant reduction in age-related muscle and bone loss.Female mice without PAI-1 maintained stronger grip strength and greater muscle mass in their lower limbs. They also showed less cortical bone loss in their femurs and tibias. In contrast, male mice did not experience the same benefits, despite also showing increased levels of PAI-1 with age. These results suggest that PAI-1 contributes to aging-related decline in a sex-specific manner.“The present study found that lower limb muscle mass, gastrocnemius and soleus muscle tissue weights, and grip strength were significantly lower in 24-month-old male and female wild-type mice than in their 6-month-old counterparts.”PAI-1 plays key roles in blood clotting, inflammation, and cellular senescence—a process in which aging cells release harmful molecules that affect nearby tissues. One of these molecules, interleukin-6 (IL-6), is a major driver of inflammation. The researchers found that aged female mice lacking PAI-1 had lower IL-6 levels in both muscle and blood, suggesting that PAI-1 may contribute to muscle and bone loss by promoting inflammation. These protective effects were also not associated with changes in muscle protein turnover or reductions in fibrous tissue, reinforcing the idea that PAI-1’s impact is likely driven by inflammatory signaling.This study highlights PAI-1 as a promising therapeutic target for slowing or preventing age-related declines in muscle and bone health, particularly in women. Since postmenopausal women are especially vulnerable to osteoporosis and frailty, a better understanding of how PAI-1 contributes to aging could lead to new strategies for maintaining strength and mobility in later life. Further research is needed to explore how PAI-1 interacts with other age-related biological changes and why its effects differ between sexes.DOI - https://doi.org/10.18632/aging.206318Corresponding author - Hiroshi Kaji - hkaji@med.kindai.ac.jpAbstract video - https://www.youtube.com/watch?v=hg4qKf-oO2ISubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsTo learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@Aging-USLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — October 21, 2025 — A new #editorial was #published in Aging-US on October 13, 2025, titled “Longevity clinics: between promise and peril.”In this editorial, Marco Demaria, Editor-in-Chief of Aging-US, from the European Research Institute for the Biology of Ageing (ERIBA), University Medical Center Groningen (UMCG), University of Groningen (RUG), reviews the rapid rise of longevity clinics worldwide. Longevity clinics have emerged globally in response to increasing demand for personalized, preventive healthcare. Located in countries such as the United States, Switzerland, and the United Arab Emirates, these centers offer advanced diagnostic services, including genomic testing, advanced imaging, and multi-omics profiling. Their goal is to extend healthspan—the number of years a person lives in good health—through customized lifestyle interventions, nutritional guidance, and, in some cases, experimental therapies.“Longevity clinics embody an important vision: healthcare is personalized, preventive, and engaged.”Although the concept of proactive aging care is attractive, the editorial raises serious concerns about the scientific and ethical foundations of these clinics. Many operate outside conventional medical systems and lack connections to academic geroscience. This disconnection allows them to market expensive interventions without sufficient clinical validation. Program costs can range from €10,000 to over €100,000 per year, limiting access to wealthy individuals while leaving out populations most at risk for premature aging.Despite these challenges, Dr. Demaria notes that longevity clinics may contribute meaningfully to innovation. By collecting extensive, long-term health data from clients, these clinics have the potential to identify early biomarkers of aging and detect signs of age-related diseases. Unlike traditional clinical trials, which are limited in scope and duration, longevity clinics track a wide range of health data over time. When paired with artificial intelligence tools, this information could help advance the science of healthy aging.However, several risks remain. Many clinics lack standardized protocols, and the tools they use, such as biological age calculators or hormone therapies, often lack accuracy or clear clinical value. Without proper guidelines, clients may receive advice that is confusing or not scientifically supported. This can reduce public trust in the broader field of longevity research.To ensure these clinics contribute positively to health innovation, the editorial outlines different key steps: greater collaboration with academic researchers, the adoption of standardized protocols, increased transparency, and work toward regulatory clarity. Broader access must also be considered by developing scalable and more affordable models, possibly through partnerships with public health systems.Ultimately, longevity clinics represent both a major opportunity and a serious concern. If integrated responsibly with science, policy, and public health, they could support a shift toward personalized, preventive healthcare. Without this alignment, however, they risk reinforcing inequality and weakening the credibility of the science behind aging.DOI - https://doi.org/10.18632/aging.206330Corresponding author - Marco Demaria — m.demaria@umcg.nlAbstract video - https://www.youtube.com/watch?v=Bt84xBdii0sTo learn more about the journal, visit https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — October 17, 2025 — A new #research paper was #published in Volume 17, Issue 9 of Aging-US on September 8, 2025, titled, “Runx1 overexpression induces early onset of intervertebral disc degeneration.”In this study, led by first author Takanori Fukunaga from Emory University School of Medicine and corresponding author Hicham Drissi from Emory and the Atlanta VA Medical Center, researchers found that the Runx1 gene, when overactive in spinal disc cells, can accelerate age-related degeneration of the intervertebral discs. The findings offer new insight into the genetic factors that drive disc aging and suggest possible directions for treating chronic back pain.Intervertebral discs cushion the spine and support movement. Their deterioration is a major cause of lower back pain, especially with aging. At the center of each disc is the nucleus pulposus (NP), a gel-like core that contains proteins such as collagen and aggrecan, which help retain water and maintain structure. As people age, NP cells often lose their function, contributing to disc breakdown.Using a genetically modified mouse model, the researchers activated Runx1 specifically in NP cells. These mice developed signs of disc degeneration by five months of age, which is much earlier than normal. The overexpression of Runx1 led to the loss of healthy NP cells, an increase in abnormal cell types, and damage to disc structure. Levels of essential proteins like aggrecan and type II collagen decreased, while type X collagen increased, signaling unhealthy tissue changes.“To achieve NP-specific postnatal overexpression of Runx1, we crossed Krt19CreERT mice with Rosa26-Runx1 transgenic mice previously generated in our laboratory.”A key finding was that Runx1 overactivity did not kill cells directly. Instead, it caused premature cellular aging, known as senescence. Senescent cells lose the ability to repair tissue, creating an environment that accelerates degeneration. Markers of senescence were significantly elevated in the affected discs.The researchers also observed a dose-dependent response. The more Runx1 was activated, the more severe the degeneration was. This suggests that targeting Runx1 may be a promising strategy to prevent or slow disc aging.Overall, this study highlights the genetic and cellular processes that contribute to intervertebral disc degeneration, a leading cause of disability. By identifying Runx1 as a potential driver of early disc aging, the research opens new opportunities for intervention and treatment of degenerative spine conditions.DOI - https://doi.org/10.18632/aging.206316Corresponding author - Hicham Drissi - hicham.drissi@emory.eduAbstract video - https://www.youtube.com/watch?v=BPwWbVBPIUMSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206316Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - cell senescence, aging, Runx1, nucleus pulposus, intervertebral disc degenerationTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@Aging-USLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
As people age, it is common to experience some memory lapses or slower thinking. Although this is often a normal part of aging, it can still affect a person’s quality of life. Scientists have been investigating ways to slow or prevent cognitive decline, and growing evidence points to the potential role of social interaction.Recently, a study using rats found that long-term social connection may help protect the brain from age-related memory decline. This work, titled “The impact of long-term social housing on biconditional association task performance and neuron ensembles in the anterior cingulate cortex and the hippocampal CA3 region of aged rats,” was recently published in Aging-US (Volume 17, Issue 9).Full blog - https://aging-us.org/2025/10/how-long-term-social-connection-supports-brain-health-and-memory-in-aging/Paper DOI - https://doi.org/10.18632/aging.206310Corresponding author - Anne M. Dankert - adankert@unc.eduAbstract video - https://www.youtube.com/watch?v=poNnPz1ti6QSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206310Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, aging, environmental enrichment, working memory, complex cognition, immediate early genesTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — October 14, 2025 — A new #research paper was #published in Volume 17, Issue 9 of Aging-US on August 30, 2025, titled, “Glycocalyx-targeted therapy prevents age-related muscle loss and declines in maximal exercise capacity.”In this study, led by Daniel R. Machin from the University of New Mexico School of Medicine and the University of Utah, researchers found that protecting a fragile layer lining blood vessels, known as the glycocalyx, can prevent muscle deterioration and help maintain physical performance during aging. They also discovered that a supplement containing high-molecular-weight hyaluronan (HMW-HA), a key component of the glycocalyx, enabled older mice to preserve muscle mass and exercise capacity. These findings suggest that targeting the glycocalyx may offer a new approach to reduce frailty and support mobility in older adults.As this layer degrades with age, it contributes to cardiovascular and muscular decline by impairing blood flow and vascular health. The study examined how preserving the glycocalyx using a therapy called Endocalyx™ affects physical function in aging mice.Researchers first studied genetically modified mice lacking Has2, the enzyme responsible for producing HMW-HA. These mice had a thinner glycocalyx, reduced exercise performance, and lower mitochondrial function in their muscles, even though muscle size remained normal. This indicated that glycocalyx damage alone can directly impair physical performance.The team then gave older mice a diet containing Endocalyx™ for 10 weeks. Compared to untreated controls, these mice maintained muscle mass and performed better on treadmill tests. Notably, the treated mice did not show the typical age-related decline in muscle strength and endurance. While the supplement did not fully restore youthful performance, it significantly slowed physical deterioration, suggesting a protective benefit. In contrast, untreated older mice lost both body mass and muscle volume during the same period.“Taken together, these findings provide direct evidence of a role for HMW-HA in the modulation of exercise capacity.”This research builds on prior evidence that the glycocalyx is essential for healthy blood vessel function. Since muscle health depends on proper blood flow and oxygen delivery, restoring the glycocalyx may help maintain strength and mobility with age. While more research is needed to confirm these results in humans, the findings point to a potential therapeutic approach to promote healthier aging.DOI - https://doi.org/10.18632/aging.206313Corresponding author - Daniel R. Machin — dmachin@salud.unm.eduAbstract video - https://www.youtube.com/watch?v=S7HjCeXT8fUSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206313Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, glycocalyx, hyaluronanTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Federica Grosso from the Institute for Genetic and Biomedical Research (IRGB) of the National Research Council (CNR) in Monserrato, Italy, describes a #research paper she co-authored that was #published in Volume 17, Issue 8 of Aging-US, entitled “Causal relationships between gut microbiome and hundreds of age-related traits: evidence of a replicable effect on ApoM protein levels.”DOI - https://doi.org/10.18632/aging.206293Corresponding author - Serena Sanna - serena.sanna@cnr.itVideo interview - https://www.youtube.com/watch?v=qYg42_gn_pwAbstractIn the past 20 years, the involvement of gut microbiome in human health has received particular attention, but its contribution to age-related diseases remains unclear. To address this, we performed a comprehensive two-sample Mendelian Randomization investigation, testing 55130 potential causal relationships between 37 traits representing gut microbiome composition and function and age-related phenotypes, including 1472 inflammatory and cardiometabolic circulating plasma proteins from UK Biobank Pharma Proteomic Project and 18 complex traits. A total of 91 causal relationships remained significant after multiple testing correction (false discovery rate p-value <0.05) and sensitivity analyses, notably two with the risk of developing age-related macular degeneration and 89 with plasma proteins. The link between purine nucleotides degradation II aerobic pathway and apolipoprotein M was further replicated using independent genome-wide association study data. Finally, by taking advantage of previously reported biological function of Faecalibacterium prausnitzii we found evidence of regulation of six proteins by its function as mucosal-A antigen utilization. These results support the role of gut microbiome as modulator of the inflammatory and cardiometabolic circuits, that may contribute to the onset of age-related diseases, albeit future studies are needed to investigate the underlying biological mechanisms.Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206293Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, causal inference, aging, gut microbiome, inflammatory proteins, age-related macular degenerationTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — October 9, 2025 — A new #research paper was #published in Volume 17, Issue 9 of Aging-US on August 22, 2025, titled, “The impact of long-term social housing on biconditional association task performance and neuron ensembles in the anterior cingulate cortex and the hippocampal CA3 region of aged rats.”The research team led by Anne M. Dankert from Providence College and University of North Carolina, Chapel Hill, showed that aged rats who lived in socially enriched environments throughout life retained better memory and cognitive flexibility than those housed alone. This study highlights the importance of social interaction in protecting the aging brain.Cognitive decline, such as memory loss and reduced problem-solving ability, affects many people over the age of 65. While many factors contribute to age-related cognitive decline, this study suggests that one key factor may be surprisingly simple: long-term social connection. To explore how social interaction might influence memory performance and brain activity, the researchers designed a study using rats as a model for aging in humans.“Cognitive decline and changes in neuronal activity are hallmarks of aging.”They compared three groups of rats: young adults, aged rats housed alone, and aged rats housed socially in groups. All groups had access to the same physical enrichment, such as exercise and stimulating objects, but only some experienced lifelong social companionship. The team tested these animals on a complex memory challenge known as the biconditional association task, which requires animals to make context-based decisions—an ability that typically declines with age.The results showed that aged rats living in social groups performed just as well as young adults on the memory task, while those housed alone showed significant impairments. Socially housed rats also made fewer working memory errors and required less effort to complete cognitive tasks, suggesting not only better performance but more efficient brain function. These benefits were not observed in aged rats who received only environmental enrichment without social interaction.Brain imaging revealed additional differences between the groups. Socially housed aged rats showed increased activity in the hippocampus, particularly in the CA3 region, which plays a key role in forming and separating memories. In contrast, aged rats that lived alone had lower activity in this region, which may explain their poorer performance. Interestingly, socially housed rats also showed reduced overactivity in the anterior cingulate cortex—a brain area involved in attention and decision-making—suggesting a more balanced and efficient neural response.This research provides new insight into how lifelong social experiences shape brain health during aging. While earlier studies have shown that physical activity and cognitive stimulation help preserve cognitive function, this study identifies social interaction as an independent and powerful protective factor. The findings are consistent with human studies showing that older adults who remain socially active tend to experience slower cognitive decline and stronger brain function.Overall, these results emphasize that brain aging is not inevitable but may be influenced by our social environments. This research suggests that fostering lifelong social connections could be a critical, low-cost strategy to protect memory and mental flexibility in older adults.DOI - https://doi.org/10.18632/aging.206310Corresponding author - Anne M. Dankert - adankert@unc.eduAbstract video - https://www.youtube.com/watch?v=poNnPz1ti6Qhttps://www.aging-us.com/MEDIA@IMPACTJOURNALS.COM
Dr. Leonard Egede, Dr. Rebekah Walker, and Dr. Obinna Ekwunife from the Department of Medicine at the University of Buffalo, NY, describe their #research paper #published in Volume 17, Issue 8 of Aging-US, entitled “Longitudinal relationship between social and CVD risk factors in older adults with prediabetes: the HRS 2006-2016.”#interview #authorinterview #aging #prediabetes #cardiovascular #health #openaccess #openscience #peerreviewed #journal #publication #publishing #mededDOI - https://doi.org/10.18632/aging.206308Corresponding author - Leonard E. Egede - legede@buffalo.eduVideo interview - https://www.youtube.com/watch?v=1MSTk3GQAGAVideo transcript - https://aging-us.net/2025/10/08/behind-the-study-social-and-cardiovascular-risk-factors-in-older-adults-with-prediabetes/AbstractBackground: This study examines how multiple social risk factors influence cardiovascular disease (CVD) risk control over time in older adults with prediabetes using a nationally representative cohort.Methods: Data from the Health and Retirement Study (HRS) included 5,086 U.S. adults aged 50+ with prediabetes. Five social risk domains (economic stability, environment, education, healthcare, and social context) were examined as independent variables, while CVD risk factors included glycemic control (HbA1c), systolic blood pressure (SBP), and cholesterol ratio (total cholesterol/high-density lipoprotein). Mixed-effects models assessed relationships between social risk factors and CVD outcomes, adjusting for age, gender, race, and marital status.Results: The sample had an average age of 68.6 years, with 60.2% female, and 70.97% identifying as non-Hispanic Black. Average HbA1c was 5.7, SBP 129.4, and cholesterol ratio 3.85. Limited education was consistently associated with increased CVD risk—HbA1c (β = 0.03, 95% CI: 0.01–0.06, p < 0.001), SBP (β = 4.34, 95% CI: 2.96–5.71, p < 0.001), and cholesterol ratio (β = 0.08, 95% CI: 0.01–0.16, p < 0.05) —in the fully adjusted model. Medication cost-related non-adherence was significantly associated with higher HbA1c levels (β = 0.03, 95% CI: 0.002–0.06, p < 0.05). Difficulty paying bills and lack of health insurance were both significantly associated with higher cholesterol levels (β = 0.03, 95% CI: 0.002–0.06, p < 0.05) and (β = 0.22, 95% CI: 0.15–0.30, p < 0.001), respectively.Conclusions: Social risk factors, particularly limited education, significantly impact CVD risk in older adults with prediabetes.Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206308Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, prediabetes, social determinants of health, health equity, cardiovascular health, population healthTo learn more about the journal, visit https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — October 7, 2025 — A new #research paper was #published in Volume 17, Issue 9 of Aging-US on August 27, 2025, titled, “Deregulated miR-145 and miR-27b in Hutchinson-Gilford progeria syndrome: implications for adipogenesis.”In this study, led by first author Felix Quirin Fenzl and corresponding author Karima Djabali from the Technical University of Munich (TUM), researchers identified that miR-145-5p and miR-27b-3p interfere with the formation of fat cells in children with Hutchinson-Gilford progeria syndrome (HGPS), a rare and fatal premature aging disorder. Their findings help explain why patients often experience fat loss and related metabolic complications and suggest new potential therapeutic strategies.Hutchinson-Gilford progeria syndrome is a genetic condition that causes rapid aging in children, often leading to early death due to heart disease. Although affected children appear healthy at birth, they soon develop signs of accelerated aging, including hair loss, stiff joints, and a significant reduction in fat tissue. While certain treatments can slow disease progression, many aspects, such as the loss of fat tissue, remain poorly understood.“Overall, this study provides the first comprehensive miRNA profiling of HGPS and control fibroblasts across different stages of cellular senescence.”This study focused on how microRNAs—tiny molecules that help regulate gene expression—contribute to the disease. To explore this, the researchers used skin-derived stem cells from both healthy individuals and HGPS patients. When they transformed these cells into fat cells, the HGPS-derived stem cells formed significantly fewer fat cells. This difference was linked to unusually high levels of miR-145-5p and miR-27b-3p. These molecules were found to silence important genes required for fat cell growth and function. When the researchers blocked these microRNAs, fat cell formation improved. The team also examined fat tissue from a mouse model of HGPS. Similar to the human cells, these mice showed increased levels of miR-145-5p and miR-27b-3p and impaired fat development. These results confirm that these two microRNAs play a central role in the loss of fat tissue seen in the disease. Importantly, reducing their activity could become a promising therapeutic strategy for restoring fat tissue in affected individuals.Although further research is needed before developing treatments, this study represents a step forward in understanding the molecular causes of lipodystrophy, a condition in which the body cannot form healthy fat tissue, in HGPS. It also opens the door for future therapies that could improve quality of life and health outcomes for patients. In the long term, similar approaches might benefit people with other metabolic diseases, such as obesity or diabetes, where fat cell function is also disrupted.DOI - https://doi.org/10.18632/aging.206309Corresponding authors - Karima Djabali — djabali@tum.deAbstract video - https://www.youtube.com/watch?v=b0ksC3cvdZ0Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206309Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, Hutchinson-Gilford progeria syndrome (HGPS), progerin, microRNAs, adipogenesisTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — October 3, 2025 — A new #research perspective was #published in Volume 17, Issue 9 of Aging-US on August 26, 2025, titled “Analysis of the current state of frailty indexes and their implementation for aging intervention studies.” In this work, led by first author Oliver G. Frost from Loughborough University alongside corresponding authors Abdelhadi Rebbaa and Amit Sharma, from the Lifespan Research Institute, the authors explore growing concerns about the lack of standardization in how frailty is measured in rodent aging studies, which may limit the development of effective interventions targeting age-related decline.Frailty, a key indicator of deteriorating health in older adults, is increasingly assessed in preclinical models using frailty indexes (FIs). These indexes quantify health deficits, such as reduced mobility, cognitive decline, or physical weakness. However, this perspective highlights that FI methodologies vary significantly across studies, from the selection of parameters to the cut-off thresholds used, resulting in inconsistent outcomes that affects reproducibility and translational value.The authors reviewed 18 rodent studies and found substantial variation in how frailty is defined and measured. Some FIs rely on clinical observations, such as appearance or beahaviour, while others focus on physical performance metrics like grip strength or locomotion. In several cases, applying different FIs to the same group of animals produced contradictory results, underscoring the importance of harmonized protocols.To illustrate these issues, the researchers applied an 8-item FI to mice of different ages and found that even young mice were sometimes scored as frail, depending on the scoring method and reference values. This finding emphasizes the need for consistent baselines and controlled environments, especially when comparing across studies. The authors recommend using each animal as its own baseline in longitudinal studies, a strategy that enhances reliability without adding significant cost.“Sex as a biological variable in FIs is an important consideration, as there is a known difference between male and female frailty onset and progression.” The authors also discuss emerging automated tools, such as video-based open-field testing, which can reduce observer bias and improve reproducibility. In the future, broader health indicators, such as cognition, circadian rhythms, social behavior, and body composition, may further enhance frailty assessments.Overall, this work underscores the urgent need for standardized, transparent, and reproducible methods for evaluating frailty in preclinical aging studies. Improved consistency in frailty scoring will better inform the development of healthspan-extending therapies and enhance the translational relevance of animal models.DOI - https://doi.org/10.18632/aging.206307Corresponding authors - Abdelhadi Rebbaa - rebbaa@gmail.com, and Amit Sharma - amit.sharma@sens.orgAbstract video - https://www.youtube.com/watch?v=eha3XA9LyWASign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206307Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, frailty, rodents, frailty index, phenotypeTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
As life expectancy increases, there is growing interest not only in extending lifespan but also in improving the quality of those additional years. To address the physical and cognitive decline that often accompanies aging, researchers have explored a variety of strategies. Many of these focus on a single biological factor, such as reducing inflammation or stimulating stem cell activity. However, aging is a complex process involving multiple, interconnected changes in the body.Recognizing this, researchers at the University of California, Berkeley proposed a more comprehensive approach: targeting multiple aging-related pathways simultaneously. Their study, titled “Sex-specific longitudinal reversal of aging in old frail mice,” was recently featured on the cover of Aging-US (Volume 17, Issue 9).Full blog - https://aging-us.org/2025/10/new-anti-aging-combo-boosts-lifespan-in-old-male-mice/Paper DOI - https://doi.org/10.18632/aging.206304Corresponding author - Irina M. Conboy - irina@generationlab.coAbstract video - https://www.youtube.com/watch?v=bpWxDd7hHhMSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206304Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, lifespan, healthspan, Alk5 inhibitor, oxytocin, sex-specific differencesTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — October 1, 2025 — A new #research paper #featured as the #cover of Volume 17, Issue 9 of Aging-US was published on August 21, 2025, titled “Sex-specific longitudinal reversal of aging in old frail mice.” The study, led by first author Cameron Kato and corresponding author and Aging-US Editorial Board Member Irina M. Conboy from the University of California, Berkeley, reports that a combination of oxytocin and an Alk5 inhibitor (OT+A5i) significantly extended both lifespan and healthspan in frail, elderly, male mice. These rejuvenating effects were not seen in female mice, highlighting key biological differences between the sexes in their response to aging therapies.The researchers tested a dual-drug approach targeting two biological pathways that change with age. Oxytocin, a hormone that declines with aging and supports tissue repair, was combined with an Alk5 inhibitor that blocks the TGF-beta pathway. TGF-beta becomes overactive with age and contributes to chronic inflammation and tissue damage. In this study, frail mice at 25 months of age—roughly equivalent to 75 human years—were treated regularly with the OT+A5i combination.Male mice receiving the therapy lived over 70% longer than untreated controls and showed significant improvements in physical endurance, agility, and memory. According to hazard ratio analysis, the treated males were nearly three times less likely to die at any given time than untreated males. “Treatment of old frail male mice with OT+A5i resulted in a remarkable 73% life extension from that time, and a 14% increase in the overall median lifespan.”The therapy also reduced “biological noise” in circulating blood proteins—an established marker of aging—bringing those levels back to a more youthful state. Short-term benefits, were seen in both sexes, however, after four months of continuous treatment, only the male mice showed sustained improvement in systemic protein balance. Female mice did not experience significant gains in lifespan or healthspan, though middle-aged females did show improved fertility after treatment.These results underscore the importance of understanding sex-specific biology when developing treatments for aging. While the reasons for these differences remain unclear, the findings provide a new model for studying and designing longevity therapies.Oxytocin is already FDA-approved, and Alk5 inhibitors are currently in clinical trials, suggesting that this approach could be translated to humans. With strong results in aged and frail male animals, OT+A5i appears to be a promising candidate for improving late-life health and survival.DOI - https://doi.org/10.18632/aging.206304Corresponding author - Irina M. Conboy - irina@generationlab.coAbstract video - https://www.youtube.com/watch?v=bpWxDd7hHhMSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206304Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, lifespan, healthspan, Alk5 inhibitor, oxytocin, sex-specific differencesTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
In this episode of the Longevity & Aging Series, Girish Harinath from AgelessRx joins host Dr. Evgeniy Galimov to discuss a research paper he co-authored in Volume 17, Issue 4 of Aging-US, titled “Influence of rapamycin on safety and healthspan metrics after one year: PEARL trial results.”DOI - https://doi.org/10.18632/aging.206235Corresponding author - Stefanie L. Morgan - stefanie@agelessrx.comVideo interview - https://www.youtube.com/watch?v=7-NvskI8Ve0Longevity & Aging Series - https://www.aging-us.com/longevityAbstractDesign: This 48-week decentralized, double-blinded, randomized, placebo-controlled trial (NCT04488601) evaluated the long-term safety of intermittent low-dose rapamycin in a healthy, normative-aging human cohort. Participants received placebo, 5 mg or 10 mg compounded rapamycin weekly. The primary outcome measure was visceral adiposity (by DXA scan), secondary outcomes were blood biomarkers, and lean tissue and bone mineral content (by DXA scan). Established surveys were utilized to evaluate health and well-being. Safety was assessed through adverse events and blood biomarker monitoring.Results: Adverse and serious adverse events were similar across all groups. Visceral adiposity did not change significantly (ηp2 = 0.001, p = 0.942), and changes in blood biomarkers remained within normal ranges. Lean tissue mass (ηp2 = 0.202, p = 0.013) and self-reported pain (ηp2 = 0.168, p = 0.015) improved significantly for women using 10 mg rapamycin. Self-reported emotional well-being (ηp2 = 0.108, p = 0.023) and general health (ηp2 = 0.166, p = 0.004) also improved for those using 5 mg rapamycin. No other significant effects were observed.Conclusions: Low-dose, intermittent rapamycin administration over 48 weeks is relatively safe in healthy, normative-aging adults, and was associated with significant improvements in lean tissue mass and pain in women. Future work will evaluate benefits of a broader range of rapamycin doses on healthspan metrics for longevity, and will aim to more comprehensively establish efficacy.Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206235Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, rapamycin, geroscience, longevity, healthspanTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — September 24, 2025 — A new #research paper was #published in Volume 17, Issue 8 of Aging-US on August 7, 2025, titled, “What is the clinical evidence to support off-label rapamycin therapy in healthy adults?”In this study, led by Jacob M. Hands from The George Washington University School of Medicine and Health Sciences, researchers analyzed current research to determine whether low-dose rapamycin can extend healthspan or delay aging in healthy adults. While studies in animals have shown promising results, this review found no clear clinical evidence that the same benefits apply to humans. The findings point to the urgent need for larger, better-designed human trials before recommending rapamycin for off-label use to prevent aging.Rapamycin, originally developed as a drug to suppress the immune system, has gained interest as a possible anti-aging therapy. It works by blocking a key cellular pathway called mTOR, which plays a role in growth and metabolism. In animal studies, blocking this pathway has extended lifespan. However, the translation of these results to humans remains uncertain. The current study examined clinical trials and observational studies involving healthy adults who took low doses of rapamycin or similar drugs.“This paper has reviewed trials of low-dose mTOR inhibition therapy in human subjects.”Some trials showed encouraging signs. For example, older adults treated with low-dose mTOR inhibitors showed stronger immune responses and fewer respiratory infections. Other studies suggested possible improvements in subjective well-being and physical performance, such as walking speed and strength. Still, none of the trials directly showed that rapamycin extends life or clearly slows the aging process. One small study using a biological aging model (PhenoAge) suggested that users might have reduced their biological age by nearly four years, but the estimate was based on average values, not individual patient data.There are also concerns about side effects. While short-term use seems safe, some studies reported increases in blood lipids and markers of inflammation. Research on muscle health produced contradictory findings—some studies suggest rapamycin might reduce the body’s ability to build muscle. The impact on mental health is also unclear, with a few participants reporting increased anxiety during treatment.The researchers emphasize that rapamycin’s role in human aging is still uncertain. Off-label use is growing among longevity clinics and individuals seeking anti-aging solutions, but there is no standard dose, and long-term safety is unknown. The authors advise that off-label use should be approached with caution, including careful monitoring and full disclosure about the limited evidence.Overall, while animal studies have demonstrated promising effects, human trials have not yet shown that rapamycin can safely or effectively slow aging or extend lifespan. More rigorous and well-controlled studies are necessary before the drug can be considered a reliable option for healthy adults interested in longevity interventions.DOI - https://doi.org/10.18632/aging.206300Corresponding author - Jacob M. Hands - jacobhands@gwu.eduAbstract video - https://www.youtube.com/watch?v=cdWUenvB_mYSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — September 23, 2025 — A new #research paper was #published in Volume 17, Issue 8 of Aging-US on August 7, 2025, titled “Senescent cell heterogeneity and responses to senolytic treatment are related to cell cycle status during senescence induction.”This study, led by first authors Francesco Neri and Shuyuan Zheng, together with corresponding authors Denis Wirtz, Pei-Hsun Wu, and Birgit Schilling from the Buck Institute for Research on Aging, the USC Leonard Davis School of Gerontology, and Johns Hopkins University, reveals that not all aging cells behave the same. The researchers identified key differences between senescent cell subtypes that may influence how well they respond to senolytic drugs. These findings could help guide the development of more effective therapies for age-related diseases.Senescent cells are aged or damaged cells that stop dividing and accumulate in tissues over time. While they play a role in wound healing and protecting against cancer early in life, they can drive chronic inflammation and tissue decline with age. Researchers are exploring ways to selectively remove these cells using senolytic drugs. However, the large variety of senescent cell types has made it difficult to design treatments that work for all of them. This study aimed to better understand the functional differences among senescent cell subpopulations.Using high-resolution imaging, the team analyzed thousands of human endothelial and fibroblast cells growing in the lab. They observed that cells that exited the cell cycle (stopped dividing) in a later phase showed stronger signs of senescence and were more sensitive to senolytic treatment. These cells also produced more IL-6, a molecule associated with inflammation. The findings suggest that DNA content, which varies depending on the cell cycle phase, plays an important role in how aging cells function and how they respond to drugs.“We found that G2-arrested senescent cells feature higher senescence marker expression than G1-arrested senescent cells.”This is the first clear evidence that senescent cells do not all respond equally to treatment. The results suggest that future senolytic therapies could be more successful if they are designed to target specific subtypes of senescent cells, especially those with greater inflammatory potential.While this research was conducted in laboratory cell cultures, it provides a foundation for studying how these findings apply to living tissues. Future work will examine whether similar patterns occur in the body and how this knowledge could lead to more precise and effective treatments for age-related conditions. Understanding the diversity of aging cells is key to developing therapies that are both safer and more targeted.DOI - https://doi.org/10.18632/aging.206299Corresponding authors - Denis Wirtz — wirtz@jhu.edu, Pei-Hsun Wu — pwu@jhu.edu, and Birgit Schilling — bschilling@buckinstitute.orgAbstract video - https://www.youtube.com/watch?v=x8bhKEFLzqASign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206299Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, cellular senescence, imaging, heterogeneity, senolytics, cell cycleTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — September 18, 2025 — A new #research paper was #published in Volume 17, Issue 8 of Aging-US on August 9, 2025, titled “The myokine FGF21 associates with enhanced survival in ALS and mitigates stress-induced cytotoxicity.”In this study, led by first author Abhishek Guha and corresponding author Peter H. King from the University of Alabama at Birmingham and the Birmingham Veterans Affairs Medical Center, researchers discovered that a hormone called FGF21, which is released by muscles, is elevated in people with amyotrophic lateral sclerosis (ALS) and may play a protective role. These findings are especially relevant because ALS is a fatal and currently incurable neurodegenerative disease.Amyotrophic lateral sclerosis is an age-related and progressive condition that affects the nerve cells responsible for muscle control. While some treatments can slow the disease, there is still a need to understand why ALS progresses at different rates in different individuals.“In a prior muscle miRNA sequencing investigation, we identified altered FGF pathways in ALS muscle, leading us to investigate FGF21.”The research team analyzed muscle biopsies, spinal cord tissue, and blood samples from ALS patients and found that FGF21 levels were significantly elevated. This increase was particularly evident in atrophied muscle fibers—those that had shrunk due to nerve loss—and in the surrounding tissue. Importantly, patients with higher plasma levels of FGF21 showed slower loss of function and longer survival, with some living more than six years after diagnosis.Using animal models and cultured cells, the researchers demonstrated that FGF21 levels rise even in the early, symptom-free stages of ALS. The hormone appeared to protect both muscle and motor neurons from stress-related damage. When added to stressed cells, FGF21 improved cell survival and reduced markers of cell death. In human muscle cells, FGF21 also supported the formation of new muscle fibers, a process known as myogenesis.Blood tests revealed that patients with higher levels of FGF21 not only experienced slower disease progression but also tended to have a higher body mass index (BMI), a factor previously associated with longer survival in ALS. This suggests that FGF21 may reflect a patient’s ability to counteract ALS through natural protective mechanisms. It could also serve as a biomarker to monitor disease severity and potentially guide treatment decisions.The study also investigated how FGF21 communicates with cells. It found that the hormone’s activity depends on a protein called β-Klotho, which was also altered in ALS-affected tissues. These changes were especially noticeable in motor neurons and muscle cells under stress, further highlighting FGF21’s role in the body’s response to damage.While the study does not show that FGF21 can be used as a treatment, it highlights the hormone as a promising target for future research, clinical trials, and strategies to slow ALS progression by leveraging the body’s natural protective systems.DOI - https://doi.org/10.18632/aging.206298Corresponding author - Peter H. King - phking@uabmc.eduAbstract video - https://www.youtube.com/watch?v=zEGMxQrxZxESubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, fibroblast growth factor, 21 β-Klotho, ALS biomarker, human skeletal muscle, motor neuronsTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — September 16, 2025 — A new #research paper was #published in Volume 17, Issue 8 of Aging-US on August 6, 2025, titled “Age-related trends in amyloid positivity in Parkinson’s disease without dementia.”In this study, led by first author Keiko Hatano and corresponding author Masashi Kameyama from the Tokyo Metropolitan Institute for Geriatrics and Gerontology in Japan, researchers found that patients with Parkinson’s disease (PD) diagnosed in their 80s showed a significantly higher rate of amyloid positivity—an indicator associated with Alzheimer’s disease—compared to those diagnosed at a younger age. Importantly, none of the participants had dementia. These findings suggest that older patients with PD may face a greater risk of future cognitive decline and could benefit from early screening for Alzheimer’s-related brain changes.Amyloid-beta is considered a key marker of cognitive decline. While it is known that amyloid accumulation contributes to PD with dementia, its role in patients who have not developed cognitive problems remains less understood. This study aimed to explore how age influences amyloid buildup in people with PD who do not yet show signs of dementia.The researchers analyzed data from 89 individuals with PD and no signs of dementia. Participants were divided into two age-based groups: those diagnosed before age 73 (LOW group) and those diagnosed at age 73 or older (HIGH group). Using cerebrospinal fluid samples, they measured levels of amyloid-beta, a standard method for detecting early Alzheimer’s-related changes. The findings revealed that 30.6% of the older group tested positive for amyloid, compared to just 10.0% in the younger group.“[…] we elucidated the prevalence of amyloid positivity in patients with PD without dementia, whose mean age at diagnosis was 80.2 years, using CSF Aβ42 levels.”Interestingly, both age groups of Parkinson’s patients had a lower rate of amyloid positivity than cognitively normal individuals of the same age in the general population. This unexpected result suggests that PD may alter how amyloid accumulates in the brain, possibly shortening the phase in which amyloid builds up silently before symptoms appear. The authors suggest that amyloid buildup could accelerate the transition from healthy cognition to dementia in patients with PD. The study also observed age-related associations with other biological markers of Alzheimer’s disease, such as tau protein levels. As the global population continues to age and the number of older adults diagnosed with PD grows, identifying early warning signs of cognitive decline becomes increasingly important. These findings may help inform future screening approaches and support the development of therapies aimed at delaying or preventing dementia in people with Parkinson’s disease.DOI - https://doi.org/10.18632/aging.206297Corresponding author - Masashi Kameyama - kame-tky@umin.ac.jpAbstract video - https://www.youtube.com/watch?v=AP8S9evzCJwSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206297Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, amyloid positivity, Parkinson's disease without dementia, cerebrospinal fluid Aβ42To learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Idiopathic Pulmonary Fibrosis (IPF) is a progressive lung disease that primarily affects people over the age of 60. It causes scarring in the lung tissue, which gradually reduces lung capacity and makes breathing difficult. Despite years of research, the exact causes of IPF remain largely unknown, and current treatments mainly aim to slow its progression rather than reverse or cure the disease.Because IPF tends to develop later in life, researchers have long suspected a connection with biological aging. This is the focus of a recent study by scientists from Insilico Medicine. Their research, titled “AI-driven toolset for IPF and aging research associates lung fibrosis with accelerated aging,” was published recently in Aging-US, Volume 17, Issue 8.Full blog - https://aging-us.org/2025/09/ai-tools-reveal-how-ipf-and-aging-are-connected/Paper DOI - https://doi.org/10.18632/aging.206295Corresponding author - Alex Zhavoronkov - alex@insilico.comAbstract video - https://www.youtube.com/watch?v=24lX2lHbt7oSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206295Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, IPF, generative AI, transformer, proteomicsTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — September 11, 2025 — A new #research paper was #published in Volume 17, Issue 8 of Aging-US on August 8, 2025, titled “AI-driven toolset for IPF and aging research associates lung fibrosis with accelerated aging.”In this study, researchers Fedor Galkin, Shan Chen, Alex Aliper, Alex Zhavoronkov, and Feng Ren from Insilico Medicine used artificial intelligence (AI) to investigate the similarities between idiopathic pulmonary fibrosis (IPF), a severe lung disease, and the aging process. Their findings show that IPF is not simply accelerated aging, but a distinct biological condition shaped by age-related dysfunction. This insight may lead to a new approach in how scientists and clinicians treat this complex disease.IPF mainly affects individuals over the age of 60. It causes scarring of lung tissue, making it harder to breathe and often leading to respiratory failure. Current treatments can slow the disease but rarely stop or reverse its progression. The researchers used AI to identify shared biological features between aging and fibrosis, finding new potential targets for therapy.The team developed a “proteomic aging clock” based on protein data from more than 55,000 participants in the UK Biobank. This AI-driven tool accurately measured biological age and found that patients with severe COVID-19, who are at increased risk for lung fibrosis, also showed signs of accelerated aging. This suggests that fibrosis leaves a detectable biological trace, supporting the use of aging clocks in studying age-related diseases.“For aging clock training, we used the UK Biobank collection of 55319 proteomic Olink NPX profiles annotated with age and gender.”They also developed a custom AI model, ipf-P3GPT, to compare gene activity in aging lungs versus those with IPF. Although some genes were active in both, many showed opposite behavior. In fact, more than half of the shared genes had inverse effects. This means IPF does not just speed up aging but also disrupts the body’s normal aging pathways.The study identified unique molecular signatures that distinguish IPF from normal aging. While both involve inflammation and tissue remodeling, IPF drives more damaging changes to lung structure and repair systems. This difference could guide the development of drugs that specifically target fibrosis without affecting normal aging.By combining AI with large-scale biological data, the study also introduces a powerful toolset for examining other age-related conditions such as liver and kidney fibrosis. These models may support personalized treatments and expand understanding of the relationships between aging and disease, opening new directions for therapy development.DOI - https://doi.org/10.18632/aging.206295Corresponding author - Alex Zhavoronkov - alex@insilico.comAbstract video - https://www.youtube.com/watch?v=24lX2lHbt7oSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206295Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, IPF, generative AI, transformer, proteomicsTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — September 9, 2025 — A new #research paper was #published in Volume 17, Issue 8 of Aging-US on August 1, 2025, titled “Causal relationships between gut microbiome and hundreds of age-related traits: evidence of a replicable effect on ApoM protein levels.”In this study, Federica Grosso, Daniela Zanetti, and Serena Sanna from the Institute for Genetic and Biomedical Research (IRGB) of the National Research Council (CNR), Italy, uncovered new associations between gut microbiome and the aging process. The researchers found that certain microbial characteristics may causally influence proteins in the blood linked to inflammation and heart health. These findings could help explain how age-related diseases like cardiovascular conditions and macular degeneration are influenced by changes in the gut ecosystem.The gut microbiome, the collection of microorganisms living in the digestive system, plays a major role in immune function and metabolic health. As people age, this microbial community shifts, often leading to imbalances associated with inflammation and chronic disease. To explore how these changes might affect the body, the researchers used Mendelian Randomization—a method that leverages genetic data—to test over 55,000 possible causal connections between gut microbial characteristics and age-related health indicators.The study identified 91 significant causal relationships. Among them, the researchers found that higher levels of certain gut bacteria were associated with increased risk of age-related macular degeneration. Another finding was the association between a metabolic pathway in the gut, called “purine nucleotides degradation II,” and lower levels of apolipoprotein M (ApoM), a protein that helps protect against heart disease. This result was validated using data from an independent study, strengthening the evidence.“Unlike previous studies, we performed replication analyses for the significant results using independent GWAS datasets, a fundamental step that has often been overlooked.”The study also revealed how some bacteria may affect protein levels differently depending on a person’s blood type. Specifically, in individuals with blood type A, certain gut microbes that can break down a sugar called GalNAc may influence proteins related to inflammation and cardiovascular health. This suggests that personalized approaches to managing age-related diseases could consider both gut microbiota and genetic factors like blood type.The research team followed strict guidelines to reduce false findings and confirmed its key results in independent datasets. By carefully testing for reverse causality and other biases, the authors provided strong evidence that the gut microbiome can influence critical aspects of aging biology.Although more research is needed to fully understand the biological pathways involved, these findings suggest that targeting the gut microbiota might help delay or reduce age-related inflammation and disease. The study lays a foundation for future therapeutic strategies that could include diet, probiotics, or other microbiome-based interventions.DOI - https://doi.org/10.18632/aging.206293Corresponding author - Serena Sanna - serena.sanna@cnr.itAbstract video - https://www.youtube.com/watch?v=CWky6jlHKUsSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
As the global population grows older, understanding what drives the aging process is becoming increasingly important. Diseases like Alzheimer’s, cardiovascular conditions, and cancer are more common with age, yet many current treatments only manage symptoms rather than addressing the underlying biological causes.One contributor to aging is the buildup of “senescent” cells—cells that have stopped dividing but do not die. These cells can harm nearby tissues by releasing molecular signals, a process known as secondary senescence.Scientists have found that senescent cells release tiny particles called exosomes. A research team from The Buck Institute for Research on Aging recently discovered that these exosomes carry aging-related messages through the bloodstream. Their study, titled “Exosomes released from senescent cells and circulatory exosomes isolated from human plasma reveal aging-associated proteomic and lipid signatures,” was featured as the cover article in Aging (Aging-US), Volume 17, Issue 8.Full blog - https://aging-us.org/2025/09/how-exosomes-spread-aging-signals-and-could-support-anti-aging-research/Paper DOI - https://doi.org/10.18632/aging.206292Corresponding author - Birgit Schilling - bschilling@buckinstitute.orgVideo short - https://www.youtube.com/watch?v=tcyAZahw-g8Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206292Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, proteomics, senescence, exosomes, data-independent acquisitionsTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — September 4, 2025 — A new #research perspective was #published in Volume 17, Issue 8 of Aging (Aging-US) on August 16, 2025, titled “Age-related diseases as a testbed for anti-aging therapeutics: the case of idiopathic pulmonary fibrosis.”In this research perspective, Alex Zhavoronkov, Dominika Wilczok, Feng Ren, and Fedor Galkin, from Insilico Medicine, Buck Institute for Research on Aging, and Duke University, propose a new method to evaluate age-related diseases based on how closely they align with the biological processes of aging. Their analysis shows that idiopathic pulmonary fibrosis (IPF), a progressive lung condition, is one of the diseases most strongly associated with aging. This makes IPF a promising model for testing new anti-aging therapies with the potential to treat multiple age-related conditions.“This perspective explores how aging-related diseases (ARDs) can serve as experimental platforms for discovering new geroprotective interventions.”While many age-related diseases are used as models for aging research, not all accurately reflect the biology of aging. To address this, the authors developed a scoring system that measures how closely a disease is connected to the key hallmarks of aging, such as inflammation, genetic instability, and impaired cellular repair. Using this system, they evaluated 13 common age-related diseases and found that IPF had a particularly high overlap with aging biology.IPF is a chronic disease that causes scarring in the lungs and a rapid decline in lung function. In contrast to the gradual loss of function seen in normal aging, IPF progresses more than five times faster. The authors highlight that IPF shares nearly all of the biological features associated with aging. These similarities make IPF a strong candidate for studying aging and testing therapies that target its underlying causes.The authors also discuss different therapies currently being developed for IPF that are also designed to address aging itself. These include drugs that clear senescent cells, activate telomerase to maintain chromosome health, or repair damaged signaling between cells. Some of these treatments, such as senolytic combinations and AI-discovered compounds like rentosertib, are already showing early promise in preclinical or clinical trials.In addition, the authors point out that IPF’s fast progression and clearly measurable outcomes offer an advantage for clinical testing. If a therapy proves effective in IPF, it may also be useful for other conditions that share similar aging-related mechanisms, including diabetes, arthritis, and heart disease. This approach could accelerate drug development and reduce costs by focusing on therapies that target shared biological pathways.Overall, this perspective supports a shift in pharmaceutical research toward treating aging as an underlying cause of many chronic diseases. By positioning IPF as a model for aging-related drug development, the authors propose a strategic pathway for testing and expanding anti-aging therapies across a wide range of health conditions.DOI - https://doi.org/10.18632/aging.206301Corresponding author - Alex Zhavoronkov – alex@insilico.comVideo short - https://www.youtube.com/watch?v=p5ur7itzvSISubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — September 2, 2025 — A new #research paper featured on the #cover of Volume 17, Issue 8 of Aging (Aging-US) was #published on July 30, 2025, titled “Exosomes released from senescent cells and circulatory exosomes isolated from human plasma reveal aging-associated proteomic and lipid signatures.”In this study, led by first authors Sandip Kumar Patel and Joanna Bons, along with corresponding author Birgit Schilling from The Buck Institute for Research on Aging, researchers found that exosomes—tiny particles released by cells—carry molecular signatures that indicate both biological aging and cellular senescence. These signatures include proteins, lipids, and microRNAs associated with inflammation, oxidative stress, and tissue remodeling. The findings could enhance our understanding of biological aging and help in developing future anti-aging therapies.Senescence is a state in which cells stop dividing but remain metabolically active. These cells often release harmful substances, known collectively as the senescence-associated secretory phenotype (SASP), that can affect nearby tissues. This study shows that exosomes are an important component of this secretory profile.The researchers analyzed exosomes from senescent human lung cells and from the blood plasma of both young and older adults. They identified over 1,300 proteins and 247 lipids within these particles. Many of these molecules were significantly altered with age.“In parallel, a small human plasma cohort from young (20–26 years) and old (65–74 years) individuals revealed 1,350 exosome proteins and 171 plasma exosome proteins were altered in old individuals.”Exosomes from older individuals contained more inflammation-related proteins and fewer antioxidants, while those from senescent cells showed lipid changes associated with membrane integrity and cellular stress. These changes suggest that exosomes may play a role in spreading senescence to nearby cells, a process known as secondary senescence.The study also identified distinct patterns in microRNAs—small molecules that regulate gene expression—found in the blood of older adults. Some of these, including miR-27a and miR-874, have previously been associated with cognitive decline and chronic illnesses, highlighting their potential as biomarkers for biological aging.Although the study involved a limited number of samples, it provides strong early evidence that exosomes reflect the molecular changes associated with aging. By showing how these particles carry and possibly spread aging-related signals throughout the body, the research opens new possibilities for diagnosing and treating age-related diseases.DOI - https://doi.org/10.18632/aging.206292Corresponding author - Birgit Schilling – bschilling@buckinstitute.orgVideo short - https://www.youtube.com/watch?v=tcyAZahw-g8Keywords - aging, proteomics, senescence, exosomes, data-independent acquisitionsSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — August 27, 2025 — A new #research paper was #published in Volume 17, Issue 7 of Aging (Aging-US) on July 24, 2025, titled “RNA-binding protein AUF1 suppresses cellular senescence and glycolysis by targeting PDP2 and PGAM1 mRNAs.”In this study, Hyejin Mun, Chang Hoon Shin, Mercy Kim, Jeong Ho Chang, and Je-Hyun Yoon from the University of Oklahoma and Kyungpook National University investigated how changes in cellular metabolism contribute to aging. Their findings offer potential targets for therapies aimed at slowing or reducing the effects of aging.As cells age, they often lose their ability to divide and begin releasing harmful signals that damage nearby tissues. This process, called cellular senescence, is linked to many age-related diseases. A key feature of senescent cells is their altered metabolism, where they use more glucose and oxygen, even when oxygen levels are low. This leads to the production of inflammatory substances and fatty acids, which can accelerate tissue damage. The study examined how these metabolic changes are controlled at the molecular level.Researchers found that AUF1, a protein that binds to RNA, normally helps prevent aging by breaking down two enzymes involved in glucose metabolism: PGAM1 and PDP2. When AUF1 is missing or inactive, these enzymes build up. This causes the cell to produce more energy and inflammatory molecules, which are common features of senescent cells.“Our high throughput profiling of mRNAs and proteins from Human Diploid Fibroblasts (HDFs) revealed that the expression of pyruvate metabolic enzymes is inhibited by the anti-senescent RNA-binding protein (RBP) AUF1 (AU-binding Factor 1).”The team also identified another protein, MST1, which becomes active during cellular stress and aging. MST1 modifies AUF1 in a way that stops it from doing its protective job. As a result, PGAM1 and PDP2 accumulate, leading to faster aging of the cell. Experiments using human fibroblast cells and mouse models confirmed that higher levels of these enzymes are linked to stronger signs of cellular aging.These findings improve our understanding of how metabolism affects the aging process. They highlight the MST1-AUF1-PDP2/PGAM1 pathway as a key factor in the metabolic shift seen in aging cells. Since these enzymes and proteins are already known to be involved in other diseases, existing or future therapies might be used to block this pathway and reduce the effects of aging.This study offers a new direction for senotherapy—a field focused on treating or removing aging cells. By adjusting glucose metabolism through AUF1 and its targets, scientists believe it may be possible to slow aging or limit its effects on tissue function. More research is needed, but these insights could lead to new strategies for managing age-related diseases and promoting healthier aging.DOI - https://doi.org/10.18632/aging.206286Corresponding authors - Jeong Ho Chang - jhcbio@knu.ac.kr, and Je-Hyun Yoon - jehyun-yoon@ouhsc.eduVideo short - https://www.youtube.com/watch?v=Gbu6USUSkggSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206286Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, AUF1, MST1, senescence, glycolysisTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — August 26, 2025 — A new #research paper was #published in Volume 17, Issue 7 of Aging (Aging-US) on July 21, 2025, titled “Association of DNA methylation age acceleration with digital clock drawing test performance: the Framingham Heart Study.”In this study, led by first author Zexu Li from the Department of Anatomy and Neurobiology at Boston University Chobanian and Avedisian School of Medicine, and corresponding author Chunyu Liu from Boston University Chobanian and Avedisian School of Medicine and Boston University School of Public Health, researchers found that individuals with signs of faster biological aging had lower scores on a digital cognitive test taken seven years later. The findings suggest that the rate at which a person ages at the molecular level may be associated with how well their brain functions as they grow older.Using data from the Framingham Heart Study, the researchers examined the relationship between biological aging and cognitive health. They used DNA methylation (DNAm) patterns—chemical changes that occur in the DNA with aging, known as epigenetic aging—to estimate biological age acceleration, and used the digital Clock Drawing Test (dCDT) to assess cognitive performance. The dCDT is a computerized version of a traditional pen-and-paper test that evaluates memory, thinking speed, and motor control. It provides an overall score and measures performance in specific areas such as spatial reasoning and movement.Among 1,789 participants, higher levels of epigenetic age acceleration were associated with significantly lower cognitive scores, particularly those over age 65. Of all the epigenetic aging markers examined, the DunedinPACE measure showed the strongest association with reduced brain function in both younger and older adults. Other measures, such as Horvath and PhenoAge, were associated with lower scores only in older adults. Key areas affected included motor skills and spatial reasoning.The researchers also studied blood-based protein markers used in an aging measure called GrimAge. Two proteins, PAI1 and ADM, were closely associated with lower cognitive scores, especially in older individuals. These results suggest that declines in brain and motor functions may reflect broader aging-related changes throughout the body.“Digital cognitive measures displayed stronger associations with most DNAm aging metrics among older compared to younger participants, likely to reflect the cumulative and nonlinear age influences on both brain health and DNAm.”This study supports the idea that epigenetic age may be a more accurate predictor of cognitive decline than chronological age. The dCDT, which is easy to use, automated, and more precise than traditional tools, may help detect early signs of brain aging. When combined with DNAm measures, it could become a valuable part of regular health screenings.Overall, the findings provide strong evidence that faster biological aging is associated with cognitive decline. This research may lead to better ways of identifying and monitoring brain health in aging populations.DOI - https://doi.org/10.18632/aging.206285Corresponding author - Chunyu Liu - liuc@bu.eduVideo short - https://www.youtube.com/watch?v=4hyjDqnPs8wSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — August 21, 2025 — A new #research paper was #published in Volume 17, Issue 7 of Aging (Aging-US) on July 17, 2025, titled “The influence of cancer on a forensic age estimation tool.”In this study by Charlotte Sutter, Daniel Helbling, Cordula Haas and Jacqueline Neubauer from the Zurich Institute of Forensic Medicine, University of Zurich and Onkozentrum Zurich, the researchers investigated how cancer might affect the accuracy of forensic tools used to estimate a person’s age from blood samples.DNA methylation is a natural chemical modification of DNA that changes with age. Forensic scientists can use these changes to predict someone’s age from biological traces, such as blood found at a crime scene. However, medical conditions like cancer can alter these patterns and potentially reduce the accuracy of such predictions. This study investigated whether various cancer types influence the DNA markers used in age estimation.“Our study is among the first to show whether it might be necessary to account for the influence of cancer on forensic age estimation tools in order to enhance estimation accuracy as much as possible.”The researchers applied the VISAGE enhanced age estimation tool, a widely used DNA methylation-based method, to blood samples from 100 cancer patients and 102 healthy individuals. Age predictions in the control group were generally accurate, with small average errors. Patients with solid tumors, including breast and lung cancers, showed only slightly less accurate results. In contrast, individuals with blood cancers, particularly chronic lymphocytic leukemia (CLL) and acute myeloid leukemia (AML), sometimes had large errors, with ages overestimated by as much as 50 years. Despite these few extreme cases, the study found that cancer does not typically have a strong impact on the accuracy of this forensic tool. Most cancer patients, even those undergoing treatment, had DNA methylation patterns similar to those of healthy individuals. The researchers found no consistent differences based on cancer type, stage, or treatment, except in isolated cases involving aggressive forms of cancer.The findings support the continued use of current forensic age estimation methods. While aggressive cancers may occasionally affect prediction accuracy, such cases are rare. The researchers suggest noting these conditions as a possible factor in unusually large errors, without requiring changes to standard practice.This study provides valuable information about how health conditions, such as cancer, may influence DNA-based age estimation. It strengthens confidence in the reliability of forensic age prediction tools, even when applied to individuals with a medical history of cancer.DOI - https://doi.org/10.18632/aging.206281Corresponding author - Cordula Haas - cordula.haas@irm.uzh.chVideo short - https://www.youtube.com/watch?v=lcpwE50O4ssSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206281Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, forensic age, estimation age prediction, cancer, DNA methylation, age accelerationTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — August 19, 2025 — A new #research paper was #published in Volume 17, Issue 7 of Aging (Aging-US) on July 7, 2025, titled “Epigenetic age and accelerated aging phenotypes: a tumor biomarker for predicting colorectal cancer.”In this study led by Su Yon Jung from the University of California, Los Angeles, researchers found a strong association between accelerated epigenetic aging and an increased risk of colorectal cancer in postmenopausal women. The study also indicated that lifestyle factors influence this risk.Colorectal cancer is one of the leading causes of cancer-related deaths worldwide, particularly in people over the age of 50. However, individuals do not all age at the same biological rate. Two people of the same chronological age can differ in their biological aging, which reflects the condition of their cells and tissues. This study focused on a specific measure of biological aging known as epigenetic aging, which is based on chemical changes to DNA.The researchers used data from the Women’s Health Initiative Database for Genotypes and Phenotypes (WHI-dbGaP), which includes genetic and health information from postmenopausal white women aged 50 to 79. They applied three established “epigenetic clocks” to estimate epigenetic age from blood samples collected up to 17 years before a colorectal cancer diagnosis. These clocks measure how quickly a person is aging at the molecular level by tracking DNA methylation. Women with a higher epigenetic age than expected were significantly more likely to develop colorectal cancer“[…]we examined biological aging status in PBLs via three well-established epigenetic clocks—Horvath’s, Hannum’s and Levine’s […].”The study also explored the role of lifestyle in modifying this risk. Women who consumed more fruits and vegetables showed no increased risk, even if they were epigenetically older. In contrast, women with both lower fruit and vegetable intake and signs of accelerated aging were up to 20 times more likely to develop colorectal cancer. This suggests that a healthy diet may help reduce cancer risk associated with biological aging.Another key finding involved women who had both ovaries removed before natural menopause. These women had a higher epigenetic age and, when combined with accelerated aging, a greater likelihood of developing colorectal cancer. This highlights the potential influence of hormonal and reproductive factors on aging and disease risk.The researchers validated their findings across several independent datasets, supporting the potential of blood-based epigenetic aging markers as early indicators of colorectal cancer risk. These markers could help guide early detection and prevention strategies in aging populations. However, the authors emphasize the need for independent large-scale replication studies.Overall, this study contributes to a better understanding of the association between epigenetic aging and cancer. It also supports the idea that modifiable lifestyle factors may reduce disease risk, even among those aging more rapidly at the cellular level.DOI - https://doi.org/10.18632/aging.206276Corresponding author - Su Yon Jung - sjung@sonnet.ucla.eduVideo short - https://www.youtube.com/watch?v=cq1MphQKmSkSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
A new #study published as the #cover of Aging (Aging-US) Volume 17, Issue 7, explores how factors in young human blood may affect the biological age of human skin. Researchers from Beiersdorf AG, Research and Development Hamburg in Germany, used a microphysiological co-culture system—a lab-based model simulating human circulation—to test the effects of young versus old blood serum on skin cells. The findings suggest that bone marrow-derived cells play a key role in converting blood-borne signals into effects that support skin rejuvenation.Understanding Skin Aging and Systemic InfluenceAs we age, the skin’s ability to regenerate declines, while its biological age increases. This contributes to visible signs of aging and a weakened barrier function. While cosmetic treatments can improve appearance, they rarely target the cellular processes underlying skin aging.Animal studies have shown that exposure to young blood can promote tissue repair and rejuvenation, likely due to molecules circulating in the bloodstream. However, reproducing these effects in human skin has proven difficult. Applying young serum directly to skin tissue has not produced significant results, indicating that additional cellular interactions may be required.Full blog - https://aging-us.org/2025/08/skin-rejuvenation-how-young-blood-and-bone-marrow-influence-it/Paper DOI - https://doi.org/10.18632/aging.206288Corresponding author - Elke Grönniger - elke.groenniger@beiersdorf.comVideo short - https://www.youtube.com/watch?v=_4spcgzPcEkSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206288Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, skin rejuvenation, microphysiological systems, systemic factors, bone marrow model, human serumTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — August 14, 2025 — A new #research paper was #published in Volume 17, Issue 7, of Aging (Aging-US) on July 3, 2025, titled “Frailty associates with respiratory exacerbations and mortality in the COPDGene cohort.”In this study, led by first author Eleanor Kate Phillips from Brigham and Women’s Hospital and corresponding author Dawn L. DeMeo from Brigham and Women’s Hospital and Harvard Medical School, researchers investigated how frailty impacts lung health and survival in individuals with a history of cigarette smoking. They found that frailty raises the risk of lung attacks and death, even in smokers with preserved lung function. This result shows why all current and former smokers should be checked for frailty.Frailty is a condition that makes the body more vulnerable to illness, especially in older adults. This study focused on more than 2,600 adults with a history of heavy smoking, many of whom showed no signs of lung damage on standard tests. At the second follow-up visit, participants were categorized as robust, prefrail, or frail and followed for about three years. Researchers tracked how often they experienced respiratory attacks, such as episodes of severe coughing or breathlessness, and whether they survived during that period.“COPDGene is a cohort study of individuals aged 45–80 with a minimum 10 pack-year smoking history.”The results showed that people who were frail had a three- to five-fold higher chance of developing serious or frequent respiratory attacks compared to those who were robust. These risks were not limited to people with chronic lung disease. In fact, many frail participants with normal lung function still faced a significantly higher chance of lung attacks and death. Even those in the “prefrail” stage, a milder form of frailty, were more likely to experience health complications.The research team also found that frailty was associated with an accelerated pace of biological aging, measured using a DNA-based test called DunedinPACE. This supports the idea that frailty may reflect deeper biological changes in the body that go beyond what traditional lung function tests can detect. These findings challenge the idea that standard lung tests can rule out future respiratory complications in people with a history of smoking. Altogether, the study shows that simple frailty checks could help identify early health problems, allowing for timely interventions that may prevent hospitalizations and potentially save lives. The study suggests that frailty screening may be a valuable tool in public health efforts to reduce respiratory disease and improve outcomes for aging adults.DOI - https://doi.org/10.18632/aging.206275Corresponding author - Dawn L. DeMeo - redld@channing.harvard.eduVideo short - https://www.youtube.com/watch?v=G1XQhQN6PQ8Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206275Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, frailty, cigarette smoking, respiratory exacerbations, COPD, epigenetic agingTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — August 12, 2025 — A new #research perspective was #published in Aging (Aging-US) on July 8, 2025, titled “Exercise as a geroprotector: focusing on epigenetic aging.”In this perspective, led by Takuji Kawamura from Tohoku University, researchers reviewed existing evidence from scientific studies showing that regular exercise, physical activity, and fitness may influence epigenetic aging and potentially reverse it, offering a promising way to extend healthspan and improve long-term health.Epigenetic aging refers to changes in the body’s DNA that reflect how quickly a person is aging at the molecular level. It is measured using epigenetic clocks, which analyze patterns of DNA methylation, a chemical modification that can affect gene activity. Unlike chronological age, which simply counts the number of years lived, epigenetic aging presents a more accurate picture of how well the body’s cells and tissues are functioning. This process is influenced by various factors, including lifestyle, and has become a powerful tool for studying aging.This perspective highlights that while general physical activity, such as walking or doing household tasks, offers health benefits, structured exercise routines that are planned, repetitive, and goal-directed appear to have stronger effects on slowing epigenetic aging. Physical fitness, especially high cardiorespiratory capacity, is also closely associated with slower epigenetic aging.The authors also discuss key findings from both human and animal studies. In mice, structured endurance and resistance training reduced age-related molecular changes in muscle tissue. In humans, multi-week exercise interventions demonstrated reductions in biological age markers in blood and skeletal muscle. One study found that sedentary middle-aged women reduced their epigenetic age by two years after just eight weeks of combined aerobic and strength training. Another study showed that older men with higher oxygen uptake levels, a key measure of cardiovascular fitness, had significantly slower epigenetic aging.“These findings suggest that maintaining physical fitness delays epigenetic aging in multiple organs and supports the notion that exercise as a geroprotector confers benefits to various organs.”The research also examines which organs benefit most from exercise. While skeletal muscle has been a central focus, new evidence shows that regular physical training may also slow aging in the heart, liver, fat tissue, and even the gut. In addition, Olympic athletes were found to have slower epigenetic aging than non-athletes, suggesting that long-term, intensive physical activity may have lasting anti-aging effects.The authors call for further research to understand why some individuals respond more strongly to exercise than others and how different types of training influence aging in various organs. They also point out the importance of developing personalized exercise programs to maximize anti-aging benefits. Overall, the findings support the growing recognition that maintaining physical fitness is not only essential for daily health but may also serve as one of the most effective tools for slowing the body’s internal aging process.DOI - https://doi.org/10.18632/aging.206278Corresponding author - Takuji Kawamura - takuji.kawamura.b8@tohoku.ac.jpVideo short - https://www.youtube.com/watch?v=Wro3_wBovdETo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — August 11, 2025 — Aging (Aging-US) is proud to support a milestone event for the global senescence and aging research community.This coming September 16-19, 2025, Rome, Italy will host two back-to-back events that will define the next chapter of senescence science and translation:-10th Annual International Cell Senescence Association (ICSA) Conference-Senotherapeutics Summit – organized with the Phaedon InstituteThis combined program could not come at a more important time. The field is entering a transformative phase:-Multiple clinical trials on senolytics and senomorphics are now reporting results, offering the first real-world evidence of their therapeutic potential.-Exciting new discoveries in senescence mechanisms, biomarkers, and tissue-specific roles are reshaping our understanding of when and how to target these cells.For the first time, the leading fundamental science meeting on cellular senescence will be directly connected with a global summit dedicated to the clinical and commercial development of senotherapeutics. This unique integration will allow participants to seamlessly move from bench to bedside discussions, exploring both the latest research and its translation into therapies that could transform how we approach aging and age-related diseases.Highlights include:-Keynotes from pioneers driving both discovery science and translational innovation-Sessions on mechanisms, biomarkers, and emerging targets-Industry and regulatory panels on clinical trial design, safety, and approval pathways-Case studies from ongoing and completed human trials-Networking with leaders from academia, biotech and pharmaCelebrate a decade of ICSA and help chart the path for the next generation of senescence science and therapeutics.Registration is still open: https://icsa2025rome.com/To learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Reddit - https://www.reddit.com/user/AgingUS/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — August 1, 2025 — A new #research paper featured on the #cover of Volume 17, Issue 7 of Aging (Aging-US) was #published on July 25, 2025, titled “Systemic factors in young human serum influence in vitro responses of human skin and bone marrow-derived blood cells in a microphysiological co-culture system.”The study, led by first author Johanna Ritter and corresponding author Elke Grönniger from Beiersdorf AG, Research and Development Hamburg, shows that components in young human blood serum can help restore youthful properties to skin, but only when bone marrow cells are also present. This discovery highlights the role of bone marrow in supporting skin health and may allow for novel approaches aimed at slowing or reversing visible signs of aging.The research explored how factors present in blood serum, already known to influence aging in animal studies, act on human cells. Using an advanced system that mimics human circulation, the researchers connected a 3D skin model with a 3D bone marrow model. They found that young human serum alone was not enough to rejuvenate skin. However, when bone marrow cells were present, these serum factors changed the activity of those cells, which then secreted proteins that rejuvenated skin tissue.“Interestingly, we detected a significant increase in Ki67 positive cells in the dynamic skin model co-cultured with BM model and young serum compared to the model co-cultured with BM and old serum, indicating an improved regenerative capacity of the tissue.”Detailed analysis indicated that young serum stimulated the bone marrow to produce a group of 55 proteins, with 7 of them demonstrating the ability to boost cell renewal, collagen production, and other features associated with youthful skin. These proteins included factors that improved energy production in cells and reduced signs of cellular aging. Without the interaction between skin and bone marrow cells, these rejuvenating effects did not occur.This finding explains why earlier experiments in mice, where young and old animals shared a blood supply, showed rejuvenation across organs. It suggests that bone marrow-derived cells are critical messengers that transform signals from blood into effects on other tissues, including the skin.While these results are preclinical and not from human trials, they offer a starting point for new strategies in regenerative medicine and skin care. By identifying specific proteins that may carry rejuvenating signals, the study points to a new way to address age-related changes. Researchers emphasize that further studies will be needed to confirm these effects in humans and to test how these proteins can be safely and effectively applied in future therapies.Overall, this research is an important step in understanding how young blood serum factors influence human tissue and could guide the development of novel methods to maintain healthier skin as people age.DOI - https://doi.org/10.18632/aging.206288Corresponding author - Elke Grönniger - elke.groenniger@beiersdorf.comVideo short - https://www.youtube.com/watch?v=_4spcgzPcEkSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206288Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 30, 2025 — A new #research paper was #published in Aging (Aging-US) on July 23, 2025, titled “Second generation DNA methylation age predicts cognitive change in midlife: the moderating role of childhood socioeconomic status.”In this study, led by Sophie A. Bell and Eric Turkheimer from the University of Virginia, researchers investigated how biological aging, measured through DNA methylation, is connected to changes in thinking skills during midlife and whether childhood socioeconomic status influences this relationship. Biological age provides a picture of how the body is aging that goes beyond simply counting years. In this study, researchers used both first- and second-generation DNA methylation clocks—tools that track chemical changes in DNA as markers of aging. GrimAge and PhenoAge, the second-generation clocks designed to reflect broader health and aging processes, were more accurate at predicting long-term changes in Intelligence Quotient (IQ) than the first-generation models that only estimated chronological age. The study analyzed 287 participants from the Louisville Twin Study, which is a long-term project that has followed twins from childhood into midlife.“DNAmAge was estimated with five commonly used algorithms, or epigenetic clocks (Horvath, Horvath Skin and Blood, GrimAge, and PhenoAge).”The results showed that twins with more rapid epigenetic aging had a larger drop in IQ scores. This pattern remained even after considering genetic background and early family environment, made possible by the twin-based design. Importantly, the relationship was strongest in twins who had grown up in families with lower socioeconomic status. This finding suggests that early-life disadvantage may make individuals more vulnerable to the effects of biological aging on brain health.This research adds knowledge to earlier work showing that childhood poverty can influence long-term health. It also highlights the value of second-generation epigenetic clocks as early indicators of brain aging. Unlike the first generation of clocks, these newer tools capture broader biological changes such as inflammation, disease risk, and behaviors like smoking.Although smoking partly explained the results because it strongly influences DNA methylation, it did not fully account for the association between accelerated biological aging and cognitive decline. This suggests that both life experiences and lifestyle factors shape body and brain aging.By combining decades of developmental data with a genetically informed twin design, the study provides new evidence that biological aging, especially when shaped by childhood adversity, is a key factor in midlife cognitive decline. These findings may inform early health strategies that consider both social and biological risks and support the use of second-generation methylation clocks to predict age-related cognitive changes.DOI - https://doi.org/10.18632/aging.206284Corresponding authors - Sophie A. Bell - bvf7pa@virginia.edu, and Eric Turkheimer - ent3c@virginia.eduVideo short - https://www.youtube.com/watch?v=vopDdS1olXwSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206284Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 28, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 6, on June 13, 2025, titled “Development of a novel transcriptomic measure of aging: Transcriptomic Mortality-risk Age (TraMA).”In this study, led by Eric T. Klopack from the University of Southern California, researchers created a new RNA-based aging measure that predicts health risks and mortality. This measure, called Transcriptomic Mortality-risk Age (TraMA), uses gene expression data to estimate a person’s biological aging. This finding offers a new and potentially more accurate way to track aging and understand health risks, especially for older adults.Aging is a complex biological process that affects multiple systems in the body and increases the risk of disease and death. Scientists have long looked for reliable ways to measure biological aging. While DNA methylation and blood biomarkers are commonly used, this study focused on RNA—a molecule that reflects gene activity. By analyzing RNA sequencing data from nearly 4,000 U.S. adults aged 50 and older, the team developed TraMA to predict the probability of dying within four years.TraMA proved to be a strong and independent predictor of early death, multiple chronic diseases, poor cognitive function, and difficulties with daily activities. It was also tested in another large group of long-lived families and in several smaller datasets from patients with conditions like diabetes, sepsis, and cancer. The results confirmed the tool’s usefulness across different populations and health conditions.“TraMA was also externally validated in the Long Life Family Study and several publicly available datasets.”Unlike earlier RNA-based aging measures, which were often built using small or non-representative samples, TraMA was developed using modern RNA sequencing technology results and a nationally representative dataset. This increases its reliability and potential for broad public health applications. The tool also demonstrated unique advantages over popular biological aging measures like GrimAge and PhenoAge, capturing distinct aspects of aging and health decline.Importantly, TraMA tracks biological processes related to inflammation, immune function, and kidney and brain health, systems that play key roles in aging. It was also sensitive to behavioral and socioeconomic factors. For instance, smoking, obesity, and low physical activity were associated with older TraMA scores.TraMA was also sensitive to changes in biological aging. In one study, researchers measured TraMA at two different time points and found that the more recent scores were better at predicting who would die. This suggests that TraMA can track changes in a person’s aging as their health evolves. It also performed well in both large-scale surveys and small clinical samples, making it a useful tool in many types of research.By offering a new, accurate, and flexible method for measuring biological aging, TraMA may help researchers better understand how genes, lifestyle, and environment influence aging. This tool opens the door to more precise research on improving health and extending lifespan.DOI - https://doi.org/10.18632/aging.206272Corresponding author - Eric T. Klopack - klopack@usc.eduVideo short - https://www.youtube.com/watch?v=Tl0CApUz8cUSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 23, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 6, on June 16, 2025, titled “rDNA copy number variation and methylation from birth to sexual maturity.”In this study, led by first authors Alina Michler and Sarah Kießling along with corresponding author Thomas Haaf from Julius Maximilians University in Germany, researchers explored how ribosomal DNA (rDNA) copy number and methylation change from infancy to adolescence. They discovered that the epigenetic changes often associated with aging in adults do not occur before sexual maturity. This finding offers new insights into when the biological aging process truly begins.Ribosomal DNA plays a critical role in producing proteins essential for cell survival. The researchers analyzed blood samples from 280 individuals, ranging from newborns to 18 years of age, including healthy individuals and those with developmental delays. They measured the number of rDNA copies and examined how genes are switched on or off through methylation, a chemical modification of DNA. The results showed that while adults experience a gradual loss of active rDNA copies and increased methylation—a hallmark of aging—these changes were absent in children and teenagers. In fact, during childhood and adolescence, the number of active, unmethylated rDNA copies slightly increased.These findings support the long-debated idea that biological aging begins only after the body reaches reproductive maturity. Until that point, cells appear to actively maintain rDNA in a youthful state, ensuring that protein production remains efficient. This may help explain why children and teenagers are better at resisting many age-related diseases and why their cells recover more easily from stress.The study also shows that changes in rDNA copy numbers are not associated with unexplained developmental delays. This suggests these epigenetic processes are probably not involved in early-life syndromes. The findings highlight how the body works to preserve genetic stability during childhood and raise important questions about what triggers the shift to aging-related changes after puberty.“Collectively our data suggest that the rDNA hypomethylation state is actively maintained in somatic tissues of young individuals.”The insights gained from this research expand the understanding of the molecular clock of aging. They suggest potential new ways to delay aging processes by exploring how youthful rDNA methylation patterns are maintained. As scientists continue to investigate these mechanisms, the study provides a clear foundation for future research aimed at extending cellular health beyond adolescence.DOI - https://doi.org/10.18632/aging.206271Corresponding author - Thomas Haaf - thomas.haaf@uni-wuerzburg.deVideo short - https://www.youtube.com/watch?v=Ww21u33uUhkSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206271Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, absolute rDNA copy number, active rDNA copy number, deep bisulfite sequencing, developmental delay, droplet digital PCRTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
A new #study published recently in Volume 17, Issue 6, examines a novel treatment for women with ovarian failure. Researchers from IVI Clinics Alicante in Spain investigated a procedure called Stem Cell Regenera, which uses the body’s own stem cells and platelet-rich plasma to activate dormant follicles in the ovaries. This innovative protocol could expand options for patients with ovarian failure who have not responded to conventional fertility therapies.Understanding Ovarian FailureOvarian failure affects women’s ability to conceive by reducing the quantity and quality of eggs in the ovaries. Conditions like Poor Ovarian Response, Diminished Ovarian Reserve, and Premature Ovarian Insufficiency are key reasons for infertility and make it hard to use assisted reproduction methods like in vitro fertilization (IVF).Standard fertility treatments often fail to improve outcomes for these patients, leaving donor eggs as the primary alternative. However, recent advances in regenerative medicine have raised the possibility of restoring ovarian function using cellular therapies. Emerging research suggests that the right biological conditions could reactivate dormant follicles within the ovaries, potentially helping patients to use their eggs.Full blog - https://aging-us.org/2025/07/stem-cell-regenera-a-regenerative-approach-to-activating-dormant-ovarian-follicles/Paper DOI - https://doi.org/10.18632/aging.206274Corresponding author -Amparo Santamaria - Amparo.santamaria@ivirma.comAuthor interview - https://www.youtube.com/watch?v=oRFJNwnXZWISign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206274Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, Stem Cell Regenera, oocyte activation, ovarian regeneration, G-CSF, SCFE-PRP, ovarian failureTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 21, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 6, on June 27, 2025, titled “Enhancing oocyte activation in women with ovarian failure: clinical outcomes of the Stem Cell Regenera study using G-CSF mobilization of peripheral blood stem cells and intraovarian injection of stem cell factor-enriched platelet rich plasma in real-world-practice.”This study, led by Amparo Santamaria with co-authors Ana Ballester and Manuel Muñoz from IVI Clinics Alicante, evaluates the effectiveness and safety of a regenerative treatment that may enable women with ovarian failure to regain the ability to produce viable eggs. The approach combines stem cell mobilization and enriched plasma injections into the ovaries to stimulate follicle growth. It provides an alternative for patients experiencing infertility due to poor ovarian response, diminished ovarian reserve, or premature ovarian insufficiency.Researchers evaluated the Stem Cell Regenera treatment in 145 women, aged 26 to 44 years, who had not responded to conventional fertility therapies. The procedure involved mobilizing the body’s own stem cells using granulocyte colony-stimulating factor (G-CSF), followed by an injection of platelet-rich plasma enriched with stem cell factors directly into the ovaries. This method was designed to activate dormant follicles and promote ovarian regeneration.Nearly 70% of participants demonstrated oocyte activation, defined as increased follicle growth or a rise in key hormone levels. Approximately 7% achieved spontaneous pregnancies, and 14% conceived through in vitro fertilization (IVF) after treatment. These results indicate that the therapy stimulates ovarian activity and may increase the chances of conception in selected patients.“The primary outcome measures were the rate of oocyte activation, leukocytes and stem cell count, and pregnancy rates.”No severe adverse effects were reported. Most participants tolerated the treatment well, with only mild and transient symptoms such as headaches or fatigue. The use of the patient’s own cells minimized the risk of immune reactions and helped ensure the treatment was safe.The findings provide evidence of effectiveness and safety for the Stem Cell Regenera protocol in a clinical setting. While the study was retrospective observational, the outcomes support further investigation through larger controlled trials to confirm long-term benefits and identify which patient populations may gain the greatest benefit from this approach.This research contributes to the growing field of regenerative medicine in reproductive health, offering clinicians additional tools to address infertility in women with complex ovarian conditions.DOI - https://doi.org/10.18632/aging.206274Corresponding author -Amparo Santamaria - Amparo.santamaria@ivirma.comAuthor interview - https://www.youtube.com/watch?v=oRFJNwnXZWISign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206274Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, Stem Cell Regenera, oocyte activation, ovarian regeneration, G-CSF, SCFE-PRP, ovarian failureTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 17, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 6, on June 9, 2025, titled “Developing a quantitative estimate of muscle age acceleration by a novel phenotypic clock: cross-sectional study in healthy, middle-aged and older adults.”In this study, led by first authors Lucia Ventura, Antonella Cano and Marco Morrone, along with corresponding author Franca Deriu from the University of Sassari, researchers introduce a new method to predict how muscles age, offering an early warning system for sarcopenia, the condition of age-related muscle loss. The study demonstrates how a simple, low-cost approach can identify middle-aged and older adults at higher risk for declining muscle health, allowing timely preventive strategies.The researchers developed a tool called Muscle Age Acceleration (MAA), which measures how quickly an individual’s muscles are aging compared to their actual age. By analyzing physical performance tests and body composition in 215 healthy participants aged 50 to 90 years, the researchers found that about 25% of individuals experience accelerated muscle aging. These individuals had a higher probability of developing sarcopenia, despite appearing healthy and not yet having received a diagnosis of the condition.Sarcopenia reduces muscle strength and physical performance, being a growing concern for older adults. It contributes to frailty, falls, and an increased risk of disability. Despite greater awareness, this condition often goes undetected until significant muscle loss occurs. This new muscular clock offers an opportunity to detect subtle changes in muscle health before they progress to more severe stages.By using common tests such as handgrip strength, walking speed, and mobility assessments, the MAA tool can classify individuals as having accelerated, normal, or decelerated muscle aging. Those with accelerated muscle aging also showed small changes in blood markers, suggesting early and hidden inflammation linked to muscle decline. This finding indicates that MAA may act as both a predictor of muscle-related aging and an indicator of overall health risks.“According to MAA, three trajectories were identified: accelerated agers displayed higher risk for sarcopenia (19%), as compared to normal (9%; p < 0.0001) and decelerated (2%; p < 0.0001), paralleled by significant subclinical alterations of haemato-chemical markers in accelerated agers.”If validated in future studies, this innovative approach could transform how clinicians and caregivers screen for early signs of sarcopenia. Its simplicity makes it suitable for use in clinics and community settings, helping older adults maintain independence and quality of life as they age.In summary, these findings highlight the importance of monitoring muscle health and physical performance in older adults. By detecting early signs of muscle aging with tools like MAA, interventions such as exercise and dietary changes can be introduced earlier, potentially delaying or preventing sarcopenia and its complications.DOI - https://doi.org/10.18632/aging.206269Corresponding author - Franca Deriu - deriuf@uniss.itVideo short - https://www.youtube.com/watch?v=kc9i0aJNNp0Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Dr. Amparo Santamaria describes a #research paper she co-authored that was #published in Volume 17, Issue 6 of Aging (Aging-US), titled “Enhancing oocyte activation in women with ovarian failure: clinical outcomes of the Stem Cell Regenera study using G-CSF mobilization of peripheral blood stem cells and intraovarian injection of stem cell factor-enriched platelet rich plasma in real-world-practice.”DOI - https://doi.org/10.18632/aging.206274Corresponding author -Amparo Santamaria - Amparo.santamaria@ivirma.comVideo interview - https://www.youtube.com/watch?v=oRFJNwnXZWIAbstractThe study assesses the effectiveness and safety of the Stem Cell Regenera Treatment for oocyte activation in women with ovarian failure, including conditions such as Poor Ovarian Response (POR), Diminished Ovarian Reserve (DOR), and Premature Ovarian Insufficiency (POI). This retrospective observational study was conducted from January 2023 to December 2024 at the IVIRMA Alicante Clinics in Spain.Women diagnosed with ovarian failure participated in the study, which involved mobilizing Hematopoietic Stem Cells from bone marrow into peripheral blood using granulocyte colony- stimulating factor (G-CSF). This was followed by an intraovarian injection of Stem Cell Factor- enriched Platelet Rich Plasma (SCFE-PRP).The primary outcome measures were the rate of oocyte activation, leukocytes and stem cell count, and pregnancy rates. Oocyte activation was defined as an increase in total Antral Follicle Count of three or more follicles after treatment and/or at least a 20% rise in Anti-Müllerian Hormone levels. Safety was assessed based on adverse effects. Pregnancy rates were evaluated for both spontaneous gestation and following in vitro fertilization (IVF) treatment.A total of 145 women participated: the overall activation rate was 68.28%, with 7.07% achieving spontaneous gestation and 14.14% achieving pregnancy following IVF. Mobilization of CD34+ cells was successful in all participants, with an average collection of 32.96 CD34+ cells/μl. No severe adverse effects were observed. The study concluded that the Stem Cell Regenera Treatment is effective and safe for oocyte activation in women with ovarian failure in real-world practice.Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206274Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, Stem Cell Regenera, oocyte activation, ovarian regeneration, G-CSF, SCFE-PRP, ovarian failureTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 15, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 6, on June 5, 2025, titled “Senescence caused by telomerase inactivation in myeloid, mesenchymal, and endothelial cells has distinct effects on cancer progression.”In this study, first author Joseph Rupert, along with corresponding author Mikhail G. Kolonin and colleagues from The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, McGovern Medical School, at The University of Texas Health Sciences Center at Houston, investigated how aging-related changes in different cell types affect cancer progression. By turning off telomerase in specific cell populations in mice, the researchers discovered that cell aging, or senescence, can slow primary tumor growth but also trigger unexpected effects. This work sheds light on the complex relationship between aging cells and cancer and may help guide future anti-cancer strategies.The team used genetically modified mice to deactivate telomerase, the enzyme that maintains chromosome ends, specifically in immune, connective tissue, and blood vessel cells. This caused these cells to enter a state of senescence, where they stop dividing and release inflammatory signals. The researchers then implanted breast, prostate, and pancreatic cancer cells into the mice and tracked how tumors developed. They found that when telomerase was inactivated in immune cells or connective tissue cells, tumors grew more slowly. However, these tumors showed signs of increased tissue damage and potential aggressiveness.Interestingly, when telomerase was turned off in endothelial cells, which cover blood vessels, tumors shrank and became poorly supplied with blood, leading to oxygen deprivation. In the case of pancreatic cancer cells, this low-oxygen environment made them more likely to spread to the liver, highlighting a potential risk of targeting these cells.“[…] this study shows that senescence and metabolic dysfunction resulting from telomerase inactivation in distinct cells in the tumor microenvironment have different effects on tumor growth and metastasizing of carcinomas.”This research provides important insights into how aging cells within the tumor microenvironment (TME) influence cancer behavior. While senescence in certain cell types can help suppress tumor growth, it may also create conditions that favor cancer metastasis. These findings highlight the need to consider cell type-specific effects when developing therapies that target senescent cells. By mapping how different cell populations contribute to cancer progression in aging tissues, this study opens the door for more precise approaches to prevent both tumor growth and spread.DOI - https://doi.org/10.18632/aging.206268Corresponding author - Mikhail G. Kolonin - mikhail.g.kolonin@uth.tmc.eduVideo short - https://www.youtube.com/watch?v=py8wFKj7enESign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206268Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, senescence, telomerase, myeloid, mesenchymal, endothelialTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 10, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 6, on June 7, 2025, titled “Spermidine supplementation and protein restriction protect from organismal and brain aging independently.”In this study, led by YongTian Liang and Stephan J. Sigrist from Freie Universität Berlin, Charité Universitätmediz Berlin, and the Leibniz-German Center for Neurodegenerative Diseases (DZNE), researchers investigated how spermidine, a natural substance in the body, and protein intake levels influence aging in fruit flies. They found that spermidine supplementation and changes in protein intake influenced brain health and aging in distinct ways. These insights could guide the development of new strategies to slow age-related decline in humans.“In this study, we combined low- and high-protein diets (2% versus 12% yeast in food) with spermidine supplementation in aging Drosophila fruit flies.”Aging of the brain and body contributes to cognitive decline and diseases in older populations. Scientists have long explored dietary restriction and fasting as ways to slow these processes. This study reveals that spermidine supplementation supports brain health by enhancing mitochondrial function and memory, while protein restriction independently promotes longevity and protects against movement decline.The researchers discovered that spermidine improved memory and preserved physical activity in aging flies regardless of protein intake. In contrast, reducing protein alone boosted mitochondrial activity and extended lifespan without directly enhancing memory. Importantly, the combined approach of protein restriction and spermidine supplementation provided additive benefits, suggesting potential for synergistic effects.This work highlights that spermidine acts through a pathway involving hypusination, a vital process where cells modify proteins to support energy production and repair, while protein restriction works via nutrient-sensing pathways that promote longevity. These independent mechanisms may explain why combining the two interventions offers greater protection against aging effects.Although conducted in flies, the study underscores the possibility of designing dietary and supplement-based interventions to combat human age-related decline. As spermidine levels naturally decline with age, supplementation combined with moderated protein intake could offer a safe way to promote brain health and longevity in humans.The authors point out that it takes further studies in mammals and humans to validate these results. If confirmed, such strategies could lead the way for accessible approaches to promote healthy aging and reduce the burden of cognitive disorders in older populations.DOI - https://doi.org/10.18632/aging.206267Corresponding authors - YongTian Liang - yongtian.tim.liang@gmail.com, and Stephan J. Sigrist - stephan.sigrist@fu-berlin.deVideo short - https://www.youtube.com/watch?v=QfxpK9tka7USign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206267Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, brain aging, spermidine, protein restriction, mitochondriaTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 8, 2025 — As populations worldwide continue to age, understanding the mechanisms and manifestations of cognitive aging is increasingly urgent for science, medicine, and society. Age-related cognitive decline ranges from mild memory lapses to the onset of dementia, and is shaped by a complex interplay of molecular, cellular, systemic, and social determinants.In this special collection, Aging (Aging-US) seeks to bring together cutting-edge research that spans the cellular and molecular underpinnings of cognitive aging with insights into the psychosocial, behavioral, and environmental factors that modulate its course. By integrating basic biology with translational and societal dimensions, this collection aims to foster a holistic understanding of how and why cognitive function changes with age—and what can be done to preserve it.We welcome original research articles, reviews, and perspectives across model systems and human studies, particularly those that promote interdisciplinary insights and translational potential.POTENTIAL TOPICSMolecular and Cellular Mechanisms-Senescence, inflammation, and neurodegeneration in cognitive decline-Mitochondrial dysfunction and oxidative stress in aging neurons-Neurovascular aging and blood-brain barrier integrity-Single-cell and spatial transcriptomics of the aging brain-mTOR, autophagy, and proteostasis in age-related cognitive impairment-The role of glial cells (microglia, astrocytes) in brain aging Genetics and Biomarkers-Genetic risk factors and epigenetic modifications associated with cognitive aging-Biomarkers of cognitive resilience and vulnerability-Neuroimaging and fluid-based biomarkers in aging populationsInterventions and Lifestyle Factors-Cognitive benefits of caloric restriction, exercise, or senolytic therapies-Preclinical and clinical trials targeting aging pathways to prevent cognitive decline-Impact of sleep, nutrition, and metabolic health on cognition in older adults-Use of cognitive strategies and compensatory techniques to maintain or enhance function in agingEnvironmental and Social Contexts-Impact of social isolation, education, and socioeconomic status on cognitive trajectories-Lifelong cognitive reserve and its determinants-Cross-cultural and demographic studies on aging and cognition-Digital health tools for monitoring or enhancing cognitive function in the elderlySUBMISSION DETAILS:-Submission Deadline: March 31, 2026-Manuscript Format: Please follow the journal’s submission guidelines-Peer Review: All submissions will undergo a rigorous peer-review process-Submission Link: https://aging.msubmit.net/cgi-bin/main.plexTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 8, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 6, on May 30, 2025, titled “Impact of waist-to-hip and waist-to-height ratios on physical performance: insights from the Longevity Check-up 8+ project.”In this study, researchers led by first author Anna Maria Martone and corresponding author Elena Levati from the Fondazione Policlinico Universitario “Agostino Gemelli” IRCCS and Università Cattolica del Sacro Cuore found that adults with higher waist-to-hip and waist-to-height ratios tend to have poorer physical performance. These simple body shape measures emerged as important tools for assessing strength and mobility, which are essential for maintaining independence as people age.The analysis included data from more than 10,000 Italian adults aged 18 to 98 years who participated in the Longevity Check-up 8+ project, a nationwide health initiative aimed at promoting healthy lifestyles and raising awareness of cardiovascular risks. Researchers measured participants’ waist-to-hip (WHR) and waist-to-height (WHtR) ratios and assessed their physical function using the five-repetition chair stand test, a standard evaluation of lower body strength and mobility.“Among 10690 participants (mean age 57.0 ± 14.8 y; 54% females), men exhibited higher WHR and WHtR and a higher prevalence of abnormal values (61% and 71%).”The results showed that individuals with higher waist-to-hip and waist-to-height ratios took longer to complete the test, reflecting reduced physical function. Even after adjusting for lifestyle factors such as diet, exercise habits, and cardiovascular health, these ratios remained strongly linked to poorer performance. The waist-to-height ratio, in particular, proved to be a more effective predictor of physical ability across different age and gender groups.These findings highlight how abdominal fat, already tied to serious health risks like heart disease and diabetes, may also impair mobility and independence as people age. Monitoring waist measurements could help identify individuals at risk of functional decline, offering a simple tool to support public health in aging populations.The waist-to-height ratio is especially valuable because of its simplicity and practicality. Requiring only waist and height measurements, it can be easily used in clinical settings and community health programs to screen for potential mobility issues. Encouraging healthy waist sizes through balanced diets and regular exercise could help preserve physical performance and delay age-related decline. These findings may guide future prevention strategies. By identifying individuals at higher risk, healthcare professionals can implement targeted interventions to support long-term health and independence.DOI - https://doi.org/10.18632/aging.206260Corresponding author - Elena Levati - elena.levati01@icatt.itVideo short - https://www.youtube.com/watch?v=WqGlZ1qGZPISign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206260Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, physical performance, body composition, waist-to-hip ratio, waist-to-height ratio, chair-stand testTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
A new study published recently as the cover of Aging Volume 17, Issue 6, describes a new method to estimate how fast the brain is aging. By analyzing lipids, or fat molecules, in brain tissue, researchers from the National University of Singapore and Hanze University of Applied Sciences created a biological “clock” called DoliClock. This innovation highlights how conditions such as autism, schizophrenia, and Down syndrome are associated with accelerated brain aging.Understanding Brain AgingAs people grow older, their brains naturally change. However, in many neurological disorders, these changes seem to appear earlier and progress more rapidly. Disorders like autism, schizophrenia, and Down syndrome reduce quality of life and contribute to premature death. Scientists have long searched for better ways to measure biological age in the brain to understand these processes and develop strategies to slow them down.Most existing methods for estimating biological age rely on genetic markers, such as DNA methylation, which are chemical modifications of DNA. While useful, these approaches may not fully capture the complexity of aging, especially in the brain. Lipids, which are essential components of brain cells and play important roles in energy storage and signaling, offer another perspective.Full blog - https://aging-us.org/2025/07/doliclock-a-lipid-based-clock-for-measuring-brain-aging/Paper DOI - https://doi.org/10.18632/aging.206266Corresponding author - Brian K. Kennedy - bkennedy@nus.edu.sgVideo short - https://www.youtube.com/watch?v=-FEiyj9PjBESign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206266Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, aging clock, down syndrome, autism, schizophrenia, dolicholTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Dr. Andres Cardenas, from the Department of Epidemiology and Population Health at Stanford University, joins host Dr. Evgeniy Galimov to discuss a research paper he co-authored in Volume 17, Issue 2 of Aging (Aging-US), titled “Exposome-wide association study of environmental chemical exposures and epigenetic aging in the National Health and Nutrition Examination Survey.”DOI - https://doi.org/10.18632/aging.206201Corresponding author - Andres Cardenas - andresca@stanford.eduVideo interview - https://www.youtube.com/watch?v=A1I6qoVwkfMLongevity & Aging Series - https://www.aging-us.com/longevityAbstractEpigenetic clocks can serve as pivotal biomarkers linking environmental exposures with biological aging. However, research on the influence of environmental exposures on epigenetic aging has largely been limited to a small number of chemicals and specific populations. We harnessed data from the National Health and Nutrition Examination Survey 1999-2000 and 2001-2002 cycles to examine exposome-wide associations between environmental exposures and epigenetic aging. A total of 8 epigenetic aging biomarkers were obtained from whole blood in 2,346 participants ranging from 50-84 years of age. A total of 64 environmental exposures including phthalates, metals, pesticides, dioxins, and polychlorinated biphenyls (PCBs) were measured in blood and urine. Associations between log2-transformed/standardized exposure measures and epigenetic age acceleration (EAA) were assessed using survey-weighted generalized linear regression. A 1 standard deviation (SD) increase in log2 serum cadmium levels was associated with higher GrimAge acceleration (beta = 1.23 years, p = 3.63e-06), higher GrimAge2 acceleration (beta = 1.27 years, p = 1.62e-05), and higher DunedinPoAm (beta = 0.02, p = 2.34e-05). A 1 SD increase in log2 serum cotinine levels was associated with higher GrimAge2 acceleration (beta = 1.40 years, p = 6.53e-04) and higher DunedinPoAm (beta = 0.03, p = 6.31e-04). Associations between cadmium and EAA across several clocks persisted in sensitivity models adjusted for serum cotinine levels, and other associations involving lead, dioxins, and PCBs were identified. Several environmental exposures are associated with epigenetic aging in a nationally representative US adult population, with particularly strong associations related to cadmium and cotinine across several epigenetic clocks.Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206201Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, epigenetic aging, environmental exposures, exposome, epigeneticsPlease visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 2, 2025 — A new #research perspective was #published in Aging (Aging-US) Volume 17, Issue 6, on May 29, 2025, titled “Peto’s paradox’s relevance is off the scale.”In this perspective, Dr. Mirre J.P. Simons from the University of Sheffield argues that Peto’s paradox—a well-known concept in cancer biology—remains a vital framework for understanding cancer resistance in large animals. Dr. Simons challenges recent claims that dismiss the paradox and emphasizes that the unexpectedly low cancer rates in large species still require explanation. This insight is especially relevant for aging and cancer research.Peto’s paradox highlights a puzzling observation: larger animals like elephants and whales, despite having far more cells than smaller animals, do not have proportionally higher cancer rates. If each cell had an equal chance of turning cancerous, bigger animals should develop cancer much more frequently. But in reality, they do not. This suggests that evolution has equipped these animals with powerful biological defenses against cancer.“The field of comparative biology into ageing and cancer was given a strong impetus when Peto identified that humans have substantially more cells than mice, but do not have substantially larger incidence of cancer.”Dr. Simons explains that recent studies showing small increases in cancer with body size do not disprove the paradox. The expected increase, based on basic mathematical models, would be massive—many times greater than what is observed. Instead of rejecting Peto’s paradox, the field should focus on understanding how large animals suppress cancer so effectively.The author points out that the key to resolving this paradox may lie in traits that evolved alongside body size, such as tissue environments or specialized cell-control mechanisms. These features might reduce the probability of cancer developing, even in animals with millions or billions more cells than humans.Importantly, this perspective underscores the clinical potential of studying species that resist cancer naturally. Studying these natural defenses may help researchers uncover new ways to understand, prevent, or manage cancer. Because cancer risk increases with age in most species, understanding how some animals limit both aging and cancer may also help explain how these two processes are connected.Dr. Simons cautions against oversimplifying cancer biology by focusing only on genetic mutations. Instead, understanding how cells interact with their environment, known as the tissue microenvironment, may offer deeper insight into how cancer develops or is prevented.By reaffirming the importance of Peto’s paradox, this research perspective encourages the scientific community to explore the evolutionary tools nature uses to fight cancer. These insights could improve our understanding of cancer and inspire new strategies to support healthier aging.DOI - https://doi.org/10.18632/aging.206258Corresponding author - Mirre J.P. Simons - m.simons@sheffield.ac.ukVideo short - https://www.youtube.com/watch?v=sDaq07zX2TMSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206258Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, cancer, evolutionTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 1, 2025 — A new #research paper, featured on the #cover of Aging (Aging-US) Volume 17, Issue 6, was #published on June 4, 2025, titled “DoliClock: a lipid-based aging clock reveals accelerated aging in neurological disorders.”This study, led by first author Djakim Latumalea from the National University of Singapore and Hanze University of Applied Sciences, with corresponding author Brian K. Kennedy from the National University of Singapore, introduces DoliClock, a biological aging clock based on lipid profiles in the human brain. The researchers found that individuals with autism, schizophrenia, and Down syndrome show signs of accelerated brain aging compared to individuals without these conditions. The discovery offers a new approach to measuring brain aging using lipid markers instead of traditional DNA-based methods.The team developed DoliClock using lipidomic data from post-mortem prefrontal cortex samples. Lipids are fat-like molecules that play a key role in brain health. Changes in lipid patterns can reflect the biological age of brain tissue. The study focused on a specific class of lipids called dolichols, which increase gradually with age. The DoliClock model was trained to predict biological age by analyzing levels of dolichols and other lipid molecules. It accurately estimated brain age and revealed higher aging rates in individuals with neurological disorders.One notable finding was a sharp increase in lipid profile variability—also known as entropy—around the age of 40. This suggests a disruption in lipid metabolism during midlife, possibly caused by changes in the mevalonate pathway, a critical biological process involved in producing lipids like cholesterol and dolichol. These disruptions may contribute to aging-related brain decline.The study also found that dolichol levels could serve as reliable biomarkers of aging. Their consistent increase with age and strong influence on DoliClock’s predictions make them especially useful. In individuals with autism, schizophrenia, and Down syndrome, the clock indicated more advanced biological brain aging than expected, supporting the idea that these conditions are associated with premature aging.DoliClock offers a new perspective in aging research, complementing existing biological clocks based on DNA or protein markers. Because it relies on lipids, it may detect aspects of aging that other tools cannot. While the current model is based on brain tissue samples, future research may examine whether similar lipid patterns can be identified in more accessible fluids such as blood or cerebrospinal fluid.“These findings suggest that lipidomics can provide valuable insights into the molecular mechanisms of brain aging and neurological disorders.”This study highlights the growing potential of lipidomics in the study of aging and neurological disorders. It opens the door to new biomarkers that could help researchers and clinicians better monitor brain aging and develop more targeted interventions for age-related and neurodevelopmental diseases.DOI - https://doi.org/10.18632/aging.206266Corresponding author - Brian K. Kennedy - bkennedy@nus.edu.sgVideo short - https://www.youtube.com/watch?v=-FEiyj9PjBESubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Recent discoveries in #aging research reveal a powerful insight: the biological changes that lead to chronic #diseases begin far earlier than most people realize—often in midlife, well before symptoms appear. This early phase offers a valuable opportunity for prevention. As highlighted in a recent editorial by Marco Demaria, Editor-in-Chief of Aging and a researcher at the European Research Institute for the Biology of Ageing (ERIBA), University Medical Center Groningen, and the University of Groningen (RUG), the aging process itself – not just the diseases it produces – can and should be a primary focus of healthcare. The Problem with Traditional MedicineWhile modern healthcare has extended lifespan and improved treatment for many diseases, it tends to be insufficient in addressing the complex needs of aging populations. Older individuals frequently experience multiple chronic conditions simultaneously, such as cardiovascular disease, diabetes, cancer, and neurodegenerative disorders. This state of multimorbidity complicates care, increases the use of multiple medications, and reduces quality of life. The dominant traditional healthcare system, which typically begins only after symptoms appear, is costly and insufficient for addressing the interconnected nature of these conditions.A New Model for Healthcare: Insights from the EditorialIn his recent editorial, “Rethinking healthcare through aging biology,” published in Aging Volume 17, Issue 5, Dr. Demaria outlines a shift from disease-specific treatment to targeting the biological mechanisms of aging itself, a more integrated and forward-looking approach. He presents three evolving healthcare models.Full blog - https://aging-us.org/2025/06/a-new-vision-for-healthcare-addressing-aging-before-disease-begins/Paper DOI - https://doi.org/10.18632/aging.206262Corresponding author - Marco Demaria - m.demaria@umcg.nlVideo short - https://www.youtube.com/watch?v=xR-16cjHnQYSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206262Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, healthcare, senolytics, epigenetics, medical educationTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 25, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 5, on May 28, 2025, titled “Investigating telomere length in progeroid syndromes: implications for aging disorders.”In this study, led by first author Luma Srour and corresponding authors Yosra Bejaoui and Nady El Hajj, from Hamad Bin Khalifa University, Qatar Foundation, researchers investigated whether shortened telomeres, a marker of cellular aging, are present across various rare genetic disorders that mimic early aging, known as progeroid syndromes. The study found that telomere shortening, also called telomere attrition, is not a shared characteristic of all these disorders. This finding is important because it challenges the belief that telomere loss is a common thread in premature aging and could help refine how these syndromes are studied and treated.Progeroid syndromes are rare conditions that cause individuals to display symptoms of aging far earlier than expected. While some of these syndromes share signs of typical aging, others arise from very different genetic alterations. Researchers focused on comparing telomere length in individuals with several of these syndromes to better understand how aging develops at the cellular level. Telomeres are protective ends of chromosomes that shorten as cells divide, acting as a biological clock linked to aging and disease.Using DNA methylation data from blood samples, the team analyzed telomere length in patients with six progeroid syndromes: Werner Syndrome, Hutchinson-Gilford Progeria Syndrome, Berardinelli-Seip Congenital Lipodystrophy type 2, Dyskeratosis Congenita, Cerebroretinal Microangiopathy with Calcifications and Cysts, and Wiedemann-Rautenstrauch Syndrome. They found significant telomere shortening only in classical Werner Syndrome, Berardinelli-Seip Congenital Lipodystrophy type 2, and Dyskeratosis Congenita. Other syndromes, including the widely studied Hutchinson-Gilford Progeria Syndrome, did not show this pattern.“To investigate whether progeroid syndromes have telomere attrition, we calculated telomere length using the DNAmAge web-based calculator.”The findings suggest that telomere shortening cannot be used as a universal marker for all forms of premature aging. In fact, some syndromes linked to DNA repair problems showed telomere damage, while others with different genetic mutations did not. These results indicate that the underlying biology of each syndrome is crucial in determining whether telomere shortening plays a role. Researchers also compared telomere lengths in people with genetic variants known to protect against age-related diseases. Those with protective genes had longer telomeres than people with progeroid syndromes.This study challenges assumptions about aging in rare disorders and highlights the need for more personalized approaches in aging research. By identifying which syndromes involve telomere attrition, it opens new avenues for treating or delaying aging-related symptoms. Future research may explore other biological factors behind premature aging and how genetic differences influence the aging process.DOI - https://doi.org/10.18632/aging.206255Corresponding authors - Yosra Bejaoui - yob4003@qatar-med.cornell.edu, and Nady El Hajj - nelhajj@hbku.edu.qaVideo short - https://www.youtube.com/watch?v=T8vjIuYHaFgTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 24, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 5, on May 20, 2025, titled “Short-term moderate caloric restriction in the rhesus macaque attenuates markers of ovarian aging in select populations.”In this study, led by first author Emma S. Gargus and corresponding author Francesca E. Duncan from Feinberg School of Medicine at Northwestern University, researchers explored how dietary changes impact ovarian aging in female rhesus macaques. They found that a three-year moderate reduction in caloric intake preserved a youthful distribution of ovarian follicles and reduced age-related tissue stiffness. These findings are relevant to women’s health as they suggest that caloric restriction (CR) may help delay the decline in reproductive function associated with aging.Ovarian aging, which leads to reduced fertility and hormone production, is one of the earliest signs of aging in women. This study investigated whether a 30% reduction in caloric intake could protect the ovaries from age-related damage in nonhuman primates (NHP), whose reproductive biology closely mirrors that of humans. Ovaries were collected from young (10–13 years) and old (19–26 years) rhesus macaques who were either on a diet of moderate caloric restriction or a control diet for three years.“To test the effect of CR on follicle number, follicles were analyzed in histological sections from animals across experimental cohorts: Young Control, Young CR, Old Control, Old CR (n = 4–8/group).”Although total follicle numbers still declined with age, caloric restriction helped maintain the types of follicles most associated with reproductive potential. In older monkeys who were still cycling, even if irregularly, caloric restriction preserved more primordial follicles, the key indicators of ovarian reserve, than in those on a normal diet.The benefits of caloric restriction were also seen in the structure of ovarian tissue. Normally, aging leads to fibrosis, a stiffening of the ovarian environment caused by increased collagen and decreased hyaluronic acid. This study showed that caloric restriction reduced this fibrotic process, suggesting a more supportive environment for maintaining reproductive health.While the diet did not stop the overall loss of follicles with age, it improved the proportion of younger, more viable follicles in aging ovaries. The timing of the dietary intervention also appeared to matter. Positive effects were more noticeable in older animals with irregular cycles than in those who had completely stopped cycling. This indicates that starting caloric restriction at a certain point in the reproductive lifespan may yield the best results.This research is an important step to identifying lifestyle-based strategies that can extend reproductive longevity. Although further studies are needed to test these findings in humans, the work supports the potential of moderate dietary changes to delay ovarian aging and help preserve fertility later in life.DOI - https://doi.org/10.18632/aging.206253Corresponding author - Francesca E. Duncan - f-duncan@northwestern.eduVideo short - https://www.youtube.com/watch?v=AvgZR3X3nyUSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206253Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Dr. Josh Mitteldorf summarizes his #research perspective #published in Volume 17, Issue 5 of Aging (Aging-US), titled “Methylation clocks for evaluation of anti-aging interventions.”DOI - https://doi.org/10.18632/aging.206245Corresponding author - Josh Mitteldorf - aging.advice@gmail.comAuthor interview - https://www.youtube.com/watch?v=efgNvr5ezTkVideo short - https://www.youtube.com/watch?v=YjUvpqMzCGcAbstractMethylation clocks have found their way into the community of aging research as a way to test anti-aging interventions without having to wait for mortality statistics. But methylation is a primary means of epigenetic control, and presumably has evolved under strong selection. Hence, if methylation patterns change consistently at late ages it must mean one of two things. Either (1) the body is evolved to destroy itself (with inflammation, autoimmunity, etc.), and the observed methylation changes are a means to this end; or (2) the body detects accumulated damage, and is ramping up repair mechanisms in a campaign to rescue itself. My thesis herein is that both Type 1 and Type 2 changes are occurring, but that only Type 1 changes are useful in constructing methylation clocks to evaluate anti-aging interventions. This is because a therapy that sets back Type 1 changes to an earlier age state has stopped the body from destroying itself; but a therapy that sets back Type 2 changes has stopped the body from repairing itself. Thus, a major challenge before the community of epigenetic clock developers is to distinguish Type 2 from Type 1. The existence of Type 1 epigenetic changes is in conflict with conventional Darwinian thinking, and this has prompted some researchers to explore the possibility that Type 1 changes might be a form of stochastic epigenetic drift. I argue herein that what seems like directed epigenetic change really is directed epigenetic change. Of five recent articles on “stochastic methylation clocks,” only one (from the Conboy lab) is based on truly stochastic changes. Using the Conboy methodology and a methylation database, I construct a measure of true methylation drift, and show that its correlation with age is too low to be useful.Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206245Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, methylation, stochastic, entropy, programmed aging, aging clock, epigenetic clockTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 18, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 5, on May 12, 2025, titled “Frailty transitions in electronic health records: who first? what first?”The study, led by Fabienne Hershkowitz Sikron from Meuhedet HMO, analyzed how frailty develops over time in older adults using electronic health record data from nearly 120,000 individuals aged 65 and above. Researchers found that frailty worsened in over 13% of participants within a year, particularly among women, adults aged 85 or older, and people with chronic illnesses, while nearly 3% showed signs of improvement. The findings highlight early indicators of decline that could help guide preventive care and improve outcomes for aging populations.Frailty is a condition marked by increased vulnerability to health complications and tends to change gradually. The study used the Meuhedet Electronic Frailty Index (MEFI) to track yearly transitions in frailty among older adults in Israel. While many people remained in the same frailty category, a significant proportion experienced deterioration in just one year, and a smaller group improved.“Worsening frailty is defined as a higher frailty level one year later in 2024 compared to 2023. A new frailty deficit is defined as a deficit appearing in 2024 that was not present in 2023.”Those most at risk of worsening included adults over 85, women, individuals from lower socio-economic backgrounds, and members of the Arab sector. Additional predictors of decline included recent hospitalizations, multiple chronic diseases, and signs of cognitive or mobility issues. Importantly, the first signs of worsening were often not new chronic conditions but more manageable health deficits such as sleep disturbances, muscle weakness, hearing loss, and memory decline. Those who improved were more likely to be younger, male, from higher socio-economic backgrounds, and have fewer chronic conditions and hospitalizations.The study also found that common chronic illnesses like diabetes and hypertension were often already present and did not usually signal the beginning of frailty progression. Instead, declines in overall function and quality of life were more frequently the first new issues to appear. This suggests that early intervention on modifiable health deficits could delay or prevent further decline.This work is one of the first large-scale, real-world studies to identify both who is most likely to worsen first and what health problems typically appear first. The authors emphasize the importance of using routinely collected electronic medical data to monitor frailty and tailor care. By doing so, health providers can implement timely strategies to reduce disease burden and support aging individuals in maintaining independence.These findings support the creation of proactive health programs focused on maintaining physical strength, cognitive function, and sensory abilities. Preventing frailty progression can reduce hospitalizations, ease disease burden, and help older adults maintain independence and a higher quality of life.DOI - https://doi.org/10.18632/aging.206247Corresponding author - Fabienne Hershkowitz Sikron - fabian_hershkowitz@meuhedet.co.ilVideo short - https://www.youtube.com/watch?v=4xa11ApI4hoSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 17, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 5, on May 1, 2025, titled “Oxytocin modulates insulin and GLP-1 secretion in pancreatic islets.”In this study, scientists from Fukushima Medical University School of Medicine investigated how the hormone oxytocin (Oxt) influences insulin levels by acting on specific cells in the pancreas. The team led by first author Kasumi Hattori and corresponding authors Kenju Shimomura and Yuko Maejima discovered that oxytocin may indirectly increase insulin secretion by triggering another hormone, GLP-1, from within the pancreas. This finding could lead to new strategies for improving blood sugar control in people with diabetes.Oxytocin is commonly known for its roles in childbirth and social bonding, but scientists have also been exploring its effects on metabolism. While previous studies offered mixed results about whether oxytocin raises or lowers blood sugar, this research brings new clarity. The study focused on oxytocin’s impact on insulin and a hormone called GLP-1, which helps regulate insulin production. Researchers tested this by using mice with and without oxytocin receptors and found that oxytocin’s ability to raise insulin levels depended on the presence of these receptors and high blood sugar conditions.Researchers found that oxytocin stimulates the release of “intra-islet GLP-1,” a form of GLP-1 produced inside the pancreas rather than the intestine. In the pancreas, insulin is produced by beta cells, while alpha cells produce glucagon, a hormone that raises blood sugar. But recent research, including this study, has shown that alpha cells can also release GLP-1, which in turn helps beta cells secrete insulin. Oxytocin appears to increase this internal GLP-1 release, especially when blood sugar levels are high, thereby leading to insulin release in a natural and targeted way.In this study researchers were also able to detect the difference between oxytocin’s effect on blood sugar and its effect on insulin. They observed that right after oxytocin was given, blood sugar levels rose in all mice—even in those that lacked oxytocin receptors. However, only the mice with working oxytocin receptors showed a later increase in insulin. This suggests that oxytocin may trigger insulin production through a separate, receptor-dependent pathway involving the hormone GLP-1."WT mice showed a significant increase in insulin levels at 15-min, while OxtR KO mice did not."This indirect action—oxytocin triggering alpha cells to release GLP-1, which then acts on beta cells—may represent a novel mechanism for controlling insulin release. It also explains why oxytocin does not increase insulin in low-glucose conditions, making it a potentially safer option for regulating blood sugar.As treatments for type 2 diabetes increasingly focus on GLP-1–based drugs, this study opens the door to using oxytocin or similar compounds to naturally enhance the body’s own insulin-producing system. With further research, this mechanism could help develop new therapies that better mimic the body’s natural glucose control, particularly beneficial for older adults with diabetes.DOI - https://doi.org/10.18632/aging.206244Corresponding authors - Kenju Shimomura - shimomur@fmu.ac.jp, and Yuko Maejima - maejimay@fmu.ac.jpVideo short - https://www.youtube.com/watch?v=C0K6uDX4z8UTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 12, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 5, on May 3, 2025, titled “APOE genotype and biological age impact inter-omic associations related to bioenergetics.”In this study, led by first author Dylan Ellis and corresponding author Noa Rappaport from the Institute for Systems Biology, researchers discovered that different versions of the APOE gene—particularly ε2 and ε4—are linked to metabolic patterns associated with aging and Alzheimer’s disease risk. Both variants were linked to increased levels of diacylglycerols, a type of fat molecule connected to insulin resistance and inflammation, suggesting shared disruptions in how the body regulates energy.The research team analyzed data from over 2,200 adults without an Alzheimer’s diagnosis, exploring how APOE genotypes influence biological age, a measure of health that reflects how quickly or slowly someone is aging at a cellular level. They found that the same metabolic disturbances seen in ε2 carriers were also present in people considered biologically older, revealing unexpected overlap between genetic risk and aging-related metabolic changes.To examine these connections in more detail, the researchers used a multi-omics approach, combining blood-based metabolism and protein data, gut bacteria analysis from stool samples, and clinical chemistry data. This method allowed them to map how genetic differences and biological aging affect the body’s energy systems. They observed altered connections between glucose metabolism, inflammatory markers, and key molecules that play roles in energy production, indicating early disruptions that could contribute to age-related diseases.One of the study’s surprising findings was that the ε2 variant, usually associated with longer life and reduced Alzheimer’s risk, showed metabolic traits similar to those found in insulin-resistant individuals. This suggests that ε2 may carry metabolic disadvantages earlier in life, with its protective effects becoming more pronounced later. Conversely, ε4—linked to greater Alzheimer’s risk—may exert its influence based on interactions with lifestyle factors like diet, sex, and overall health status.“‘Omics association patterns of ε2-carriers and increased biological age were also counter-intuitively similar, displaying significantly increased associations between insulin resistance markers and energy-generating pathway metabolites.”By identifying these shared biological signatures, this study offers a new framework for understanding how genes and metabolism work together to influence aging. These findings could support more personalized health strategies aimed at delaying biological aging and reducing the risk of chronic diseases. As aging populations grow worldwide, understanding these pathways is essential to improving healthspan.DOI - https://doi.org/10.18632/aging.206243Corresponding author - Noa Rappaport - noa.rappaport@isbscience.orgVideo short - https://www.youtube.com/watch?v=75hZQoO5U0USign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206243Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, apolipoprotein E (APOE), biological age, metabolism, Alzheimer’s disease (AD), insulin resistanceTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
As we age, our brains become more sensitive to stress and disease. A recent study sheds light on a lesser-known risk: reduced oxygen levels. The study, titled “Defining the hypoxic thresholds that trigger blood-brain barrier disruption: the effect of age” and recently published as the cover for Volume 17, Issue 5 of Aging (Aging-US), found that low oxygen—also called hypoxia—can harm the aging brain by disrupting the blood-brain barrier (BBB). This damage may contribute to cognitive decline, memory problems, and an increased risk of dementia.Understanding Hypoxia in the BrainThe brain relies on a steady supply of oxygen to stay healthy. When oxygen levels fall—a condition known as hypoxia—the brain undergoes changes to adapt. These changes include the remodeling of blood vessels and, importantly, a weakening of the blood-brain barrier. The BBB acts as a filter, protecting brain tissue from harmful substances. When it breaks down, it can lead to inflammation, brain cell damage, and cognitive issues.Hypoxia is common in older adults, especially those with conditions like sleep apnea, chronic obstructive pulmonary disease (COPD), heart failure, and asthma. That is why understanding the connection between low oxygen and the aging brain is crucial for preventing long-term neurological damage.Full blog - https://aging-us.org/2025/06/oxygen-deprivation-and-the-aging-brain-a-hidden-trigger-for-cognitive-decline/Paper DOI - https://doi.org/10.18632/aging.206241Corresponding author - Richard Milner - rmilner@sdbri.orgVideo short - https://www.youtube.com/watch?v=Nr6rTm7aJRoSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206241Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, blood-brain barrier integrity, endothelial, proliferation, microglia, chronic mild hypoxia, hypoxic thresholdTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 10, 2025 — The Ride for Roswell, one of the USA’s largest cycling events supporting cancer research, returns to Buffalo on Saturday, June 28, 2025. Hosted annually by Roswell Park Comprehensive Cancer Center, this community-wide event brings together riders, volunteers, and supporters to raise funds for cancer research, celebrate survivors, and honor those lost to the disease. Among the returning participants is the Open Access Team, led by team captain Sergei Kurenov. This year, the team is once again proudly sponsored by Impact Journals, the publisher of open access journals Aging, Oncotarget, Genes & Cancer, and Oncoscience.“For the last 10 years, I have continuously participated in the Ride for Roswell in honor of those who have bravely fought cancer,” said Kurenov. “This journey is deeply personal for me. My father battled cancer, and some of my closest friends have fought through prostate and lung cancer with incredible strength.”This year, the Open Access Team rides in honor of Dr. Mikhail (Misha) Blagosklonny, a visionary scientist who dedicated his career to advancing cancer and aging research. As the founding Editor-in-Chief of Aging, Oncotarget and Oncoscience, Dr. Blagosklonny was a pioneer of open-access publishing. His groundbreaking work on mTOR signaling and rapamycin transformed our understanding of cancer biology and healthy lifespan extension.The 2025 Ride for Roswell features nine route options, ranging from 4 to 100 miles, all beginning at the University at Buffalo North Campus. Riders from across the USA and beyond are invited to participate and make a meaningful impact in the fight against cancer.This ride is more than just a journey on two wheels—it’s a commitment to building a future where no one has to fear a cancer diagnosis. There is still time to support the Open Access Team in the 2025 Ride for Roswell. Whether by donating, joining the team, or sharing their story, every action brings us closer to better treatments, deeper understanding, and, ultimately, a cure.Visit the Open Access Team page - https://give.roswellpark.org/site/TR/SpecialEvents/General?team_id=23320&pg=team&fr_id=2020To learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 10, 2025 — A new #research perspective was #published in Aging (Aging-US) Volume 17, Issue 5, on May 5, 2025, titled “Methylation clocks for evaluation of anti-aging interventions.”In this perspective article, Dr. Josh Mitteldorf explores how current epigenetic clocks—used to estimate biological age—might mislead scientists trying to evaluate anti-aging therapies. The paper challenges a widespread assumption: that all changes in DNA methylation with age are equally valid for measuring biological decline. Dr. Mitteldorf proposes that failing to distinguish between different types of epigenetic changes could lead to inaccurate conclusions, potentially even favoring treatments that reduce repair processes rather than extend healthy lifespan.Methylation clocks have become a popular tool in aging research. These clocks use patterns of DNA methylation, a form of gene regulation that changes over time, to predict a person’s biological age. Because human aging trials are long and expensive, these clocks offer a faster way to evaluate whether a therapy slows or reverses aging. However, this article warns that not all methylation changes are equal in meaning or effect.The perspective identifies two main categories of methylation changes that occur with age. One type, called 'Type 1,' seems to support the idea that aging may be programmed, with gene activity changing in ways that could cause damage, such as more inflammation or increased cell loss. The second type, “Type 2,” involves increased gene activity aimed at repairing age-related damage. If a therapy reduces the activity of Type 2 genes, it may appear to slow aging while actually interfering with the body’s repair response.“Paradoxically, an intervention that “sets back” the body’s methylation clock to a younger state is shutting off vital repair mechanisms, so it is likely inimical to health and longevity.” This distinction is important because most methylation clocks, including popular models like GrimAge, do not separate these two types. As a result, they may incorrectly suggest that a treatment is reversing aging when it is only suppressing beneficial repair mechanisms. According to Dr. Mitteldorf, this could lead researchers to draw the wrong conclusions and unintentionally slow down progress in anti-aging research.The author also addresses a growing trend in the scientific community that aims to explain age-related methylation as random drift rather than directed change. In a pilot analysis using publicly available data, Dr. Mitteldorf attempted to construct a clock based purely on stochastic, or random, changes. The results showed a weak correlation with age, suggesting that random drift is an unreliable basis for assessing biological aging.Dr. Mitteldorf argues that most age-related methylation changes are likely intentional and regulated, rather than random. If so, epigenetic clocks must be refined to reflect the biological purpose behind methylation shifts. Without distinguishing between changes that indicate damage and those that indicate repair, current clocks may not only mismeasure age but also misguide intervention strategies.This article highlights the urgent need to improve how methylation data are interpreted before such clocks can reliably assess anti-aging therapies. A clearer understanding of these molecular patterns could help reshape the future of aging research and therapy evaluation.DOI - https://doi.org/10.18632/aging.206245Corresponding author - Josh Mitteldorf - aging.advice@gmail.comTo learn more about the journal, please visit our website at https://www.Aging-US.com.MEDIA@IMPACTJOURNALS.COM
Dr. Stefanie Morgan joins Dr. Robert Dudley from AgelessRx to discuss a #research paper she co-authored that was #published in Volume 17, Issue 4 of Aging, entitled “Influence of rapamycin on safety and healthspan metrics after one year: PEARL trial results.”DOI - https://doi.org/10.18632/aging.206235Corresponding author - Stefanie L. Morgan - stefanie@agelessrx.comAuthor interview - https://www.youtube.com/watch?v=2qlIiVh2OJsVideo short - https://www.youtube.com/watch?v=z5j2nyK2HZ8AbstractDesign: This 48-week decentralized, double-blinded, randomized, placebo-controlled trial (NCT04488601) evaluated the long-term safety of intermittent low-dose rapamycin in a healthy, normative-aging human cohort. Participants received placebo, 5 mg or 10 mg compounded rapamycin weekly. The primary outcome measure was visceral adiposity (by DXA scan), secondary outcomes were blood biomarkers, and lean tissue and bone mineral content (by DXA scan). Established surveys were utilized to evaluate health and well-being. Safety was assessed through adverse events and blood biomarker monitoring.Results: Adverse and serious adverse events were similar across all groups. Visceral adiposity did not change significantly (ηp2 = 0.001, p = 0.942), and changes in blood biomarkers remained within normal ranges. Lean tissue mass (ηp2 = 0.202, p = 0.013) and self-reported pain (ηp2 = 0.168, p = 0.015) improved significantly for women using 10 mg rapamycin. Self-reported emotional well-being (ηp2 = 0.108, p = 0.023) and general health (ηp2 = 0.166, p = 0.004) also improved for those using 5 mg rapamycin. No other significant effects were observed.Conclusions: Low-dose, intermittent rapamycin administration over 48 weeks is relatively safe in healthy, normative-aging adults, and was associated with significant improvements in lean tissue mass and pain in women. Future work will evaluate benefits of a broader range of rapamycin doses on healthspan metrics for longevity, and will aim to more comprehensively establish efficacy.Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206235Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, rapamycin, geroscience, longevity, healthspanTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Buffalo, NY — June 4, 2025 — The Longevity & Aging Series has been honored with the Silver Award for “Excellence in Video/Film” at the inaugural EPIC Awards celebration on May 29, 2025, during the Society for Scholarly Publishing (SSP) 47th Annual Meeting in Baltimore, Maryland.The EPIC Awards recognize the achievements of those who are advancing scholarly publishing through creativity, collaboration, and cutting-edge innovation. The Longevity & Aging Series, hosted by Aging (Aging-US) Editorial Board member Dr. Evgeniy Galimov, stood out for its impactful storytelling, production quality, and commitment to advancing understanding in the field of aging research.The Longevity & Aging Series brings together leading experts to discuss the latest developments in the biology of aging, healthy longevity, and interventions to improve healthspan. Now in its third season, the series is a trusted resource for scientists, clinicians, and the broader public interested in the future of aging research.For more information about the Aging (Aging-US) Longevity & Aging Series and to view the award-winning videos, please visit our show page or YouTube channel. If you are interested in becoming a guest or would like to know more about the series, please email us at media@impactjournals.com.Longevity & Aging Series Show Page - https://www.aging-us.com/longevityAging-US YouTube Channel - https://www.youtube.com/@AgingJournalTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/LinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc
BUFFALO, NY — June 4, 2025 — A new #editorial was #published in Aging (Aging-US) Volume 17, Issue 5, on May 29, 2025, titled “Rethinking healthcare through aging biology.”In this scientific editorial, Aging (Aging-US) Editor-in-Chief Marco Demaria from the European Research Institute for the Biology of Ageing (ERIBA), University Medical Center Groningen (UMCG) and the University of Groningen (RUG), advocates for healthcare reform that addresses the biological drivers of aging rather than individual chronic conditions. The article proposes that targeting the root causes of age-related diseases through aging biology could revolutionize preventive care, extend healthspan, and reduce long-term healthcare costs. This proactive approach aligns with a growing body of aging research focused on improving healthy longevity.Dr. Demaria explains that today’s disease-focused model is inadequate for aging populations, who often suffer from multimorbidity—the presence of multiple chronic illnesses like cancer, heart disease, and type 2 diabetes. These overlapping conditions, rooted in common aging mechanisms, overwhelm healthcare systems and lead to complex treatments with limited success. The editorial suggests that identifying and intervening in the biological aging process could prevent such diseases before they emerge.In the editorial, Dr. Demaria outlines three healthcare paradigms. The first is the existing system, which reacts to disease after symptoms appear. The second involves intervening once age-related damage begins, using new tools such as senolytics, which eliminate harmful senescent cells, and rapalogs, which regulate cellular metabolism. The third and most forward-looking model focuses on preventing aging-related damage before it starts. This strategy supports lifelong biological balance and seeks to avoid early molecular decline through continuous health maintenance.Prevention is key in this model. Lifestyle choices—such as exercise, a healthy diet, quality sleep, and stress reduction—play a vital role in slowing the aging process. Dr. Demaria also points to the promise of biological age diagnostics—tools or tests that estimate a person’s biological age—which allow people to track their physiological aging and adopt personalized interventions. Additionally, optimizing maternal nutrition and early-life health can contribute to lifelong disease prevention.To support this shift, the editorial calls for major changes in medical education. Physicians must be trained in geroscience, healthspan optimization, and personalized preventive care. This knowledge will prepare future clinicians not just to treat disease, but to delay or prevent it altogether. Collaboration among healthcare providers, researchers, and policymakers will be essential for building this new system.“The third paradigm—preventing aging-related damage—demands a systemic shift toward predictive and preventative research, with an emphasis on multi-omic data, lifestyle interventions, and early-life interventions.”By redefining medicine around the science of aging, Dr. Demaria’s editorial highlights the path toward healthier aging, longer life expectancy, and a more sustainable healthcare future.DOI - https://doi.org/10.18632/aging.206262Corresponding author - Marco Demaria - m.demaria@umcg.nlVideo short - https://www.youtube.com/watch?v=xR-16cjHnQYTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 3, 2025 — A new #research paper was #published in Aging (Aging-US) on May 1, 2025, as the #cover of Volume 17, Issue 5, titled “Defining the hypoxic thresholds that trigger blood-brain barrier disruption: the effect of age.”In this study, researchers Arjun Sapkota, Sebok K. Halder, and Richard Milner from San Diego Biomedical Research Institute investigated how aging affects the brain’s vulnerability to low oxygen, or hypoxia. Using C57BL/6J mice ranging from 2 to 23 months of age, they identified specific oxygen levels that disrupt the blood-brain barrier (BBB)—a critical structure that protects brain tissue from harmful substances. The findings are important for understanding age-related cognitive decline and the potential risks faced by individuals with chronic oxygen-limiting conditions such as asthma, sleep apnea, emphysema, and heart disease.The BBB is essential for maintaining brain health. In this study, mild and prolonged hypoxia—called chronic mild hypoxia—was found to compromise the BBB in mice. Older mice showed significantly more BBB disruption than younger ones. Notably, barrier weakening and blood vessel changes occurred at oxygen levels of just 15% in aged mice, compared to 13% in young mice. These data suggest that the aging brain is more sensitive to oxygen deprivation, even at levels that may be considered only mildly hypoxic.The researchers also determined when this vulnerability emerged. The BBB showed increased sensitivity to low oxygen not only in aged mice but also in mice as young as 2 to 6 months, with a second spike occurring between 12 and 15 months—equivalent to middle age in mice. These findings may reflect age-dependent changes in brain vascular function and remodeling capacity.“Hypoxia-induced endothelial proliferation was relatively constant across the age range, but advanced age strongly enhanced the degree of BBB disruption (4-6-fold greater in 23 months vs. 2 months old).”Another key focus was microglial activation, a sign of brain inflammation. Aged mice exhibited higher microglial activation across all oxygen levels, including normal conditions. Chronic microglial activation is closely linked to neuroinflammation and has been implicated in diseases such as Alzheimer’s. While the rate of blood vessel formation was constant across ages, the degree of BBB disruption increased sharply with age, suggesting that repair mechanisms may weaken over time.These results may help explain why older adults with chronic hypoxia-related diseases are at higher risk for neurodegeneration and cognitive decline. The study also draws attention to the risks of high-altitude exposure for aging populations, where oxygen levels naturally drop.Altogether, these findings underscore the importance of protecting brain health in older individuals by managing oxygen exposure and reducing hypoxia-related risks. The researchers emphasize the need to develop new therapies that support blood-brain barrier integrity, particularly in aging populations exposed to chronic or intermittent low-oxygen conditions.DOI - https://doi.org/10.18632/aging.206241Corresponding author - Richard Milner - rmilner@sdbri.orgVideo short - https://www.youtube.com/watch?v=Nr6rTm7aJRoKeywords - aging, blood-brain barrier integrity, endothelial, proliferation, microglia, chronic mild hypoxia, hypoxic thresholdTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — May 23, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 4, on April 1, 2025, titled “Examining frailty phenotypes of community-dwelling older adults in Taiwan using the falls risk for older people in the community – Taiwan version (Tw-FROP-Com).”A research team led by first author Ya-Mei Tzeng and corresponding authors Yu-Tien Chang and Yaw-Wen Chang from the National Defense Medical Center studied older adults in Taiwan and found that unintentional weight loss is the most significant individual predictor of fall risk among the common signs of frailty. This finding highlights the importance of early detection and tailored interventions to reduce fall-related injuries among aging populations.Falls are a major cause of injury-related death in seniors, especially in low- and middle-income countries. In Taiwan, they rank as the second leading cause of accidental death among those aged 65 and older. The researchers evaluated five signs of frailty—weakness, slowness, exhaustion, low physical activity, and unintentional weight loss—using a locally adapted fall risk screening tool, Tw-FROP-Com. Frailty is a condition marked by reduced strength, stamina, and resilience, making older adults more vulnerable to accidents and illness.The study analyzed data from 375 older adults participating in a fall prevention program in Keelung City. Of these, 18.7% were classified as frail, and nearly one-third had experienced a fall in the past year. All five frailty signs were associated with increased fall risk, but statistical analysis showed that unintentional weight loss had the strongest association, even after adjusting for factors like age and previous falls.Rather than relying on a broad frailty label, this study found that analyzing each frailty feature individually provided more accurate predictions of fall risk. Weight loss, in particular, was also associated with conditions such as malnutrition, muscle decline, or chronic illness.“Treating frailty as five distinct components provided a more precise prediction of fall risk than using a dichotomous frailty measure (Yes/No).”The findings support the use of accessible screening tools like Tw-FROP-Com in everyday healthcare settings. Because it does not require complex equipment or physical testing, it can be widely applied to identify older adults at risk. Interventions such as nutritional support, physical activity, and weight monitoring can then be offered before a fall occurs.The researchers recommend that public health programs and healthcare providers focus on each specific frailty sign, especially unintentional weight loss, rather than relying only on overall frailty status. As the global population ages, targeted fall prevention strategies like these may help older adults live healthier, more independent lives.Paper DOI: https://doi.org/10.18632/aging.206231Corresponding authors: Yu-Tien Chang – greengarden720925@gmail.com; Yaw-Wen Chang- yawwenc@office365.ndmctsgh.edu.twKeywords: aging, frailty, fall risk, fried frailty criteria, older adults, Tw-FROP-ComSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, epigenetics, DNA methylation, diet, biological clockTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
In a world where we are living longer but not always healthier, scientists are searching for ways to add life to our years, not just years to our lives. A recent study published in Aging (Aging-US), Volume 17, Issue 4, led by researchers at the National University of Natural Medicine, suggests that certain common foods, already known for their health benefits, might also help slow or even reverse epigenetic or biological aging. These foods, rich in specific plant compounds, appear to influence our DNA in ways that may slow down the body’s epigenetic clock.Full blog - https://aging-us.org/2025/05/study-identifies-foods-that-may-reverse-biological-age-and-promote-healthy-aging-in-men/Paper DOI - https://doi.org/10.18632/aging.206240Corresponding author - Ryan Bradley - rbradley@nunm.eduVideo short - https://www.youtube.com/watch?v=T6I33AIAIFMSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206240Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, epigenetics, DNA methylation, diet, biological clockTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — May 20, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 4, on April 17, 2025, titled “Dietary associations with reduced epigenetic age: a secondary data analysis of the methylation diet and lifestyle study.”In this study, researchers led by first author Jamie L. Villanueva from the University of Washington and the National University of Natural Medicine, along with corresponding author Ryan Bradley from the National University of Natural Medicine and University of California, investigated how diet influences epigenetic aging. They found that certain plant-based foods containing natural compounds called methyl adaptogens were associated with a decrease in epigenetic age. This effect was measured using DNA methylation, a marker that reflects how the body ages at the cellular level. The findings suggest that targeted food choices may help slow the aging process.Epigenetic age refers to how old a person’s cells appear biologically, rather than their actual age in years. DNA methylation patterns, which are chemical tags on DNA, can indicate whether someone is aging faster or slower than expected. For this study, researchers used Horvath’s epigenetic clock, a widely accepted tool, to measure changes in epigenetic age.The analysis included healthy men aged 50 to 72 who had previously completed an eight-week program featuring a plant-based, nutrient-rich diet, along with guidance on exercise, sleep, and stress management. Researchers focused on individual dietary differences to understand why some participants experienced greater improvements in epigenetic age than others.The study found that those who ate higher amounts of methyl adaptogen foods—including turmeric, rosemary, garlic, berries, green tea, and oolong tea—experienced greater reductions in epigenetic age. These benefits remained significant even after accounting for weight changes and participants’ starting epigenetic age, suggesting that the foods themselves had a direct impact on aging markers.“In hierarchical linear regression, foods investigated as polyphenolic modulators of DNA methylation (green tea, oolong tea, turmeric, rosemary, garlic, berries) categorized in the original study as methyl adaptogens showed significant linear associations with epigenetic age change (B = -1.21, CI = [-2.80, -0.08]), after controlling for baseline epigenetic age acceleration and weight changes.”The natural compounds in methyl adaptogen foods are known to influence how genes behave by affecting DNA methylation. Previous studies have shown that these compounds may support healthy aging and help lower the risk of conditions such as heart disease and cognitive decline.While this study involved a relatively small group of middle-aged men, it adds knowledge to growing global research showing that diets rich in polyphenols—found in vegetables, fruits, and teas—are associated with slower aging. These findings support earlier results from studies on Mediterranean and traditional Japanese diets, both known for their health benefits.Future research should include larger and more diverse populations and use updated epigenetic aging tools to confirm these results. Based on current evidence, this study highlights a practical, food-based strategy that may help reduce epigenetic aging and support long-term health.DOI - https://doi.org/10.18632/aging.206240Corresponding author - Ryan Bradley - rbradley@nunm.eduTo learn more about the journal, connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
In this #episode of the Longevity & Aging Series, Dr. Shubhankar Suman from the Department of Oncology at Georgetown University Medical Center joins host Dr. Evgeniy Galimov to discuss a #research paper he co-authored in Volume 17, Issue 1 of Aging (Aging-US), titled: “Senolytic agent ABT-263 mitigates low- and high-LET radiation-induced gastrointestinal cancer development in Apc1638N/+ mice.”DOI - https://doi.org/10.18632/aging.206183Corresponding author - Shubhankar Suman - ss2286@georgetown.eduAuthor interview - https://www.youtube.com/watch?v=ClLO0ERwC0MVideo short - https://www.youtube.com/watch?v=M_WEht4vy4wSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206183Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, senescence-associated secretory phenotype, senolytic agent, carcinogenesis, inflammation, β-cateninTo learn more about Aging (Aging-US), please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — May 14, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 4, on April 10, 2025, titled “Impact of Factor Xa inhibitors on cardiovascular events in older patients with nonvalvular atrial fibrillation.”In this study, first author Masahiko Takahashi and corresponding author Keisuke Okawa led a research team from Kagawa Prefectural Central Hospital and Hyogo Medical University that investigated whether Factor Xa inhibitors (Xa-Is)—a type of blood thinner—can reduce the risk of heart-related complications in patients over 80 with nonvalvular atrial fibrillation (NVAF). The study found that patients using Xa-Is experienced significantly fewer cardiovascular problems than those on other anticoagulants. This finding is especially relevant, as older adults face a high risk of both stroke and heart disease.Atrial fibrillation is a common heart rhythm disorder, particularly in the elderly, that increases the risk of blood clots, heart failure, and stroke. Anticoagulants are often prescribed to prevent clots, but not all types have the same effects on heart health. This study focused on comparing Xa-Is—specifically rivaroxaban, apixaban, and edoxaban—with commonly used drugs such as warfarin and dabigatran.Researchers followed more than 1,000 patients aged 80 and above for up to five years to assess the long-term impact of these medications on cardiovascular outcomes. Patients who used Xa-Is had significantly lower rates of heart failure, artery disease, and cardiovascular death. The risk of cardiovascular problems in the Xa-I group was less than half that of those on non-Xa-I medications. These benefits remained even after adjusting for factors like age, existing heart conditions, and kidney function. Additionally, stroke and all-cause death rates were notably lower in the Xa-I group. “Xa-Is may be useful for not only anticoagulation but also the prevention of cardiovascular events in very old patients with NVAF.”What makes Xa-Is different, according to the researchers, is their ability to inhibit a specific biological pathway—known as Factor Xa–PAR2—that contributes to inflammation, fibrosis, and damage in blood vessels and heart tissue. This effect extends beyond their traditional role in preventing blood clots. Although the study was conducted at a single medical center in Japan, its rigorous design and long follow-up period enhance the reliability of the findings for real-world clinical decision-making.While further studies, especially across multiple centers, are needed to confirm the full range of benefits, this study strongly suggests that Xa-Is may offer broader cardiovascular protection for very old patients. The findings could influence how clinicians choose blood thinners for elderly individuals with atrial fibrillation, potentially improving both survival and quality of life in this growing population.DOI - https://doi.org/10.18632/aging.206238Corresponding author - Keisuke Okawa - k-ookawa@chp-kagawa.jpVideo short - https://www.youtube.com/watch?v=YtbYpfVDVDISign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206238Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, Factor Xa inhibitor, atrial fibrillation, older patient, cardiovascular eventsTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Werner syndrome is a rare condition marked by accelerated aging. A recent study, featured as the cover paper in Aging (Aging-US), Volume 17, Issue 4, led by researchers at the University of Oslo and international collaborators, suggests that nicotinamide adenine dinucleotide (NAD+), a vital molecule involved in cellular energy production, may be key to understanding this disease and developing future strategies to manage it.Understanding Werner SyndromeWerner syndrome (WS) is a rare genetic condition that causes people to age more quickly than normal. By their 20s or 30s, individuals with WS often show signs typically associated with older age, such as cataracts, hair loss, thinning skin, and heart disease. This premature aging is caused by mutations in the WRN gene, which normally helps repair DNA and protect cells from damage. While the WRN gene’s role in maintaining genetic stability is well understood, the reasons behind the rapid decline of cells in WS patients are still not fully clear.The Study: Investigating NAD+ in Werner SyndromeNicotinamide adenine dinucleotide levels naturally decline with age. In the study titled “Decreased mitochondrial NAD+ in WRN deficient cells links to dysfunctional proliferation,” researchers investigated whether this decline is more severe in people with WS and whether restoring NAD+ levels could help slow the aging process in these patients.Full blog - https://aging-us.org/2025/05/fighting-premature-aging-how-nad-could-help-treat-werner-syndrome/Paper DOI - https://doi.org/10.18632/aging.206236Corresponding author - Evandro F. Fang - e.f.fang@medisin.uio.noVideo short - https://www.youtube.com/watch?v=WpRpi8TYPfUSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206236Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, Werner syndrome, premature aging, NAD+, mitochondria, proliferationTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — May 13, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 4, on April 7, 2025, titled “Pharmacological recapitulation of the lean phenotype induced by the lifespan-extending sulfur amino acid-restricted diet.”In this study, the research team, led by first author Naidu B. Ommi and corresponding author Sailendra N. Nichenametla from the Orentreich Foundation for the Advancement of Science Inc., investigated whether the drug buthionine sulfoximine (BSO) could replicate the effects of sulfur amino acid restriction (SAAR), a challenging diet known to reduce obesity. The study found that BSO produced similar reductions in fat mass and weight gain. This drug-based approach may offer a simpler and safer treatment for obesity, especially for those unable to follow strict dietary plans.Obesity and metabolic disorders raise the risk of chronic illnesses like heart disease, diabetes, and Alzheimer’s disease. While SAAR, a diet low in the amino-acids methionine and cysteine, has shown powerful health benefits in animal studies, its translation to humans has been limited by adherence challenges. This new study explored whether BSO, a compound that lowers glutathione (GSH) levels in the body, could mimic SAAR’s effects without dietary restriction.Researchers tested four groups of obese mice on high-fat diets. One group received the SAAR diet, another was given a regular diet plus BSO, while two control groups received either no treatment or a supplement that increased GSH levels. The BSO-treated mice showed lower fat mass, reduced liver fat, and prevented weight gain, results comparable to those on the SAAR diet. These benefits occurred without reducing food intake or muscle mass, making BSO a particularly promising treatment option.“BSO mice exhibited all SAAR-induced changes, with two notable differences, i.e., a smaller effect size than that of the SAAR diet and a higher predilection for molecular changes in kidneys than in the liver.”Additional findings revealed that both the SAAR diet and BSO influenced metabolic activity by activating pathways related to fat storage, but they did so in different organs. The SAAR diet had stronger effects in the liver, while BSO acted more in the kidneys. Both interventions increased levels of the amino acid serine, which is associated with lower fat production.Unlike many obesity treatments that suppress appetite or reduce muscle, BSO helped prevent fat accumulation while preserving lean mass and food consumption. No signs of liver or kidney toxicity were observed during the 13-week study, suggesting the drug’s safety at the tested dose.Since BSO has previously been evaluated in human clinical trials for other conditions, repurposing it for metabolic diseases may be relatively straightforward. However, the researchers point out that there should be further studies in both animals and humans. If successful, this strategy could provide a practical alternative to difficult-to-maintain diets and help more people manage weight long-term.DOI: https://doi.org/10.18632/aging.206237Corresponding author: Sailendra N. Nichenametla – snichenametla@orentreich.orgVideo short - https://www.youtube.com/watch?v=AcCzYTIElGYSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords: aging, buthionine sulfoximine, thiols, serine, anti-obesity drugsTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — May 7, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 4, on April 4, 2025, titled “Influence of rapamycin on safety and healthspan metrics after one year: PEARL trial results.”A research team led by first author Mauricio Moel and corresponding author Stefanie L. Morgan from AgelessRx conducted a clinical trial to determine whether low-dose, intermittent rapamycin could safely improve healthspan in older adults. The findings suggest rapamycin may offer measurable benefits for physical function and overall well-being, reinforcing its potential as a safe intervention to support healthy aging.Aging remains the leading cause of chronic conditions such as heart disease, diabetes, and dementia. While medical advances have extended lifespan, many people still experience declining health and reduced mobility in later years. This growing gap between lifespan and healthspan has driven interest in therapies that target aging itself. Rapamycin, an FDA-approved drug originally used in transplant medicine, has drawn attention for its ability to influence aging-related pathways in animal studies. Until recently, its safety and benefits in healthy human populations were largely unknown.The PEARL trial is the longest study so far to explore rapamycin’s use for longevity in healthy aging adults. Researchers followed 114 participants aged 50 to 85 over 48 weeks in a randomized, double-blind, placebo-controlled design. Participants received either a placebo or 5 mg or 10 mg of compounded rapamycin once per week. The study’s primary goal was to measure changes in visceral fat, while secondary outcomes included lean muscle mass, blood markers, and quality-of-life assessments.The trial found that low-dose rapamycin was safe and well-tolerated, with serious side effects reported at similar rates across all groups. The most frequent minor issue among rapamycin users was mild gastrointestinal discomfort. While no significant reductions in visceral fat were observed, women taking 10 mg of rapamycin showed significant gains in lean muscle and reported reduced pain. In addition, participants taking 5 mg weekly reported improvements in emotional well-being and general health, as measured by validated surveys.“Our findings provide evidence that these rapamycin regimens are well tolerated with minimal adverse effects when administered for at least one year within normative aging individuals.”Researchers noted some limitations, including the relatively small and health-conscious participant group, which may have limited the ability to detect larger effects. The compounded form of rapamycin used also had lower absorption than commercial versions, possibly reducing its impact.Overall, the PEARL trial provides early clinical evidence that low-dose rapamycin may help support physical and emotional well-being in older adults. Further studies with larger and more diverse populations will be essential to confirm the study results and refine dosing strategies for broader application.DOI: https://doi.org/10.18632/aging.206235Corresponding author: Stefanie L. Morgan – stefanie@agelessrx.comSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords: rapamycin, aging, healthspan, longevity, geroscienceTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — May 6, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 4, on April 2, 2025, titled “Fisetin ameliorates vascular smooth muscle cell calcification via DUSP1-dependent p38 MAPK inhibition.”In this study, researchers at Johannes Kepler University Linz found that fisetin, a natural substance found in fruits and vegetables, helps protect blood vessels from hardening, which is a common problem in older adults and people with kidney disease. This discovery highlights fisetin’s potential to prevent vascular calcification and reduce cardiovascular damage caused by aging and chronic kidney disease.The research, led by first author Mehdi Razazian and corresponding author Ioana Alesutan, focused on vascular calcification—a condition in which blood vessels stiffen due to calcium deposits. This process is common in aging and chronic kidney disease and increases the risk of heart attacks and strokes. Using human and mouse study models, the researchers tested fisetin’s ability to prevent this calcification in vascular smooth muscle cells (VSMC), which play a key role in maintaining vessel health. Fisetin, known for its anti-inflammatory and antioxidant properties, significantly reduced calcium buildup and calcification markers under stress conditions that mimic disease.The team also discovered that fisetin suppresses activity in a signaling pathway called p38 MAPK, which is known to promote calcification. This effect depends on a protein called DUSP1. When DUSP1 was blocked, fisetin could no longer protect the cells, showing that this protein is essential for its anti-calcification activity. The researchers confirmed fisetin’s protective effects in isolated mouse arteries and in living mice treated with high doses of vitamin D, which typically increases arterial calcification.“Mechanistically, fisetin requires the phosphatase DUSP1 to inhibit p38 MAPK in order to mediate its protective effect on VSMC calcification.”Importantly, the researchers tested fisetin under conditions similar to human disease. When VSMCs were exposed to blood serum from kidney dialysis patients—a condition known to trigger vascular calcification—fisetin again reduced calcium buildup and protected the cells. These findings suggest fisetin could be useful in countering the harmful vascular effects seen in chronic kidney disease.This study adds to growing evidence that fisetin may protect blood vessels from aging-related damage. While more research is needed before it can be used in clinical treatments, the study highlights fisetin as a promising candidate for slowing or preventing vascular calcification. The findings could have broad implications for aging populations and individuals with kidney disease, who are at greater risk for heart problems due to vascular stiffening.Read the full paper: DOI: https://doi.org/10.18632/aging.206233Corresponding author: Ioana Alesutan – ioana.alesutan@jku.atKeywords: aging, vascular calcification, vascular smooth muscle cells, fisetin, dual-specificity phosphatase 1, p38 MAPK______To learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY – May 5, 2025 – Aging (Aging-US), #published by Impact Journals, is pleased to #announce its participation at the upcoming Society for Scholarly Publishing (SSP) 47th Annual Meeting. The #event will take place from May 28-30, 2025, in Baltimore, Maryland.Attendees are invited to visit Booth No. 209 to meet members of the Aging (Aging-US) team. The 2025 meeting theme, “Reimagining the Future of Scholarly Publishing at the Intersection of Value and Values,” underscores the urgency of adapting to rapid technological change, including AI, and addressing growing concerns around research integrity and trust. These priorities align closely with our mission to foster open, reliable, and impactful scientific communication in the field of aging and age-related diseases.In addition, the Longevity & Aging Series - hosted by Dr. Evgeniy Galimov and presented by Aging (Aging-US) - is a Finalist for a Society for Scholarly Publishing (SSP) 2025 EPIC Award in the Video/Film category. Winners will be announced at the EPIC Awards Celebration on May 29.We look forward to connecting with SSP 2025 attendees to share more about Aging (Aging-US) and our publishing initiatives.To learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Aging (Aging-US) invites #submissions for a Special Collection dedicated to the theme of cellular #senescence, spanning its basic mechanisms, physiological and pathological functions, and clinical applications.This collection is published in memory of Professor Judith Campisi, a pioneering force in the field of cellular senescence whose groundbreaking work shaped the understanding of senescence in aging, cancer, and tissue homeostasis. Her legacy continues to inspire generations of scientists working to decode the complex biology of senescent cells and their impact on health and disease.We welcome original research articles, reviews, and perspectives on topics including:-Fundamental mechanisms of senescence induction and maintenance-Regulation and context-specific roles of the senescence-associated secretory phenotype (SASP)-Beneficial and detrimental effects of senescent cells in vivo-Senescence in development, aging, regeneration, and age-related diseases-Biomarkers, imaging, and tools for senescence detection and quantification-Therapeutic targeting of senescent cells: senolytics, senomorphics, and clinical translationThis Special Collection is guest edited by Han Li and Irina Conboy, both internationally recognized leaders in the study of senescence and aging.Submission Details:-Submission Deadline: January 15, 2026-Manuscript Format: Please follow the journal’s submission guidelines-Peer Review: All submissions will undergo a rigorous peer-review process-Submission Link: https://aging.msubmit.net/cgi-bin/main.plex
BUFFALO, NY — May 1, 2025 — A new #research paper was #published in Aging (Aging-US) on April 2, 2025, as the #cover of Volume 17, Issue 4, titled “Decreased mitochondrial NAD+ in WRN deficient cells links to dysfunctional proliferation.”In this study, the team led by first author Sofie Lautrup and corresponding author Evandro F. Fang, from the University of Oslo and Akershus University Hospital in Norway, discovered that cells from people with Werner syndrome (WS)—a rare genetic disorder that causes premature aging—have low levels of a molecule called NAD+ in their mitochondria. This molecule is essential for energy production, cellular metabolism, and maintaining cell health. The researchers also found a potential way to improve cell function in WS patients, pointing to new directions for treating age-related decline and other premature aging disorders.Werner syndrome leads to signs of aging much earlier than normal, including problems such as cataracts, hair loss, and atherosclerosis by age 20 to 30. The team found that when the WRN gene is missing or damaged, cells cannot maintain healthy NAD+ levels in their mitochondria. As a result, the cells age more quickly and stop growing properly. When the researchers boosted NAD+ levels using nicotinamide riboside (a vitamin B3 compound) the affected stem cells and skin cells from patients showed less aging and improved mitochondrial activity.“Interestingly, only 24 h treatment with 1 mM nicotinamide riboside (NR), an NAD+ precursor, rescued multiple pathways in the WRN−/− cells, including increased expression of genes driving mitochondrial and metabolism-related pathways, as well as proliferation-related pathways.”The study also found that the WRN gene helps regulate other important genes that control how NAD+ is made in the body. Without WRN, this system becomes unbalanced, which affects how cells function, grow, and respond to stress. Although adding more NAD+ helped some cells look healthier, it could not completely fix the growth problems in other types of lab-grown cells. This suggests that while NAD+ supplementation is beneficial, it cannot fully replace the essential functions of the WRN gene.These findings offer new insights into the biological mechanisms of aging and reinforce the therapeutic potential of targeting NAD+ metabolism in age-related and genetic diseases. Future studies will aim to better understand how subcellular NAD+ regulation interacts with mutations like those seen in WS. Finally, this research supports ongoing efforts to develop NAD+-based treatments that could slow cellular aging and improve quality of life for patients with premature aging conditions.DOI - https://doi.org/10.18632/aging.206236Corresponding author - Evandro F. Fang - e.f.fang@medisin.uio.noVideo short - https://www.youtube.com/watch?v=WpRpi8TYPfUSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206236Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, Werner syndrome, premature aging, NAD+, mitochondria, proliferationTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Bluesky - https://bsky.app/profile/aging-us.bsky.socialPinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — April 29, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 3, on March 20, 2025, titled “Inhibition of the metalloprotease ADAM19 as a novel senomorphic strategy to ameliorate gut permeability and senescence markers by modulating senescence-associated secretory phenotype (SASP).”Researchers, led by first author Sudipta Bar and corresponding authors Amit Sharma and Pankaj Kapahi from the Buck Institute for Research on Aging, have found that the enzyme ADAM19 plays an important role in regulating aging in cells and inflammation in the gut. Their study shows that blocking ADAM19 reduced gut damage and inflammation in fruit flies, mice, and human cells. This discovery points to a new possible way to treat gut disorders related to aging by reducing the harmful signals from senescent (aging) cells.As individuals age, DNA damage can lead to the accumulation of senescent cells, contributing to tissue damage. These are cells that stop dividing and release harmful inflammatory substances called the senescence-associated secretory phenotype (SASP). In this study, researchers used fruit flies to search for genes involved in radiation-related gut damage. They identified a gene called meltrin, which is similar to human ADAM19. When meltrin was turned off, the flies had less gut leakage, less inflammation, and fewer signs of cellular aging.“Through an unbiased genome-wide association study (GWAS) utilizing 156 strains from the Drosophila Genetic Reference Panel (DGRP), we identified meltrin (the drosophila orthologue of mammalian ADAM19) as a potential modulator of the senescence-associated secretory phenotype (SASP).”To test if these results applied beyond flies, the team inhibited ADAM19 in mice using a drug called batimastat. Mice treated with the drug after chemotherapy exposure had stronger gut barriers and lower levels of inflammatory markers. The findings extended to human cell cultures, where ADAM19 inhibition reduced signs of cellular aging, including the expression of SASP proteins and β-galactosidase, a classic aging marker. Importantly, this approach does not kill aging cells like many 'senolytic' therapies but instead reduces the harmful substances they release, making it a potential "senomorphic" strategy. The study also showed that ADAM19 helps release certain SASP proteins by cutting them at the cell surface, suggesting a direct role in regulating inflammatory signals.Through proteomic analysis, the team identified 12 SASP proteins that were significantly reduced when ADAM19 was blocked. Many of these proteins are linked to inflammation, immune response, and tissue remodeling in diseases such as inflammatory bowel disease and Crohn’s disease. This connection underlines the relevance of the findings for treating chronic gut disorders in aging populations.By targeting ADAM19, researchers may have found a new way to protect gut health and lower inflammation caused by aging cells. This study offers a promising path for creating treatments that maintain healthy tissues without having to destroy aging cells, which could benefit people with gut damage related to aging or medical treatments.DOI - https://doi.org/10.18632/aging.206224Corresponding authors - Amit Sharma - amit.sharma@sens.org, and Pankaj Kapahi - pkapahi@buckinstitute.orgVideo short - https://www.youtube.com/watch?v=dRfxQ20O2fQSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsTo learn more about the journal, please visit our website at https://www.Aging-US.com.MEDIA@IMPACTJOURNALS.COM
In this #episode of the Longevity & Aging Series, Dr. Stephen Vatner from the Department of Cell Biology and Molecular Medicine at Rutgers New Jersey Medical School, joins host Dr. Evgeniy Galimov to discuss a #research perspective he co-authored in Volume 16, Issue 22 of Aging (Aging-US), titled “Brown adipose tissue enhances exercise performance and healthful longevity.”DOI - https://doi.org/10.18632/aging.206179Corresponding author - Stephen F. Vatner - vatnersf@njms.rutgers.eduAuthor interview - https://www.youtube.com/watch?v=-DE4H2DtSZgVideo short - https://www.youtube.com/watch?v=n1DvuR7owJQSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206179Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, brown adipose tissue, white adipose tissue, healthful longevity, exercise, regulator of G protein signaling 14To learn more about Aging (Aging-US), please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Bluesky - https://bsky.app/profile/aging-us.bsky.socialSpotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Aging (Aging-US) was proud to sponsor the Muscle Aging Science & Translation (MAST) Symposium, organized by the Aging Initiative at Harvard University on Friday, April 18, 2025. This important event brought together 350 participants—chosen from more than 1,300 applicants—including students, researchers, company founders, investors, and industry leaders. Together, they explored the latest research and innovations in muscle health and aging. The symposium reflected the journal’s strong commitment to supporting collaboration across fields and advancing research in aging.-Key Highlights from the MAST Symposium- Clinical Research Perspectives on Frailty The symposium opened with a strong clinical session led by experts from top institutions: Dr. Roger Fielding (Tufts University and Boston Claude D. Pepper Older Americans Independence Center) and Drs. Douglas Kiel, Shivani Sahni, and Yi-Hsiang Hsu (Harvard Medical School and Beth Israel Deaconess Medical Center).The panel discussed key topics such as the biology of frailty, how bone and muscle health are connected, and the influence of genetics, diet, and exercise on staying strong as we age. By blending real-life patient care with the latest research, the speakers shed light on the challenges of sarcopenia—the gradual loss of muscle strength and mass that occurs with age—and the new scientific approaches being developed to improve treatment.Full recap - https://aging-us.org/2025/04/agings-ongoing-support-for-scientific-innovation-sponsoring-the-muscle-aging-science-translation-symposium/Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — April 23, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 3, on March 18, 2025, titled “Epigenetic and accelerated age in captive olive baboons (Papio anubis), and relationships with walking speed and fine motor performance.”In this study, led by Sarah J. Neal from The University of Texas MD Anderson Cancer Center, researchers examined how the epigenetic age of baboons—a measure of biological aging based on DNA methylation—compared to their actual age (chronological age) and whether it related to signs of aging like slower walking or reduced hand coordination. While many baboons showed a mismatch between their epigenetic and chronological ages, these differences did not consistently align with physical performance measures.Researchers analyzed blood samples from 140 captive olive baboons (Papio anubis) to determine whether these primates, like humans, show signs of “age acceleration”—a condition where epigenetic age surpasses chronological age. The results revealed that about a quarter of the baboons exhibited accelerated aging, while another quarter showed signs of slower aging, known as “age deceleration.” “We found that epigenetic age was strongly correlated with chronological age, and that approximately 27% of the sample showed age acceleration and 28% showed age deceleration."The scientists then investigated whether these differences were reflected in physical indicators such as walking speed or fine motor skills. To do this, researchers measured walking speed by tracking how quickly baboons moved between points in their enclosures and assessed fine motor skills using a simple task that involved picking up small objects.Older baboons did tend to walk more slowly and perform worse on tasks requiring dexterity, patterns also seen in aging humans. However, these changes were more closely related to chronological age than epigenetic age. Two different methods were used to measure the gap between epigenetic and chronological age. Each method produced slightly different outcomes, highlighting the complexity of defining age acceleration. In one analysis, the oldest baboons appeared to age more slowly epigenetically, possibly reflecting selective survival, where only the healthiest individuals live into old age.This research is among the first to classify baboons based on their epigenetic aging rate and investigate how this links to real-world signs of aging. Although the findings did not provide clear evidence that epigenetic age acceleration leads to physical decline, they point to the importance of DNA methylation as a biomarker in aging research. Because baboons share many biological similarities with humans, these findings help refine how researchers measure aging and assess potential early warning signs of decline. Continued studies in baboons and other primates may improve our understanding of how epigenetic aging influences health and longevity—and could help develop better tools for predicting age-related decline in humans.DOI - https://doi.org/10.18632/aging.206223Corresponding author - Sarah Neal - SJNeal@MDAnderson.orgVideo short - https://www.youtube.com/watch?v=EFfRMFbAMqkSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206223Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — April 21, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 3, on March 14, 2025, titled “Effects of a natural ingredients-based intervention targeting the hallmarks of aging on epigenetic clocks, physical function, and body composition: a single-arm clinical trial.”A team of researchers, led by first authors Natalia Carreras-Gallo and Rita Dargham, and corresponding author Varun B. Dwaraka from TruDiagnostic, studied how a natural anti-aging supplement called the Cel System might influence the aging process. They found that participants who took the supplement for one year showed a reduction in biological age, along with improved muscle strength and body composition. The study highlights the potential of lifestyle and nutritional supplements to support healthy aging.“The Cel System supplement range was formulated to target pathways associated with the Hallmarks of Aging when combining Cel1, Cel2, and Cel3 formulas.”Cel System is a natural supplement made from a mix of plant compounds, vitamins, and antioxidants designed to target the biological mechanisms associated with aging. Over the course of a year, 51 adults between the ages of 54 and 84 participated in the clinical trial. The group included 26 men and 25 women. Researchers tracked changes in biological age using DNA-based tests known as epigenetic clocks, along with physical performance and body composition metrics. Participants were also encouraged to walk for 10 minutes and practice mindfulness for five minutes daily.Results showed that participants experienced improvements in grip strength, lower body mobility, and reductions in body weight, waist circumference, and body mass index. These physical gains were supported by slower biological aging, as measured by multiple epigenetic clocks. In addition, the supplement appeared to reduce stem cell turnover, a key marker of aging at the cellular level.The study also reported changes in immune cell composition, suggesting that the supplement may help regulate immune function as people age. Biomarkers associated with liver function also shifted, pointing to potential improvements in organ health. However, levels of inflammation markers did not significantly change.Analysis of methylation chemical marks on DNA revealed that the supplement influenced gene activity related to stress response, brain function, and cell communication. These molecular-level changes may help explain the broader benefits seen in physical and biological aging measures.Although this was a pilot study without a control group, the findings suggest that the Cel System supplement shows potential for reducing signs of aging and improving overall health. The authors suggest future randomized controlled trials with larger sample sizes to confirm these results and explore the supplement’s long-term effects on longevity.This study adds to growing evidence that targeted natural supplements may slow biological aging and extend healthspan. By combining epigenetic analysis with real-world health data, the findings offer new insight into how nutraceuticals, like Cel System, could promote long-term health and resilience.Paper: DOI: https://doi.org/10.18632/aging.206221Corresponding author: Varun B. Dwaraka – varun.dwaraka@trudiagnostic.comKeywords: aging, epigenetic age change, physiological age change, epigenetic biomarker proxies, hallmarks of aging, nutraceutical longevity interventionsTo learn more about the journal, please visit our website at www.Aging-US.com and connect with us on social media at:Facebook - www.facebook.com/AgingUS/X - twitter.com/AgingJrnlInstagram - www.instagram.com/agingjrnl/YouTube - www.youtube.com/@AgingJournalLinkedIn - www.linkedin.com/company/aging/Pinterest - www.pinterest.com/AgingUS/Spotify - open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — April 16, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 3, on March 12, 2025, titled “DNA methylation entropy is a biomarker for aging.”Researchers Jonathan Chan, Liudmilla Rubbi, and Matteo Pellegrini from the University of California, Los Angeles, led a study that discovered a new way to measure changes in DNA that can help predict a person’s age. This method focuses on how random certain chemical tags on DNA become over time. The team compared this new measurement, called methylation entropy, to existing methods and found it performed just as well—or even better. These findings support the idea that changes in our epigenetic information are closely linked to aging and could offer new tools for studying age-related diseases.The study focused on DNA methylation, a process where chemical marks are added to DNA and help control which genes are turned on or off. Scientists have traditionally measured average methylation levels to estimate biological age using “epigenetic clocks.” This study, however, takes a different approach. The researchers used buccal swabs (cells from inside the cheek) from 100 individuals between ages 7 and 84 and applied targeted bisulfite sequencing techniques to measure methylation entropy across 3,000 regions of the genome.Entropy in this context reflects how disordered or varied the methylation patterns are at certain sites on the DNA. The researchers discovered that as people age, the entropy of methylation at many locations changes in a reproducible way. Sometimes it increases, reflecting more random patterns, and sometimes it decreases, showing more uniformity. These shifts are not always tied to how much methylation is happening, which suggests entropy provides new information beyond what traditional methods can offer.To test how well this new metric could predict age, the team used both statistical and machine learning models. They found that methylation entropy predicted age as accurately as traditional methods, and the best results came from combining entropy with other measurements like average methylation and a method called CHALM. These combined models were able to estimate age with an average error of just five years."[...] methylation entropy is measuring different properties of a locus compared to mean methylation and CHALM, and that loci can become both more or less disordered with age, independently of whether the methylation is increasing or decreasing with age."This research supports the growing theory that aging is partly caused by a gradual loss of epigenetic information—the biological “instructions” that help keep our cells working properly. This insight also connects with recent studies suggesting that restoring this lost information might reverse some signs of aging. While more research is needed to study methylation entropy in other tissues, this work points to a more precise and powerful way to measure biological aging, which could influence the future of aging-related treatments and therapies.Read the full paper: DOI: https://doi.org/10.18632/aging.206220Corresponding author: Matteo Pellegrini - matteope@gmail.comSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206220Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords: entropy, DNA methylation, aging, epigenetics, epigenetic clocksTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Breast cancer survivors are living longer than ever, thanks to research and medical advances, but new studies suggest that some treatments may come with a hidden cost: accelerated aging. A recent study, titled “Accelerated aging associated with cancer characteristics and treatments among breast cancer survivors,” published in Aging (Aging-US), reveals that breast cancer and its treatments may speed up biological aging, with effects lasting up to a decade post-diagnosis.Breast Cancer and AgingBreast cancer is one of the most common cancers among women worldwide. Medical advancements have dramatically improved survival rates, making it one of the most treatable forms of cancer. Yet, many survivors report lasting symptoms like fatigue, memory issues, and reduced vitality that resemble accelerated aging. This pattern has led scientists to investigate whether treatments for breast cancer might be contributing to biological age acceleration.Full blog - https://aging-us.org/2025/04/breast-cancer-treatments-hidden-impact-accelerated-aging-among-survivors/Paper DOI - https://doi.org/10.18632/aging.206218Corresponding author - Xiao-Ou Shu - xiao-ou.shu@vumc.orgVideo short - https://www.youtube.com/watch?v=cfuyzVyDeHYSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206218Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, accelerated aging, PhenoAge, breast cancer, survivorsVisit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — April 14, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 3, on March 4, 2025, titled “Deciphering age-related transcriptomic changes in the mouse retinal pigment epithelium.”The study, led by first authors Sushil K. Dubey and Rashmi Dubey with corresponding author Mark E. Kleinman from East Tennessee State University, reveals that aging causes inflammation, oxidative stress, and gene disruption in the retinal pigment epithelium (RPE), a vital layer of cells in the eye. These changes may explain why older adults are more vulnerable to age-related eye diseases. The researchers also developed a human cell model to study retinal aging and test future therapies.The RPE plays a key role in maintaining retinal health. It recycles light-sensitive molecules, supports the visual cycle, and protects the retina from damage. When this layer becomes damaged, vision problems such as age-related macular degeneration can develop.In this study, researchers compared gene activity in RPE cells from young and aged mice. They found that aging increased the activity of genes involved in immune system responses, inflammation, and oxidative stress, three known triggers of tissue damage. At the same time, genes related to vision and light detection became less active, weakening the RPE’s ability to support healthy vision.To reinforce these findings, the research team also aged human RPE cells in the lab. Over time, these cells showed the same patterns: inflammation increased, while genes tied to visual function decreased. This human cell model offers a practical way to explore how RPE degeneration happens over time and how it might be slowed down or reversed.The research also identified “hub genes,” which are central players of the gene networks involved in RPE aging. These are connected to immune signaling, oxidative damage, and changes in the eye’s structural support. Many of these genes are already known to be involved in age-related retinal degeneration, so they may become important targets for future treatments aimed at protecting vision in older adults.“GO annotation of downregulated genes included processes related to visual perception, sensory perception of light stimulus, detection of light stimulus, detection of visible light, detection of external stimulus, detection of abiotic stimulus, phototransduction, cellular response to interferon-beta, response to interferon-beta, and response to light stimulus.”By mapping how the RPE changes with age at the molecular level, this study provides a clearer understanding of why aging leads to eye disease. It also introduces a reliable laboratory model that researchers can use to test new therapies. Altogether, the work is a key step toward developing treatments to slow or prevent vision loss tied to retinal aging.Read the full paper: DOI: https://doi.org/10.18632/aging.206219Corresponding author: Mark E. Kleinman- kleinman@etsu.edu Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords: aging, transcriptome, retinal pigment epithelium, oxidative stress, inflammation, chronological agingTo learn more about the journal, please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
Paula Cilleros-Holgado from Pablo de Olavide University discusses a #research paper she co-authored that was #published in Volume 17, Issue 2 of Aging (Aging-US), entitled “Mitochondrial dysfunction, iron accumulation, lipid peroxidation, and inflammasome activation in cellular models derived from patients with multiple sclerosis.”DOI - https://doi.org/10.18632/aging.206198Corresponding author - José Antonio Sánchez-Alcázar - jasanalc@upo.esVideo interview - https://www.youtube.com/watch?v=wIV0lAHPA_MAbstractMultiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS). Despite advancements in managing relapsing active illness, effective treatments for the irreversible progressive decline in MS remain limited.Research employing skin fibroblasts obtained from patients with neurological disorders revealed modifications in cellular stress pathways and bioenergetics. However, research using MS patient-derived cellular models is scarce.In this study, we collected fibroblasts from two MS patients to investigate cellular pathological alterations. We observed that MS fibroblasts showed a senescent morphology associated with iron/lipofuscin accumulation and altered expression of iron metabolism proteins. In addition, we found increased lipid peroxidation and downregulation of antioxidant enzymes expression levels in MS fibroblasts. When challenged against erastin, a ferroptosis inducer, MS fibroblasts showed decreased viability, suggesting increased sensitivity to ferroptosis. Furthermore, MS fibroblasts presented alterations in the expression levels of autophagy-related proteins. Interestingly, these alterations were associated with mitochondrial dysfunction and inflammasome activation. These findings were validated in 7 additional patient-derived cell lines.Our findings suggest that the underlying stress phenotype of MS fibroblasts may be disease-specific and recapitulate the main cellular pathological alterations found in the disease such as mitochondrial dysfunction, iron accumulation, lipid peroxidation, inflammasome activation, and pro-inflammatory cytokine production.Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206198Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, multiple sclerosis, iron accumulation, lipid peroxidation, inflammasome, mitochondrial dysfunctionTo learn more about Aging (Aging-US), please visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — April 9, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 3, on March 5, 2025, titled “Reproductive aging, preimplantation genetic testing for aneuploidy, and the diameter of blastocysts: does size matter?”In this study, a team led by first author Jakub Wyroba from the Malopolski Institute of Fertility Diagnostics and Treatment and Andrzej Frycz Modrzewski Krakow University, and corresponding author Pawel Kordowitzki from Harvard Medical School, Nicolaus Copernicus University, and Charité, found that the size of an embryo and whether it has started hatching can help predict its genetic health. This insight could help fertility clinics select better embryos during in vitro fertilization (IVF), especially in countries or situations where advanced genetic testing is not available.As more women are choosing to have children later in life, fertility challenges related to age are becoming more common. Older maternal age is linked with a higher risk of chromosomal problems in embryos, which can reduce the success of IVF. To identify healthy embryos, many clinics use a test called preimplantation genetic testing for aneuploidy (PGT-A). However, PGT-A is expensive and not available in all countries. This study explored whether embryo quality could be predicted using physical features alone.During IVF, embryos develop in the lab for several days before being transferred into the uterus. Around day five or six, the embryo reaches a stage called the blastocyst. At this point, it begins to break out of its outer shell, called the zona pellucida. This process is called hatching, and it is an important step before the embryo can attach to the uterus and begin a pregnancy.The researchers examined 1150 embryos from women aged 26 to 45 who underwent IVF. They looked at whether the embryos were already starting to hatch and how big they were. They then compared these features with results from genetic tests. They found that smaller embryos that were already hatching were more likely to be chromosomally normal, also called “euploid.”“Of the 1150 blastocysts that underwent PGT-A analysis in this study, 49% were aneuploid.”For women over 35, 51% of small hatching embryos were euploid, compared to just 38% of larger ones that had not started to hatch. Among younger women under 35, the difference was even greater—73% of small hatching embryos were euploid, compared to 58% of large, unhatched ones.The research team also looked at what happened after the embryos were transferred. When embryos were already known to be euploid, both large and small embryos led to similar pregnancy rates. This means the size and hatching behavior mostly matter when genetic testing is not done.This study offers new guidance for IVF clinics. Choosing a small hatching embryo may improve the chances of success, especially for women of advanced age and in clinics that do not use PGT-A. This finding could help make fertility treatment more accessible and affordable. As fertility science continues to advance, insights like this provide practical tools to improve outcomes and bring new hope to individuals and families trying to conceive through IVF.DOI: https://doi.org/10.18632/aging.206215Corresponding author: Pawel Kordowitzki- p.kordowitzki@umk.plVideo short - https://www.youtube.com/watch?v=0JJIOqWadE4Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsPlease visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — April 7, 2025 — A new #research paper was #published in Aging (Aging-US) on March 18, 2025, in Volume 17, Issue 3, titled “Mitochondrial oxidative stress or decreased autophagy in osteoblast lineage cells is not sufficient to mimic the deleterious effects of aging on bone mechanoresponsiveness.”Researchers from the University of Arkansas for Medical Sciences, led by first author Ana Resende-Coelho and corresponding authors Melda Onal and Maria Almeida, investigated why bones become less responsive to exercise as people age. They studied two well-known aging-related cellular changes: oxidative stress (a buildup of harmful molecules inside cells) and reduced autophagy (a slowdown in the cell’s ability to clean out and recycle damaged parts) to determine whether these could explain the decline in bone strength. Their findings revealed that these changes alone are not enough to account for the reduced bone-building response seen with aging.Physical activity is known to strengthen bones by creating mechanical stress, which activates bone cells like osteocytes to promote new bone formation. However, this process becomes less effective with age, increasing the risk of bone loss and fractures in older adults. The study aimed to uncover why this response weakens over time by focusing on specific age-related changes inside bone-forming cells.“The bone response to loading is less effective with aging, but the cellular and molecular mechanisms responsible for the impaired mechanoresponsiveness remain unclear.”The research team used a well-established mouse model in which pressure was applied to the tibia, simulating the effects of exercise. As expected, bones from older mice showed a weaker response compared to those of younger mice. However, when the researchers examined younger mice genetically modified to have either high oxidative stress or impaired autophagy, as seen in aging, their bones still responded normally to mechanical loading.The researchers also found that damage to the bone’s osteocyte network, a system of cells that helps sense and respond to mechanical forces, did not prevent a healthy bone-building response in mice with autophagy deficiencies. This challenges the long-standing idea that deterioration of this cell network is a main cause of age-related bone decline.These results are significant because they eliminate two widely suspected causes of the aging skeleton’s reduced responsiveness to exercise. While oxidative stress and autophagy dysfunction are common in older bone, they are not solely responsible for its reduced ability to grow stronger under physical stress. The authors suggest that future studies should explore other possible factors, such as changes in energy metabolism or how bone cells communicate.Overall, this study shows that bone aging is more complex than previously thought. Protecting bone health in older adults may require new strategies that go beyond targeting oxidative stress or autophagy.DOI - https://doi.org/10.18632/aging.206213Corresponding authors - Melda Onal - MOnal@uams.edu, and Maria Almeida - schullermaria@uams.eduVideo short - https://www.youtube.com/watch?v=fHQhA6rOaDcSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206213Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, Atg7, tibia compressive loading, Sod2, Osx1-Cre, osteocytesPlease visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — April 3, 2025 — Aging (Aging-US) is pleased to announce a special Call for Papers for a commemorative collection honoring the legacy of Dr. Mikhail (Misha) Blagosklonny, the founding editor of the journal and a pioneer in aging biology. His groundbreaking work shaped fundamental concepts in the field, particularly regarding the role of mTOR in aging and cancer, the use of rapamycin, bypassing senescence during the process of transformation, personalized medicine, and theories on why we age.This special collection will explore key themes central to Dr. Blagosklonny’s scientific contributions, with a focus on mechanistic insights, translational approaches, and theoretical perspectives. We invite original research, reviews, and perspective articles covering topics such as:The role of mTOR in aging and age-related diseasesRapamycin and other pharmacological strategies to extend lifespanSenescence bypass and its implications for cancer and regenerative medicinePersonalized medicine approaches in aging and longevity researchTheoretical models and evolutionary perspectives on agingThe special issue will be guest-edited by leading scientist in the field, David Gems, who will oversee the selection of high-quality contributions that reflect the depth and impact of Dr. Blagosklonny’s work.We encourage researchers working on these topics to submit their manuscripts and contribute to this tribute to one of the most influential figures in aging research.SUBMISSION DETAILS:Submission Deadline: December 1, 2025Manuscript Format: Please follow the journal’s submission guidelinesPeer Review: All submissions will undergo a rigorous peer-review processSubmission Link: https://aging.msubmit.net/cgi-bin/main.plexWe look forward to your contributions to this special issue and to honoring Dr. Blagosklonny’s enduring impact on the field of aging research.To learn more about Aging (Aging-US), please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Could a class of drugs that clear aging cells also help treat Alzheimer’s disease? A recent study, featured as the cover for Aging (Volume 17, Issue 3), titled “Differential senolytic inhibition of normal versus Aβ-associated cholinesterases: implications in aging and Alzheimer’s disease,” suggests they might—and with remarkable precision.Understanding Alzheimer’s DiseaseAlzheimer’s disease is a progressive neurological disorder that gradually steals memory, independence, and a person’s sense of identity. A defining feature of Alzheimer’s is the buildup of amyloid-β (Aβ) plaques—sticky protein clumps that interfere with communication between brain cells. This disruption is closely linked to changes in a group of enzymes called cholinesterases, especially acetylcholinesterase (AChE) and butyrylcholinesterase (BChE). These enzymes normally play a vital role in regulating neurotransmitters critical for memory, learning, and cognitive function. In Alzheimer’s, however, their behavior changes significantly, particularly when they interact with Aβ plaques.The Study: Exploring Senolytics for Alzheimer’s Enzyme InhibitionA research team from Dalhousie University in Canada looked into whether senolytic compounds—a class of drugs that eliminate damaged, aging cells often referred to as “zombie” cells—could also target the harmful forms of cholinesterase enzymes found in Alzheimer’s disease. Their goal was to see if these compounds could selectively inhibit the disease-associated versions of AChE and BChE, without affecting the healthy forms that are essential for normal brain function.Full blog - https://aging-us.org/2025/04/senolytic-compounds-show-promise-in-targeted-alzheimers-treatments/DOI - https://doi.org/10.18632/aging.206227Corresponding author - Sultan Darvesh - sultan.darvesh@dal.caVideo short - https://www.youtube.com/watch?v=CJQFpG9Jn6YSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206227Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, cellular senescence, β-amyloid, acetylcholinesterase, butyrylcholinesterase, cholinesterase inhibitorsAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — April 1, 2025 — A new #research paper was #published in Aging (Aging-US) on March 29, 2025, as the #cover of Volume 17, Issue 3, titled “Differential senolytic inhibition of normal versus Aβ-associated cholinesterases: implications in aging and Alzheimer’s disease.”In this study, a research team from Dalhousie University, led by Sultan Darvesh, discovered that certain anti-aging compounds, known as senolytics, can block harmful brain enzymes linked to Alzheimer’s disease (AD) without affecting healthy ones. Senolytics are compounds that help clear out damaged or “zombie” cells that build up with age and contribute to inflammation and tissue dysfunction. This work provides new insight into how AD-related damage can be precisely targeted, leading the way for safer treatments that protect memory and brain health in older adults.Alzheimer’s disease is one of the most common causes of memory loss and dementia. A hallmark of the disease is the buildup of sticky protein clumps in the brain, known as amyloid-beta plaques. Two enzymes—acetylcholinesterase (AChE) and butyrylcholinesterase (BChE)—are found near these plaques. While these enzymes play important roles in brain function, they can also contribute to AD progression when they attach to plaques. Drugs that target these enzymes are already used to help with memory, but they often block both harmful and healthy forms, which can cause unwanted side effects.To investigate a better solution, researchers tested six compounds that are known for their anti-aging or brain-boosting properties. They wanted to know if these compounds could block only the harmful AChE and BChE enzymes forms linked to Alzheimer’s disease. Using brain tissue samples from AD patients and enzyme activity assays, they discovered that compounds such as dasatinib and nintedanib, both senolytics, were able to block the forms of AChE and BChE associated with amyloid-beta plaques. These compounds did not affect normal brain enzymes, though. “We show that the selected senolytics and nootropic inhibit ChEs associated with plaques but not the enzymes associated with normal neural elements.”The study also used computer modeling to explore how these compounds interact with the enzymes. The models showed that the enzymes change shape when near plaques, making them easier for certain compounds to target. This change may explain how the drugs can selectively affect only the diseased areas of the brain.While not all compounds worked equally well, the findings offer a new strategy for treating AD. By focusing on the differences between healthy and diseased enzyme forms, researchers may be able to design more precise and effective therapies. This selective approach could improve memory, reduce inflammation, and avoid the side effects of AD’s current treatments.In summary, this research opens new possibilities for treating Alzheimer’s disease in a more targeted way. It also highlights how discoveries in aging and brain health can work together to create better therapies for neurodegenerative diseases.DOI - https://doi.org/10.18632/aging.206227Corresponding author - Sultan Darvesh - sultan.darvesh@dal.caVideo short - https://www.youtube.com/watch?v=CJQFpG9Jn6YSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206227Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsPlease visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — March 26, 2025 — A new #research paper was #published in Aging (Aging-US) on January 29, 2025, in Volume 17, Issue 2, titled “Diet, lifestyle and telomere length: using Copula Graphical Models on NHANES data.”Researchers Angelo M. Tedaldi, Pariya Behrouzi, and Pol Grootswagers from Wageningen University and Research used data from the National Health and Nutrition Examination Survey (NHANES) to explore how diet and lifestyle affect telomere length, a key marker of cellular aging. They found that inflammation—rather than diet, exercise, or smoking—had the strongest and most consistent association to telomere shortening. The findings suggest that reducing inflammation may be more effective than dietary changes in slowing down the aging process at the cellular level.Telomeres are protective caps at the ends of chromosomes that get shorter as we age. When they become too short, cells lose the ability to divide properly, which can contribute to aging and age-related diseases. Previous studies suggested that healthy habits might protect telomeres, but many focused on a small number of factors and did not account for important elements like inflammation or differences in blood cell composition. This study aimed to take a more complete, data-driven approach.The research team analyzed health data from over 7,000 U.S. adults collected between 1999 and 2002. Using a method called Copula Graphical Modeling, they examined more than 100 variables—such as diet, physical activity, smoking, and blood biomarkers—across three age groups: Young (20–39 years), Middle (40–59 years), and Old (60–84 years). They found that telomere length was most strongly associated to age, levels of C-reactive protein (CRP)—a common marker of inflammation—and gamma-tocopherol, a form of vitamin E found in the blood. Higher CRP levels were consistently associated with shorter telomeres, especially in younger and middle-aged adults.The results suggest that while lifestyle factors like diet and exercise still play a role, their impact on aging may be indirect—mainly through their influence on inflammation. This finding shifts the focus toward managing chronic inflammation as a potentially more effective way to preserve telomere length and promote healthy aging.“The central role played by CRP and the marginal role of antioxidants suggests that telomeres are particularly vulnerable not to oxidative stress, but to inflammation; and they should be protected against it.”The study challenges earlier research that looked at individual lifestyle factors isolated. By using a more advanced and inclusive method, this analysis offers a clearer picture of how health behaviors, biological markers, and aging are connected.Although this research cannot prove a cause-and-effect relationship, it strongly supports the idea that inflammation plays a key role in cellular aging. The authors recommend further long-term studies to better understand how inflammation affects telomere length over time. In the meantime, reducing chronic inflammation may be one of the most important steps to help support healthy aging and reduce the risk of age-related diseases.DOI - https://doi.org/10.18632/aging.206194Corresponding author - Angelo M. Tedaldi - angelomt1999@gmail.comVideo short - https://www.youtube.com/watch?v=C2yXfF7iY6cSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsPlease visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — March 25, 2025 — A new #research paper was #published in Aging (Aging-US) on January 31, 2025, in Volume 17, Issue 2, titled “Cysteinyl leukotriene receptor 1 modulates retinal immune cells, vascularity and proteolytic activity in aged mice.”The study, led by first author and corresponding author Andreas Koller from the University Hospital of the Paracelsus Medical University, found that blocking an inflammatory receptor called CysLTR1 in the retinas of aging mice improved retinal health. These findings suggest a new approach to slowing age-related vision loss and protecting eye health in older adults.Age-related vision problems are a growing concern worldwide, and inflammation plays a key role in damaging the retina over time. The retina is the part of the eye that captures light and sends visual signals to the brain, making it vital for clear eyesight. In this study, scientists focused on the CysLTR1 receptor, which is known to promote inflammation and is found in high amounts in the retina. They explored whether blocking this receptor could reduce the harmful effects of aging in the eye.To achieve this, researchers treated aged mice with montelukast (MTK), a drug commonly used for asthma, which specifically blocks CysLTR1. The oral treatment lasted eight weeks and results were compared with both untreated aged mice and healthy young mice. After treatment, the older mice showed major improvements in retinal health.One key finding was a reduction in immune cells called microglia, which tend to increase with age and contribute to chronic inflammation in the retina. With CysLTR1 blocked, the number of these immune cells dropped significantly, suggesting reduced retinal inflammation. Lower inflammation is linked to a lower risk of age-related eye diseases like macular degeneration.“The reduction in immune cells caused by Cysltr1 suppression may dampen neuroinflammation, a known promoter of tissue aging.”Another important result was the restoration of blood vessel function. The tiny blood vessels in the retina had narrowed in aging mice, reducing blood flow and oxygen supply to the eye. MTK treatment increased the diameter of these vessels, improving circulation and possibly helping the retina work more efficiently.The study also indicated that blocking CysLTR1 helped boost the retina’s natural ability to clear out waste proteins. As we age, this cleaning process slows down, allowing harmful material to build up in the eye. After treatment, the aged mice had stronger proteasome activity—the system responsible for breaking down cellular waste—and fewer signs of waste accumulation.Importantly, the treatment did not harm retinal nerve cells, which are essential for vision. This evidence indicates that the therapy was not only effective but also safe.While more research is needed to confirm these results in humans, this study highlights the potential of repurposing MTK to protect against age-related vision decline. Because it is already an approved drug, testing it for age-related eye diseases like macular degeneration or diabetic retinopathy could move forward more quickly. Blocking inflammation and supporting the eye’s natural cleaning systems may be a promising new way to preserve healthy vision in aging populations.DOI - https://doi.org/10.18632/aging.206193Corresponding author - Andreas Koller - a.koller@salk.atVideo short - https://www.youtube.com/watch?v=ngnrPJzHlpIPlease visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
In this installment of the Longevity & Aging Series, Dr. Julia Sidorova from the Department of Laboratory Medicine and Pathology at the University of Washington (Seattle, WA) joined host Dr. Evgeniy Galimov to discuss her co-authored research paper from Volume 16, Issue 20 of Aging (Aging-US), titled “Werner syndrome RECQ helicase participates in and directs maintenance of the protein complexes of constitutive heterochromatin in proliferating human cells.”DOI - https://doi.org/10.18632/aging.206132Corresponding Author - Julia M. Sidorova - julias@uw.eduVideo interview - https://www.youtube.com/watch?v=3yn8O-JA6GEAbstractWerner syndrome of premature aging is caused by mutations in the WRN RECQ helicase/exonuclease, which functions in DNA replication, repair, transcription, and telomere maintenance. How the loss of WRN accelerates aging is not understood in full. Here we show that WRN is necessary for optimal constitutive heterochromatin levels in proliferating human fibroblasts. Locally, WRN deficiency derepresses SATII pericentromeric satellite repeats but does not reduce replication fork progression on SATII repeats. Globally, WRN loss reduces a subset of protein-protein interactions responsible for the organization of constitutive heterochromatin in the nucleus, namely, the interactions involving Lamin B1 and Lamin B receptor, LBR. Both the mRNA level and subcellular distribution of LBR are affected by WRN deficiency, and unlike the former, the latter phenotype does not require WRN catalytic activities. The phenotypes of heterochromatin disruption seen in WRN-deficient proliferating fibroblasts are also observed in WRN-proficient fibroblasts undergoing replicative or oncogene-induced senescence. WRN interacts with histone deacetylase 2, HDAC2; WRN/HDAC2 association is mediated by heterochromatin protein alpha, HP1α, and WRN complexes with HP1α and HDAC2 are downregulated in senescing cells. The data suggest that the effect of WRN loss on heterochromatin is separable from senescence program, but mimics at least some of the heterochromatin changes associated with it.Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206132Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, Werner progeria, heterochromatin, senescence, nuclear lamina, satellite repeatsAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Could the air we breathe, the food we eat, or the chemicals in our everyday environment be accelerating our aging process? A recent study published in Aging suggests that exposure to certain environmental chemicals may be linked to faster biological aging through changes in DNA. These findings could have major implications for public health and longevity.Understanding How Scientists Measure Aging at the DNA LevelAging is not just about wrinkles and gray hair—it happens at the molecular level too. Scientists use epigenetic clocks to measure biological aging, which can differ from a person’s actual chronological age. These clocks track DNA methylation, a type of chemical modification that can change over time due to environmental factors like diet, pollution, and chemical exposure. Until now, there has been little research into how widespread environmental chemicals impact these aging markers. The Study: Investigating the Impact of Environmental Pollutants on AgingA research team led by first author Dennis Khodasevich and corresponding author Andres Cardenas from Stanford University, conducted an exposome-wide association study to examine how different environmental pollutants affect epigenetic aging. Using data from the National Health and Nutrition Examination Survey (NHANES), they analyzed blood and urine samples from 2,346 adults aged 50 to 84. The study measured 64 environmental chemicals, including heavy metals, pesticides, plastics, and tobacco-related compounds, to identify potential links to accelerated aging. The study titled “Exposome-wide association study of environmental chemical exposures and epigenetic aging in the national health and nutrition examination survey,” was published in Aging on February 11, 2025.Full blog - https://aging-us.org/2025/03/how-environmental-chemicals-may-accelerate-biological-aging/Paper DOI - https://doi.org/10.18632/aging.206201Corresponding author - Andres Cardenas - andresca@stanford.eduVideo short - https://www.youtube.com/watch?v=WcL-K399a7MSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206201Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, epigenetic aging, environmental exposures, exposome, epigeneticsAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — March 19, 2025 — A new #research paper was #published in Aging (Aging-US) on February 27, 2025, in Volume 17, Issue 2, titled “Age, sex, and mitochondrial-haplotype influence gut microbiome composition and metabolites in a genetically diverse rat model.”The research team, led by first author Hoang Van M. Nguyen and corresponding author Archana Unnikrishnan from the University of Oklahoma Health Sciences, studied how aging affects gut bacteria in a special group of rats generated to have genetic diversity similar to humans. Their research found that both biological sex and mitochondrial DNA—the small set of genes inherited only from mothers—play a key role in how gut bacteria change over time.The gut microbiome, a collection of bacteria in the intestines, affects digestion, metabolism, and even brain function. As people age, these bacteria shift, and some of these changes are linked to diseases like Alzheimer’s, Parkinson’s, and metabolic disorders. However, most studies have looked at either men or women without comparing differences between sexes, and few have explored how mitochondrial DNA might influence these changes.To better understand these factors, researchers analyzed fecal samples from the genetically diverse rats to assess gut bacteria composition and metabolic byproducts. The results showed that aging affects gut bacteria differently in males and females. More bacterial species changed with age in female rats than in males, and only a few changes were consistent across both sexes. These findings suggest that men and women may experience aging differently at the microbial level, which could impact nutrition and disease risk.“Five microbial species changed significantly with age in male rats compared to nine microbial species in female rats. Only three of these microbes changed with age in both male and female rats.”Another key discovery was that mitochondrial DNA influences how gut bacteria evolve with age. These effects were different in males and females, suggesting a deeper connection between mitochondrial function and gut health, with potential implications for personalized medicine and aging research.In addition to studying bacteria, the researchers analyzed metabolic compounds such as short-chain fatty acids and bile acids, which help with digestion. They found that aging altered these compounds based on both sex and mitochondrial DNA. For example, older female rats had higher levels of short-chain fatty acids in their feces, possibly due to differences in nutrient absorption.This study highlights new factors that shape the gut microbiome in aging populations. Understanding how biological sex and mitochondrial DNA influence these changes could lead to targeted approaches for maintaining gut health and preventing age-related diseases. These findings reinforce the importance of personalized health strategies that consider both genetic and biological differences.DOI - https://doi.org/10.18632/aging.206211Corresponding author - Archana Unnikrishnan - archana-unnikrishnan@ouhsc.eduVideo short - https://www.youtube.com/watch?v=RtsqRi2_uAISubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — March 18, 2025 — A new #research paper was #published by Aging (Aging-US) on March 7, 2025, titled “Accelerated aging associated with cancer characteristics and treatments among breast cancer survivors.”Led by first author Cong Wang and corresponding author Xiao-Ou Shu from Vanderbilt University, this study examines how breast cancer and its treatments contribute to accelerated aging in survivors. Their study revealed that breast cancer patients show signs of faster biological aging compared to cancer-free individuals, with long-term effects lasting up to ten years post-diagnosis. This finding raises concerns about the potential lasting impact of cancer therapies on aging and overall health.Breast cancer is one of the most common cancers in women worldwide, with improved treatments leading to longer survival rates. However, emerging evidence suggests that these treatments may also accelerate aging. The study used Phenotypic Age Acceleration (PAA), a biological marker that estimates a person’s aging rate based on blood tests. Researchers compared data from 1,264 breast cancer patients and 429 cancer-free controls. The results indicated that breast cancer survivors had significantly higher PAA at diagnosis and continued to show signs of accelerated aging up to ten years later.“This is the first large study with 10 years of follow-up to evaluate PAA among BC survivors.”The study found that tumor severity played a role in aging acceleration. Women with advanced-stage (Stage III/IV) or high-grade tumors showed the highest levels of aging acceleration. Additionally, treatments such as chemotherapy and endocrine therapy were linked to increased biological aging. One year after diagnosis, chemotherapy was associated with the most significant rise in PAA, while endocrine therapy had long-term effects, increasing aging markers even ten years after treatment.Interestingly, not all cancer treatments had the same effect. Surgery and radiation therapy were associated with lower aging acceleration over time. These findings suggest that systemic therapies, which affect the whole body, may contribute more to aging-related changes than localized treatments.The findings highlight the need for ongoing monitoring of breast cancer survivors beyond their initial recovery. Understanding how cancer treatments influence aging can help improve post-treatment care and potentially lead to strategies that reduce these effects. Further research is needed to explore whether lifestyle changes, medications, or other interventions could slow down aging in cancer survivors.As the number of breast cancer survivors continues to grow, addressing the long-term health consequences of cancer treatment is crucial. This study provides valuable insights into how different factors contribute to accelerated aging, helping to shape future research and healthcare approaches for breast cancer survivors.DOI - https://doi.org/10.18632/aging.206218Corresponding author - Xiao-Ou Shu - xiao-ou.shu@vumc.orgVideo short - https://www.youtube.com/watch?v=cfuyzVyDeHYSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — March 17, 2025 — Impact Journals (Aging’s publisher) is pleased to announce its participation as an exhibitor at theAmerican Association for Cancer Research (AACR) Annual Meeting 2025. The meeting is scheduled for April 25-30, 2025, at the McCormick Place Convention Center in Chicago, Illinois.This 2025 AACR Annual Meeting theme, “Unifying Cancer Science and Medicine: A Continuum of Innovation for Impact,” highlights significant advancements and groundbreaking discoveries in cancer research. Aging closely aligns with this mission, dedicated to disseminating impactful scientific research at the intersection of oncology and gerontology.Visit Booth 2815 to meet directly with members of the Aging team, explore the latest research publications, and discuss opportunities for collaboration and manuscript submissions. Aging, supported by its publisher Impact Journals, remains dedicated to promoting innovation, collaboration, and advancing scientific knowledge in aging-related cancer research.About Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — March 10, 2025 — A new #research paper was #published in Aging (Aging-US) on February 18, 2025, Volume 17, Issue 2, titled “Transcriptomic landscape of cumulus cells from patients <38 years old with a history of poor ovarian response (POR) treated with platelet-rich plasma (PRP).”Researchers from IVIRMA New Jersey, Yale School of Medicine, Yale University, and Acibadem Mehmet Ali Aydinlar University studied how a treatment called platelet-rich plasma (PRP) might help women with poor ovarian response. Their results suggest that PRP may enhance ovarian rejuvenation and improve egg quality, potentially increasing pregnancy success rates for women undergoing in vitro fertilization (IVF).Diminished ovarian reserve is a major challenge in fertility treatments, affecting many women undergoing IVF. It is associated with fewer collected eggs and lower pregnancy success rates. Some studies have explored PRP—a concentration of growth factors derived from a patient’s own blood—as a potential treatment to rejuvenate ovarian function. However, the biological effects of PRP treatment at the molecular level remain unclear.In this study, the research team, led by first author Leah M. Roberts and corresponding author Emre Seli, analyzed cumulus cells, specialized cells that surround the egg, using RNA sequencing technology. Samples were collected from women aged 18 to 37 with poor ovarian response, who either received PRP therapy or standard treatment before IVF.The results showed significant differences in gene expression between the two groups. PRP-treated samples exhibited increased activity in genes related to metabolism, cell survival, and communication between cells, all of which are crucial for egg development and fertility. One key finding was that PRP influenced carbohydrate metabolism in cumulus cells. This is essential, as cumulus cells provide energy to the developing egg, and previous research has linked metabolic health to embryo quality. PRP also appeared to regulate pathways related to cell proliferation and programmed cell death, suggesting it may help support egg survival.“Our findings indicate that PRP treatment regulates certain pathways that could contribute to follicular activation and oocyte maturation.”Although PRP has been used in medicine for wound healing and tissue repair, its role in fertility treatment is still under investigation. Some clinical trials have shown improved ovarian reserve markers after PRP treatment, while others have not found a direct benefit for pregnancy rates. This study sheds light on how PRP affects cumulus cells, offering valuable insights into its potential for improving fertility treatments.The researchers hope that further studies will help refine PRP treatments, determine the best protocols, and identify which patients may benefit the most. By understanding the molecular effects of PRP on ovarian cells, scientists may develop targeted fertility therapies to support women facing infertility due to diminished ovarian reserve.DOI - https://doi.org/10.18632/aging.206202Corresponding author - Emre Seli - emre.seli@yale.eduVideo short - https://www.youtube.com/watch?v=3Zc_0tr0S84About Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — March 12, 2025 — A new #research paper was #published in Aging (Aging-US) on February 25, 2025, Volume 17, Issue 2, titled “Epidemiology and genetic determination of measures of peripheral vascular health in the Long Life Family Study.”Researchers from multiple institutions, led by first author and corresponding author Deidra R. Fricke from the University of Pittsburgh, studied the genetic and lifestyle factors that influence peripheral artery disease (PAD), a condition that restricts blood flow to the legs. Their findings suggest that people from families with exceptional longevity have a lower risk of PAD, possibly due to inherited genetic traits or healthier lifestyle habits.Peripheral artery disease is a common but often undiagnosed condition that affects millions worldwide. It increases the risk of heart disease, stroke, and mobility issues. This study conducted using data from the Long Life Family Study (LLFS), found that individuals from long-lived families have significantly better vascular health than the general population.“Peripheral artery disease (PAD) is a major contributor to morbidity in older adults.”The researchers analyzed over 3,000 participants, including 1,090 long-lived individuals, their 1,554 children, and 362 spouses. Among the oldest participants (average age 89), about 18% had PAD. However, among their children (average age 60), only 1% had PAD—far lower than the expected 12% found in other studies. This finding suggests that certain protective factors, whether genetic or lifestyle-related, help maintain healthier arteries in these families.In the study, key risk factors for PAD were identified, including aging, high blood pressure, smoking, and hypertension medication use. Interestingly, unlike in other studies, high cholesterol and diabetes were not major risk factors in this group. This data further supports the idea that long-lived families may have genetic protective factors that contribute to better vascular health.In addition to lifestyle factors, the study found four genomic regions linked to PAD risk. Three of these were new discoveries, while the fourth was similar but not identical to previously published findings. These genetic markers may help scientists better understand why some individuals are more likely to develop PAD and how to prevent it.“We identified four genomic sites that may harbor variants associated with protection from PAD.”This research highlights the value of studying long-lived families to unlock the secrets of healthy aging and vascular health. Understanding what helps them maintain better artery function could lead to new strategies for preventing PAD, heart disease, and other age-related conditions.Paper DOI: https://doi.org/10.18632/aging.206204Corresponding author: Deidra R. Fricke — der94@pitt.eduKeywords: aging, ankle-brachial index, peripheral arterial disease, heritability, genomewide linkage analysis, genomewide association studySubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Radiation therapy or radiotherapy, is a common treatment for cancer, but its effectiveness differs across patients. A recent study published as the cover for Volume 17, Issue 2 of Aging explored why this happens. The findings provide valuable insights, particularly for brain cancers like glioblastoma (GBM) and low-grade gliomas (LGG).Understanding Glioblastoma and Low-Grade GliomasGlioblastoma and LGG are both brain tumors, but they behave in very different ways. GBM is highly aggressive, with most patients surviving only 12 to 18 months, even with surgery, chemotherapy, and radiation therapy. LGG, on the other hand, grows more slowly, and many patients live for decades with proper care.Despite their differences, LGG and GBM are biologically linked. Some LGG tumors eventually transform into GBM, making early treatment decisions critical. Given radiation therapy’s effectiveness in GBM, it has often been assumed that LGG patients would also benefit from it. However, a new study titled “Variability in radiotherapy outcomes across cancer types: a comparative study of glioblastoma multiforme and low-grade gliomas” challenges this assumption.Full blog - https://aging-us.org/2025/03/how-radiation-therapy-affects-tumors-glioblastoma-vs-low-grade-gliomas/Paper DOI - https://doi.org/10.18632/aging.206212Corresponding author - Morten Scheibye-Knudsen - mscheibye@sund.ku.dkVideo short - https://www.youtube.com/watch?v=j91rzDJHXTESign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206212Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, cancer, biomarkers, radiotherapy, GBM, LGG, survivalAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — March 3, 2025 — A new #research paper was #published in Aging (Aging-US) on February 27, 2025, as the #cover of Volume 17, Issue 2, titled “Variability in radiotherapy outcomes across cancer types: a comparative study of glioblastoma multiforme and low-grade gliomas.” An international research team, led by first author Alexander Veviorskiy from Insilico Medicine AI Limited, Abu Dhabi, UAE, and corresponding author Morten Scheibye-Knudsen from the Center for Healthy Aging, University of Copenhagen, investigated how radiotherapy affects survival in different types of cancer, with a special focus on glioblastoma multiforme (GBM) and low-grade gliomas (LGG). Their findings reveal that radiotherapy has opposite effects in GBM and LGG patients. The study highlights key biological differences between these brain cancer types, emphasizing the need for personalized treatment strategies.Radiotherapy is a standard treatment for many tumors, but its effectiveness varies widely depending on the type of cancer. The researchers began by analyzing data from 32 cancer types using information from The Cancer Genome Atlas (TCGA). They then focused on glioblastoma multiforme (GBM) and low-grade gliomas (LGG), two types of brain cancer with distinct biological behaviors. GBM is an aggressive cancer with poor survival rates, whereas LGG progresses more slowly and often has a better prognosis.“GBM and LGG are particularly interesting to study together because GBM often originates from a preexisting LGG, representing a progression from a lower-grade to a higher-grade malignancy.”The results revealed a striking contrast: patients with GBM who received radiotherapy lived longer, whereas those with LGG had shorter survival times after treatment. To understand the reasons behind this, the researchers analyzed gene expression and signaling pathways. They identify several biological processes that may influence radiotherapy outcomes.For example, GBM tumors have weaker DNA repair mechanisms, making them more vulnerable to radiation-induced damage, which allows radiotherapy to effectively kill cancer cells. In contrast, LGG tumors have stronger DNA repair systems, helping cells survive radiation better and potentially reducing the treatment’s effectiveness. Additionally, differences in immune system activity and genetic mutations—such as EGFR alterations—were linked to worse survival in LGG patients who received radiotherapy.These findings highlight the need for a more personalized approach to treating brain cancer. The study proposes that a universal approach to radiotherapy is not appropriate, particularly for patients with LGG. Instead, personalized treatment strategies based on genetic and molecular characteristics could improve patient survival outcomes. The research also raises the possibility of combining radiotherapy with targeted therapies, such as immune-boosting therapies or DNA repair inhibitors, to enhance its effectiveness.In conclusion, this study highlights the complexity of brain cancer treatment and the need for further research to refine therapeutic strategies. By understanding the molecular and genetic differences between the different types of cancers, more effective and personalized approaches can be developed to improve survival and quality of life for brain cancer patients.DOI - https://doi.org/10.18632/aging.206212Corresponding author - Morten Scheibye-Knudsen - mscheibye@sund.ku.dkVideo short - https://www.youtube.com/watch?v=j91rzDJHXTEVisit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — March 5, 2025 — A new #research paper was #published in Aging (Aging-US) on February 11, 2025, Volume 17, Issue 2, titled “Exposome-wide association study of environmental chemical exposures and epigenetic aging in the national health and nutrition examination survey.” First author Dennis Khodasevich and corresponding author Andres Cardenas from Stanford University, and colleagues from other U.S. institutions, studied how exposure to harmful chemicals in the environment affects aging. Using data from the National Health and Nutrition Examination Survey (NHANES), they discovered that cadmium, lead, and cotinine are linked to faster biological aging, a process that can increase the risk of age-related diseases.The study analyzed data from 2,346 U.S. adults aged 50 to 84 who participated in a national health survey. Researchers tested their blood and urine for 64 different chemicals, including metals, pesticides, and industrial pollutants. They assessed how these exposures influenced eight different epigenetic aging markers—biological clocks that measure how fast a person’s body is aging at the DNA level."We harnessed data from the National Health and Nutrition Examination Survey 1999-2000 and 2001-2002 cycles to examine exposome-wide associations between environmental exposures and epigenetic aging."The strongest effects were linked to cadmium, a toxic metal found in cigarette smoke and some foods. People with higher levels of cadmium in their blood showed signs of accelerated aging. Higher levels of cotinine, a chemical related to tobacco exposure, were also linked to increased biological age, reinforcing the harmful effects of smoking. Additionally, lead exposure, a heavy metal found in old paint and contaminated water, was also associated with faster aging. The researchers also found that some pollutants, including a type of PCB (PCB118) and a type of dioxin (HpCDD), were linked to slower biological aging. However, it is unclear if this fact is beneficial, as past research shows that slower aging in some cases can still be linked to health risks.This study is one of the largest to investigate how pollution affects the aging process. Unlike previous research that focused on only a few chemicals, it examined a wide range of pollutants in a diverse group of people. The findings suggest that everyday exposure to toxic substances can speed up aging at the cellular level, increasing the risk of age-related diseases.In summary, these findings raise concerns about how widespread environmental contaminants may accelerate aging and contribute to chronic diseases such as heart disease, cancer, and cognitive decline. Reducing exposure to toxic substances like cadmium and lead—found in cigarettes, polluted air, and contaminated food—could help slow biological aging and improve long-term health. These insights highlight the need for stronger environmental health policies to protect individuals from premature aging and disease.DOI - https://doi.org/10.18632/aging.206201Corresponding author - Andres Cardenas - andresca@stanford.eduVideo short - https://www.youtube.com/watch?v=WcL-K399a7MSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — February 24, 2025 — A new #researchpaper was #published in Aging (Aging-US) on January 22, 2025, in Volume 17, Issue 1, titled “EpiAge: a next-generation sequencing-based ELOVL2 epigenetic clock for biological age assessment in saliva and blood across health and disease.”The research team, experts from both industry (EpiMedTech Global, HKG Epitherapeutics Ltd) and academic institutions (McGill University, Oxford University, University of Catania, and the Research Institute-IRCCS), led by first author David Cheishvili and corresponding author Moshe Szyf, have developed EpiAgePublic, a new method to estimate biological age using only three key DNA sites in the ELOVL2 gene, a well-known marker of aging. Unlike traditional methods that require analyzing thousands of DNA regions, this approach simplifies the process while maintaining accuracy. Their findings show that EpiAgePublic performs as well as, or even better than, more complex models in predicting biological age in diverse populations.Biological age measures how fast or slow a person’s body is aging. It can be different from chronological age and is influenced by genetics, lifestyle, and health conditions. Understanding biological aging can help researchers and clinicians identify age-related diseases like Alzheimer’s disease and develop anti-aging treatments. However, many existing biological age tests rely on expensive and complicated processes. The EpiAgePublic model overcomes these challenges with a simple yet powerful approach.The study analyzed data from over 4,600 individuals across different health conditions, including Alzheimer’s disease and HIV. It confirmed that EpiAgePublic accurately tracks aging patterns and can identify factors such as chronic illness or stress that accelerate the aging process. Importantly, the researchers demonstrated that the test works well using saliva samples, offering a convenient and non-invasive alternative to blood-based tests. This makes it easier to conduct epigenetic age testing in both clinical and research settings.“The simplicity and precision of epiAgePublic, designed for compatibility with next-generation sequencing (NGS) technologies, mark a significant step forward in the field of epigenetic research.”The ability to measure epigenetic aging with a quick and cost-effective test has significant implications for healthcare, longevity research, and personalized medicine. This method could be used in hospitals, wellness clinics, and longevity studies to track aging and evaluate the effectiveness of anti-aging interventions. It may also help clinicians detect early signs of aging-related diseases, allowing for better preventive care.Finally, the study’s findings highlight the advantages of next-generation sequencing in epigenetic research, leading the way for more precise and accessible aging diagnostics. Future research will explore how this model can be expanded to other health conditions and used in routine medical practice.DOI - https://doi.org/10.18632/aging.206188Corresponding author - Moshe Szyf - moshe.szyf@epimedtech.comAuthor interview - https://www.youtube.com/watch?v=NA8Vctks0gYSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206188Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsPlease visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
In the Season 3 premiere of the Longevity & Aging Series, Dr. Yu-Xuan Lyu from Southern University of Science and Technology (Shenzhen, China) joins host Dr. Evgeniy Galimov to discuss his co-authored research paper, featured as the cover for Aging (Aging-US) Volume 16, Issue 20, titled “Longevity biotechnology: bridging AI, biomarkers, geroscience, and clinical applications for healthy longevity.”#aging #author #interview #series #biotechnology #ai #artificialintelligence #longevity #healthspan #lifespan #oa #openscience #peerreview #journal #publication #publishing #meded #agingshort #videoDOI - https://doi.org/10.18632/aging.206135Corresponding authors - Yu-Xuan Lyu - lvyx@sustech.edu.cn, Alex Zhavoronkov - alex@insilico.com, Morten Scheibye-Knudsen - mscheibye@sund.ku.dk, and Daniela Bakula - bakula@sund.ku.dkVideo interview - https://www.youtube.com/watch?v=VUfNxWdBV5kVideo short - https://www.youtube.com/watch?v=Hpfe5WJ5g7IAbstractThe recent unprecedented progress in ageing research and drug discovery brings together fundamental research and clinical applications to advance the goal of promoting healthy longevity in the human population. We, from the gathering at the Aging Research and Drug Discovery Meeting in 2023, summarised the latest developments in healthspan biotechnology, with a particular emphasis on artificial intelligence (AI), biomarkers and clocks, geroscience, and clinical trials and interventions for healthy longevity. Moreover, we provide an overview of academic research and the biotech industry focused on targeting ageing as the root of age-related diseases to combat multimorbidity and extend healthspan. We propose that the integration of generative AI, cutting-edge biological technology, and longevity medicine is essential for extending the productive and healthy human lifespan.Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206135Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, biotechnology, artificial intelligence, healthy longevityAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — February 26, 2025 — A new #research paper was #published in Aging (Aging-US) on January 27, 2025, in Volume 17, Issue 1, titled “Age-invariant genes: multi-tissue identification and characterization of murine reference genes.”Aging is a process driven by changes in gene activity, but researchers from Yale University School of Medicine and Altos Labs, led by first author John T. González and corresponding author Albert T. Higgins-Chen, have identified a set of genes that remain unchanged throughout the aging process. This discovery could improve the accuracy of aging research and provide insights into why some genes stay unchanged while others decline.“Reference genes have mostly been identified and validated in young organisms, and no systematic investigation has been done across the lifespan.”The study looked at gene activity in 17 different tissues in mice, from 1 month old to over 21 months old. Scientists used advanced bioinformatic analysis methods to analyze RNA sequencing data. They found nine genes that stayed the same across all tissues, as well as other genes that remained stable in specific tissues. These genes are usually shorter and have special DNA regions called CpG islands, which may help cells stay healthy and resist aging. Their stability throughout aging was confirmed by analyzing different datasets and using RT-qPCR.One of the most significant findings is that these stable genes are linked to essential cellular functions, such as mitochondrial activity and protein maintenance. This challenges the common belief that all aspects of aging involve gene dysregulation. Instead, the findings suggest that some cellular processes may naturally resist aging, leading the way for new research on longevity and potential anti-aging therapies.“Biological processes that change with age and those that resist age-related dysregulation are two sides of the same coin, and both will need to be investigated to fully understand aging.”Another key finding is that commonly used reference genes, such as GAPDH and ACTB, fluctuate with age, making them unreliable for aging studies. No single classical reference gene was found to be stable across all tissues. Researchers often use these reference genes as a control to measure gene activity, but if their expression changes over time, it can lead to inaccurate results. By identifying new, stable reference genes, this study provides scientists with better tools for studying aging-related diseases, regenerative medicine, and longevity science.Understanding how certain genes remain unchanged throughout life suggests that they may play a protective role in aging and could potentially be used to develop treatments that slow down age-related decline. While further research is needed, this discovery sets a new standard for measuring gene activity in aging studies and could have a significant impact on aging research and medicine.DOI - https://doi.org/10.18632/aging.206192Corresponding author - Albert T. Higgins-Chen - a.higginschen@yale.eduAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
Dr. Moshe Szyf from EpiMedTech Global in Singapore discusses a research paper he co-authored that was published in Volume 17, Issue 1 of Aging (Aging-US), entitled “EpiAge: a next-generation sequencing-based ELOVL2 epigenetic clock for biological age assessment in saliva and blood across health and disease.”DOI - https://doi.org/10.18632/aging.206188Corresponding author - Moshe Szyf - moshe.szyf@epimedtech.comVideo interview - https://www.youtube.com/watch?v=NA8Vctks0gYVideo transcript - https://www.aging-us.com/interviews/epiage-ngs-based-elovl2-epigenetic-clock-for-biological-age-assessmentSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206188Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, epigenetic clock, elovl2, next-generation sequencing, EpiAge, Alzheimer's diseaseAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — February 19, 2025 — A new #research paper was #published by Aging (Aging-US) on January 6, 2025, in Volume 17, Issue 1, titled “The profile of oxidative stress markers (arachidonic and linoleic acid derivatives) in patients with benign prostatic hyperplasia in relation to metabolic syndrome.”A team of researchers, led by first author Weronika Ratajczak and corresponding author Olimpia Sipak from Pomeranian Medical University, examined how inflammation and metabolic health contribute to benign prostatic hyperplasia (BPH), a common condition that causes prostate enlargement in aging men, leading to urinary problems. Their findings suggest that inflammatory-related molecules in the blood may play a key role in BPH development, especially in men with metabolic syndrome—a group of conditions including obesity, high blood sugar, and high cholesterol.BPH affects millions of men as they age, making urination more difficult and sometimes painful. While age and hormonal changes are known factors, the precise causes of prostate enlargement remain unclear. This study provides new evidence that inflammation, especially lipid-derived inflammatory markers, may be a driving factor behind BPH, particularly in those with poor metabolic health.The research team analyzed blood samples from 219 men, including 144 with BPH and 75 without, measuring markers related to inflammation and oxidative stress. The results showed that men with BPH had significantly higher levels of pro-inflammatory molecules such as 12S-HETE and 5-HETE while having lower levels of anti-inflammatory substances like lipoxin A4. The imbalance was even more pronounced in men with both BPH and metabolic syndrome, indicating a possible link between poor metabolic health and worsening prostate conditions.“Furthermore, there is mounting evidence that links the onset of inflammation with the development of prostate diseases, including benign prostatic hyperplasia and prostate cancer.”Metabolic dysfunction and chronic inflammation may not only contribute to BPH development but also exacerbate its severity. Monitoring metabolic health could play a role in reducing the risk of prostate enlargement.Future research is needed and may focus on whether anti-inflammatory treatments or lifestyle changes—such as improved diet, weight management, and exercise—could help slow the progression of BPH or reduce its symptoms.DOI - https://doi.org/10.18632/aging.206187Corresponding author - Olimpia Sipak - olimpiasipak-szmigiel@wp.plVideo short - https://www.youtube.com/watch?v=O0VMvqaVsUsSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206187Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, benign prostatic hyperplasia (BPH), metabolic syndrome (MetS), lipid markers, inflammation, fatty acids derivativesAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY—February 18, 2025 — A new #research paper was #published by Aging (Aging-US) on January 8, 2025, in Volume 17, Issue 1, titled “Senolytic agent ABT-263 mitigates low- and high-LET radiation-induced gastrointestinal cancer development in Apc1638N/+ mice.”Researchers Kamendra Kumar, Bo-Hyun Moon, Santosh Kumar, Jerry Angdisen, Bhaskar V.S. Kallakury, Albert J. Fornace Jr., and Shubhankar Suman from Georgetown University Medical Center explored whether a drug called ABT-263 could help reduce the risk of gastrointestinal (GI) cancer caused by radiation exposure. Their findings suggest that ABT-263, a senolytic agent, helps eliminate harmful aging cells in the gut, reducing inflammation and lowering cancer risk in mice. These results could lead to potential treatments for people exposed to radiation, including cancer patients and astronauts.Radiation exposure, whether from medical treatments, environmental sources, or space travel, can damage cells and increase the risk of GI cancer. One key factor in this process is cellular senescence, where damaged cells stop dividing but continue to release harmful molecules that promotes tumor growth. This study tested whether ABT-263, a drug designed to remove these aged cells, could lower cancer risk in a mouse model of GI cancer.In this study, researchers exposed mice to radiation and found that it increased the number of damaged cells in their intestines, leading to more tumors. However, when the mice were given ABT-263, the number of harmful cells decreased, and they developed fewer tumors. The drug also reduced inflammation and blocked signals that promote cancer growth.“Oral administration of ABT-263 in Apc1638N/+ mice resulted in a significant reduction in low-LET IR-induced intestinal tumor burden at 5 months post-exposure."These findings highlight the potential of senolytic drugs like ABT-263 as a preventive treatment for radiation-induced cancers. This approach could be especially beneficial for cancer patients undergoing radiation therapy, astronauts exposed to cosmic radiation, and individuals at risk from environmental sources such as radon gas.However, while ABT-263 showed promise, it also has known side effects, including reduced platelet counts, which can impact blood clotting. Future research will focus on optimizing senolytic treatments to ensure they are both safe and effective for human use. Scientists are also exploring alternative drugs and combination therapies that might offer the same benefits with fewer risks.This study provides strong evidence that removing senescent cells could help prevent radiation-related GI cancer. With further research, senolytic drugs may become an important tool in protecting at-risk populations from the long-term effects of radiation exposure.DOI - https://doi.org/10.18632/aging.206183Corresponding author - Shubhankar Suman - ss2286@georgetown.eduVideo short - https://www.youtube.com/watch?v=M_WEht4vy4wSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Imagine a simple topical treatment that could help aging skin heal faster, reducing recovery time from wounds and even improving skin quality. Scientists may have found exactly that. A recent study, published in Aging, reveals that a compound called ABT-263 can eliminate aging cells in the skin, boosting its ability to regenerate. Understanding How Aging Affects Skin HealingAging affects the skin’s structure and function, leading to a reduced ability to heal from wounds. Scientists have long suspected that senescent cells, also known as “zombie cells,” play a major role in this decline. These cells stop dividing but refuse to die, accumulating in tissues and releasing inflammatory molecules that impair the body’s natural repair processes.Various studies have explored senolytics, a class of drugs designed to eliminate these aging cells and restore tissue function. While these drugs have shown promise in treating diseases like osteoporosis and fibrosis, their impact on skin regeneration and wound healing has been less studied. A new study titled “Topical ABT-263 treatment reduces aged skin senescence and improves subsequent wound healing” now suggests that a topical application of the senolytic ABT-263 could significantly improve wound healing in older individuals.Full blog - https://aging-us.org/2025/02/a-new-approach-to-healing-aging-skin-insights-from-senolytic-research/Paper DOI - https://doi.org/10.18632/aging.206165Corresponding author - Daniel S. Roh - droh@bu.eduVideo short - https://www.youtube.com/watch?v=AKS7sZyEChgSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206165Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, senolytic, senescence, wound healing, ABT-263About Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY—February 12, 2025 — A new #research paper was #published in Aging (Aging-US) on January 3, 2025, in Volume 17, Issue 1, titled “Characterization of DNA methylation clock algorithms applied to diverse tissue types.”Researchers Mark Richardson, Courtney Brandt, Niyati Jain, James L. Li, Kathryn Demanelis, Farzana Jasmine, Muhammad G. Kibriya, Lin Tong, and Brandon L. Pierce from the University of Chicago and University of Pittsburgh, studied how biological aging is measured using DNA. Their study found that while commonly used “DNA methylation clocks” work well for blood samples, they may be less reliable for other tissues like the lungs, colon, and kidneys.DNA methylation clocks are widely used in forensic science, epigenetics and longevity research to estimate a person’s biological age based on chemical changes in DNA. These epigenetic clocks help scientists predict age-related diseases and assess how lifestyle factors, such as smoking, impact aging. Most were originally developed using blood samples, and their effectiveness in other tissues remains unclear. This study tested eight different DNA methylation clocks across nine human tissue types, including the lungs, prostate, ovaries, skeletal muscle, and kidneys. The researchers analyzed data from 973 tissue samples collected through the Genotype-Tissue Expression (GTEx) project.Their analysis revealed significant differences in biological age estimates across tissues. While blood samples provided the most reliable results, other tissues showed noticeable variations. For example, testis and ovary tissues appeared younger than expected, while lung and colon tissues appeared older. “These differences across tissue types were most apparent for clocks trained using DNAm from blood only (e.g., Hannum), but also present for clocks trained on multiple tissue types (e.g., Horvath, a clock designed for pan-tissue age prediction.” These findings suggest that aging may not occur at the same rate in every organ, and that standard DNA methylation clocks may not always give accurate biological age estimates outside of blood samples. The authors suggest that new, organ-specific epigenetic clocks may be needed to improve biological age prediction. Creating tissue-specific aging clocks could also improve medical diagnostics, age-related disease prevention, and health monitoring.The researchers emphasize that larger studies with more tissue-specific DNA methylation data are needed to refine these aging clocks. By improving these tools, scientists can better understand how aging affects different organs and develop more reliable methods for measuring biological age. These advancements could lead to better predictions of age-related diseases and new strategies for healthy aging.DOI - https://doi.org/10.18632/aging.206182Corresponding author - Brandon L. Pierce - brandonpierce@uchicago.eduVideo short - https://www.youtube.com/watch?v=Jz-daRsZO2oSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY—February 11, 2025 — A new #research paper was #published in Aging (Aging-US) on January 15, 2025, in Volume 17, Issue 1, titled “Association between physical activity practice and sleep quality of older people in social isolation during the COVID-19 pandemic and Health Guidelines and future studies for the post-COVID period: a systematic review.”Researchers Alexandro Andrade, Ana Cecília Rosatelli de Freitas Bastos, Anderson D’Oliveira, and Guilherme Torres Vilarino from the Santa Catarina State University (UDESC) in Brazil, conducted a systematic review to examine the relationship between physical activity (PA) and sleep quality in older adults who experienced social isolation during the COVID-19 pandemic. Their findings reveal that a decline in PA levels during social isolation negatively impacted sleep health, emphasizing the need for regular movement in aging populations.The study reviewed nine studies involving over 11,500 older adults of both sexes from China, Japan, Brazil, Scotland, Canada, Italy, and Spain. The results showed that reduced PA during the pandemic was linked to poorer sleep quality in four studies, while one study found that those who remained active had better sleep patterns. The four other studies showed no significant association.Getting enough quality sleep is essential for healthy aging, as sleep disorders have been linked to cognitive decline, depression, and reduced mental well-being. The COVID-19 pandemic worsened sleep health due to increased stress, isolation, and anxiety. Researchers suggest that staying active through walking, stretching, and structured exercise routines may help improve sleep quality and overall mental health.The researchers point out the importance of PA as an accessible way to enhance sleep quality in older adults, particularly during times of crisis. Encouraging regular exercise and movement may help prevent sleep disorders and improve overall well-being in aging populations.“PA can be considered a safe and effective practice to improve sleep quality in older adults due to its well-documented benefits in the literature.”As the world moves past the pandemic, the researchers call for public health policies that promote PA for seniors. Health professionals and caregivers should advocate for regular movement as a preventive measure against insomnia, poor sleep, and mental health issues while emphasizing the long-term consequences of physical inactivity. The study also highlights the need for further research on the most effective types and intensities of PA for improving sleep quality in older adults.“The practice of exercise and PA, individually and in groups, is recommended for this post-COVID scenario, as a measure to reduce social isolation and its negative effects and improve the quality of sleep in older adults.”Future studies should explore how different exercise routines impact sleep health, especially for older adults recovering from COVID-19 or facing ongoing sleep challenges.DOI - https://doi.org/10.18632/aging.206180Corresponding author - Alexandro Andrade - alexandro.andrade.phd@gmail.comVideo short - https://www.youtube.com/watch?v=uV4WXq7I_J0About Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Emerging research suggests that a specific type of body fat may play an important role in healthy aging and physical performance. Researchers from Rutgers New Jersey Medical School explore this topic in a recent research perspective published in Aging (Aging-US). Their work discusses new findings and emerging ideas about the role of brown adipose tissue (BAT), commonly known as brown fat.Understanding Brown FatThe human body contains different types of fat. The most common is white adipose tissue (WAT), which primarily stores excess calories. When present in large amounts, WAT contributes to health problems like obesity, type 2 diabetes, and cardiovascular disease as a result of its role in metabolic imbalance.In contrast, BAT serves a more dynamic role. Instead of storing energy, BAT burns calories to generate heat through a process called thermogenesis, powered by its high concentration of mitochondria—the energy-producing structures in cells. While BAT is abundant in newborns to help regulate body temperature, it persists in smaller amounts in adults, particularly around the neck, shoulders, and spine. According to the research perspective, titled “Brown Adipose Tissue Enhances Exercise Performance and Healthful Longevity” brown fat’s role extends beyond thermoregulation. The authors suggest that BAT can significantly improve metabolic health, enhance physical performance, and promote healthful longevity.Full blog - https://aging-us.org/2025/02/the-hidden-power-of-brown-fat-a-new-ally-in-healthy-aging/Paper DOI - https://doi.org/10.18632/aging.206179Corresponding author - Stephen F. Vatner - vatnersf@njms.rutgers.eduVideo short - https://www.youtube.com/watch?v=n1DvuR7owJQSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206179Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, brown adipose tissue, white adipose tissue, healthful longevity, exercise, regulator of G protein signaling 14About Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY—February 5, 2025 — A new #research paper was #published in Aging (Aging-US) on November 27, 2024, in Volume 17, Issue 1, titled “Neurocognitive disparities: investigating ethnicity and mental health in rural aging adults.”Researchers Carol Fadalla, Jonathan Singer,, Peter Rerick, Lauren Elliott, Elisabeth McLean, Sydnie Schneider, Lauren Chrzanowski, Veronica Molinar-Lopez, and Volker Neugebauer from Texas Tech University and the University of Central Oklahoma studied how depression and anxiety affect memory and thinking skills in Hispanic and non-Hispanic White older adults living in rural areas. They found clear differences in brain health, with Hispanic older adults scoring lower on tests of memory, attention, and problem-solving, even when their mental health was similar to non-Hispanic White participants. This suggests that Hispanic older adults may face unique challenges that affect their brain health, highlighting the need for support programs tailored to their specific needs.As the U.S. population grows older, more people are being diagnosed with conditions like Alzheimer’s disease, dementia, and other memory-related illnesses. This issue is even more serious in rural communities where healthcare services are limited. Hispanic older adults, who make up a large part of the rural population, are at an even higher risk of developing these brain health issues.In this study, researchers analyzed data from over 1,400 adults aged 40 and older from rural communities in Texas. Participants completed tests measuring memory, problem-solving, and attention, along with surveys about depression and anxiety. While depression and anxiety were linked to poorer thinking skills, they did not fully explain the brain health differences between Hispanic and non-Hispanic White participants. In fact, ethnic background alone explained about 20% of the differences in brain health, showing its strong impact on cognitive performance.The study also found that other factors, such as lifelong stress, limited access to healthcare, language barriers, discrimination, social isolation, and fewer educational opportunities, may contribute to these brain health differences. These challenges seem to affect Hispanic older adults more, increasing their risk of memory and thinking problems as they age.The researchers emphasize the need to look beyond mental health to fully understand brain health differences in older adults. They recommend that healthcare providers consider social, economic, and cultural factors when developing programs to support cognitive health. Adding memory and thinking tests to regular checkups could help detect early signs of cognitive decline. “Culturally tailored interventions targeting risk factors for neurocognitive impairment in Hispanic rural aging adults are imperative to mitigate neurocognitive disparities.”By understanding the unique challenges faced by Hispanic older adults, programs that better support brain health can be created. Involving local community leaders in designing these programs can make them more effective, helping all older adults maintain their memory and thinking skills as they age. Read the full paper: DOI: https://doi.org/10.18632/aging.206166Corresponding author: Jonathan Singer - jonsinge@ttu.eduAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com.MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY—February 4, 2025 — A new #research paper was #published by Aging (Aging-US) on December 3, 2024, in Volume 17, Issue 1, titled “Topical ABT-263 treatment reduces aged skin senescence and improves subsequent wound healing.”Researchers Maria Shvedova, Rex Jeya Rajkumar Samdavid Thanapaul, Joy Ha, Jannat Dhillon, Grace H. Shin, Jack Crouch, Adam C. Gower, Sami Gritli, and Daniel S. Roh from Boston University Aram V. Chobanian and Edward Avedisian School of Medicine have discovered that a drug called ABT-263 can significantly improve wound healing in aging skin. When applied directly to the skin of older mice, ABT-263 helps clear out old, damaged cells, known as senescent cells, and speeds up the skin’s ability to heal after injury. This finding could lead to new treatments for slow-healing wounds in older adults, especially for post-surgical recovery and chronic wound care.As people age, their bodies accumulate senescent cells—damaged cells that no longer function properly but refuse to die. The buildup of these cells in tissues like the skin slows down the body’s ability to heal after injuries. This study investigated whether ABT-263, a senolytic drug designed to target and remove senescent cells when applied topically, could enhance the skin’s natural healing process.Researchers applied ABT-263 to the skin of aged mice for five days. The treated skin showed fewer signs of cellular aging, and when small wounds were created, they healed much faster compared to untreated mice. By day 24, 80% of the mice treated with ABT-263 had fully healed wounds, compared to just 56% of untreated mice.Interestingly, ABT-263 triggered a brief spike of inflammation in the skin, which surprisingly helped the healing process. The inflammation seemed to “wake up” the skin’s repair systems, making them respond more quickly to wounds. Additionally, ABT-263 increased the activity of genes related to wound repair, such as those involved in collagen production and the growth of new blood vessels, both essential for skin strength and regeneration.The study also found that ABT-263 selectively reduced senescent cells in aged mice without affecting young mice, suggesting the drug is particularly effective in older tissues where these damaged cells accumulate. Moreover, because ABT-263 was applied directly to the skin, it avoided the common side effects associated with oral senolytic drugs.“Our study underscores the potential of topical senolytic treatments to enhance wound healing in aging skin, presenting a potentially promising strategy for preoperative care.”While the results are promising, more research is needed to confirm whether this treatment is safe and effective for humans. However, this study represents an exciting step forward in regenerative medicine, opening new opportunities to improve wound healing in aging skin.DOI - https://doi.org/10.18632/aging.206165Corresponding author - Daniel S. Roh - droh@bu.eduVideo short - https://www.youtube.com/watch?v=AKS7sZyEChgAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- January 29, 2025 – A new #editorial was #published in Volume 16, Issue 22 of Aging (Aging-US) on December 11, 2024, titled “ISarcoPRM algorithm for global operationalization of sarcopenia diagnosis.”In this editorial, Pelin Analay, Murat Kara and Levent Özçakar from Hacettepe University Medical School discuss the importance of establishing a standardized global approach to diagnosing sarcopenia, an age-related condition that leads to muscle loss and reduced strength. The authors highlight the ISarcoPRM algorithm, which suggests measuring quadriceps muscle mass instead of the commonly used appendicular lean mass (ALM) measurement. They believe this improved method could help clinicians identify sarcopenia earlier and provide better treatment options.Sarcopenia is a major health problem for older adults, making daily activities such as walking, climbing stairs, and standing up more difficult. As muscle strength declines, individuals with sarcopenia are at greater risk of falls and serious injuries, such as fractures. Early detection of sarcopenia is crucial to help older adults maintain their mobility and independence.The editorial points out that current diagnostic tools, such as dual-energy X-ray absorptiometry (DXA), may not effectively measure age-related muscle loss. Sarcopenia primarily affects fast-twitch muscle fibers, which are essential for strength and quick movements. However, DXA scans measure overall muscle mass and fail to assess these specific fibers, potentially leading to inaccurate or delayed diagnoses.The authors propose that measuring the quadriceps muscle mass—the large muscle in the thigh—is a more accurate way to diagnose sarcopenia. This muscle plays a critical role in mobility and strength, and its size and function are strongly linked to a person's overall physical performance. The editorial recommends using ultrasound (US) imaging as a practical and cost-effective solution for diagnosing sarcopenia in clinical settings. Compared to other imaging techniques, US is affordable, widely available, and well-suited for elderly patients, including those with mobility limitations or medical implants. Ultrasound is also non-invasive, making it an ideal choice for routine sarcopenia screening in hospitals, clinics, and long-term care facilities.If widely adopted, this new way of diagnosing sarcopenia could help clinicians detect it more accurately and at an earlier stage. Finding sarcopenia early allows people to start helpful treatments, like exercise, better nutrition, and healthy lifestyle changes. These steps can slow down muscle loss and help older adults stay strong and active. Finally, the authors encourage a global consensus on how to diagnose sarcopenia and suggest the ISarcoPRM method as a great option.“In conclusion, quadriceps muscle mass measurements, preferably by US and as recommended by the ISarcoPRM algorithm, holds great promise in the diagnosis of sarcopenia.”DOI - https://doi.org/10.18632/aging.206174Corresponding author - Pelin Analay - pelinanalay@yahoo.comVideo short - https://www.youtube.com/watch?v=gDcQ9w6mHyEAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- January 28, 2025 – A new #research paper was #published in Volume 16, Issue 22 of Aging (Aging-US) on December 20, 2024, titled, “Impaired renal transporter gene expression and uremic toxin excretion as aging hallmarks in cats with naturally occurring chronic kidney disease.”This study, led by researchers Qinghong Li, James A. Holzwarth, Bethany Smith, Sonia Karaz, Mathieu Membrez, Vincenzo Sorrentino, Stacie Summers, Julie Spears, and Eugenia Migliavacca from Nestlé Purina Research and Oregon State University, explores how aging affects kidney function in cats with chronic kidney disease (CKD). The researchers found that older cats have lower levels of important kidney transporter genes, which usually help remove harmful waste products from the blood. These findings could help veterinarians better understand CKD in aging cats and offer insights that may be relevant to human kidney health."Chronic kidney disease (CKD) is a naturally occurring kidney disease common in both geriatric cats and older people. Despite differing etiology, both species share many pathophysiological similarities, including chronic tubulointerstitial inflammation and fibrosis."Older cats with CKD struggle to filter toxins from their bloodstream effectively. In this study, the researchers analyzed kidney samples from two cat cohorts aged 6 to 21 years. The cohort number one included 41 colony cats: 28 control and 13 CKD cats. The cohort number two had 30 privately owned cats with 10 control and 20 CKD cats. They discovered that certain transporter genes, such as OAT1, OAT4, OATP4C1 and ABCC2, were significantly decreased in cats with CKD compared to healthy cats. The research team also found increased levels of harmful toxins in the blood of cats with CKD. Even healthy older cats had higher toxin levels compared to younger cats, showing that aging itself might contribute to declining kidney function.Monitoring kidney transporters levels and toxin buildup may help detect the disease early and improve treatment options. The researchers highlight the importance of regular veterinary check-ups to catch kidney problems early and keep cats healthier for longer.Because cats and humans share similar kidney health challenges, studying feline CKD can provide valuable insights into human kidney disease and aging. Continued research is essential to develop treatments that may improve kidney function in aging cats and potentially benefit humans as well.DOI - https://doi.org/10.18632/aging.206176Corresponding author - Qinghong Li - qinghong.li@rd.nestle.comVideo short - https://www.youtube.com/watch?v=WuEP9PXtx2ASign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206176Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, trimethylamine N-oxide, indoxyl sulfate, OAT1, OATP4C1, ABCC2About Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
“We illustrate our strategy in brain and liver tissue, demonstrating how cell-type specific epigenetic clocks from these tissues can improve tissue-specific estimation of chronological and biological age.”Aging affects everyone differently. There are two types of aging: chronological aging, which refers to the number of years a person has lived, and biological aging, which reflects how well the body is functioning based on cellular changes. A recent study published as the cover for Volume 16, Issue 22 of Aging reports a new discovery that could revolutionize the way we understand aging and its impact on health. Understanding Biological AgeBiological age reflects how well the body is aging and can vary based on lifestyle, genetics, and environmental factors. Traditionally, scientists estimate it using epigenetic clocks, which measure DNA methylation, chemical changes that occur over time. Until recently, these clocks could only provide general estimates by analyzing entire tissues, meaning they could not distinguish how different cell types aged within those tissues. A recent study titled “Cell-type Specific Epigenetic Clocks to Quantify Biological Age at Cell-Type Resolution” aims to change that.Full blog - https://aging-us.org/2025/01/how-scientists-are-measuring-aging-at-the-cellular-level/Paper DOI - https://doi.org/10.18632/aging.206184Corresponding author - Andrew E. Teschendorff - andrew@sinh.ac.cnVideo short - https://www.youtube.com/watch?v=FjJa5U2-AqQSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206184Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, DNA methylation, epigenetic clocks, cell-type deconvolution, biological aging, Alzheimer’s disease, obesityAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- January 22, 2025 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) on December 12, 2024, Volume 16, Issue 22, titled “Arginase-II gene deficiency reduces skeletal muscle aging in mice.”Researchers Matteo Caretti, Duilio Michele Potenza, Guillaume Ajalbert, Urs Albrecht, Xiu-Fen Ming, Andrea Brenna, and Zhihong Yang from the University of Fribourg found that removing a specific gene, called arginase-II (Arg-II), can slow down muscle aging in mice. Their research showed that older mice lacking this gene stayed more active and had healthier skeletal muscles compared to normal aging mice. This discovery could lead to new treatments to help people maintain muscle strength and mobility as they become older.As people age, their muscles naturally get weaker, leading to reduced physical activity and overall quality of life. This condition, known as sarcopenia, occurs because of muscle fiber loss, inflammation, and scar tissue buildup. The study found that the Arg-II gene contributes to this process.The research team compared normal mice with mice lacking the Arg-II gene and discovered that in general, the mice without the gene had improved muscle health, reduced inflammation, and fewer signs of age-related muscle decline. It was also found that older male mice deficient in the Arg-II gene were more active, particularly during their peak nighttime activity. These mice had stronger muscles and performed better in physical tests. Interestingly, the benefits of Arg-II gene removal were more pronounced in male mice compared to females, suggesting that hormonal or genetic differences might play a role in age-related muscle loss.“The improved phenotype of arg-ii-/- mice in aging is associated with reduced sarcopenia, cellular senescence, inflammation, and fibrosis, whereas age-associated decline of microvascular endothelial cell density, satellite cell numbers, and muscle fiber types in skeletal muscle is prevented in arg-ii-/- mice.”ARG-II protein was not found in muscle fibers but instead in surrounding cells such as fibroblasts and blood vessel cells, which makes scientists believe this gene influences muscle aging indirectly. Independently of that, the findings suggest that targeting the Arg-II gene could help slow down age-related muscle deterioration and improve muscle function in older adults. "[...] we demonstrate an increased arg-ii gene expression level in aging skeletal muscle and found Arg-II protein expression in endothelial cells and fibroblasts, but not in skeletal muscle fibers, macrophages, and satellite cells."While these results are promising, further research is needed to determine whether blocking the Arg-II gene in humans could provide similar benefits. Furthermore, understanding why male and female mice responded differently to the gene removal will be essential before personalized treatments for age-related muscle loss. If future studies confirm these findings in humans, targeting Arg-II could become a valuable strategy to help adults maintain muscle strength, mobility, and overall quality of life as they age.DOI - https://doi.org/10.18632/aging.206173Corresponding authors - Andrea Brenna - andrea.brenna@unifr.ch, and Zhihong Yang - zhihong.yang@unifr.chVideo short - https://www.youtube.com/watch?v=uDxSCO2Y7-wAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com.MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- January 21, 2025 — Aging (Aging-US) (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) partners with the inaugural Global Conference on Gerophysics, taking place from March 5–6, 2025, in Singapore. This groundbreaking event marks the launch of Gerophysics, an innovative field that applies theoretical physics concepts to the biology of aging, aiming to extend healthy human lifespans.The Intersection of Physics and AgingTheoretical physics has long revolutionized diverse industries—reshaping finance, powering artificial intelligence breakthroughs, and transforming our understanding of the cosmos. Now, leading experts are applying these powerful methodologies to tackle one of humanity's most profound challenges: aging. Hosted by the National University of Singapore (NUS) Yong Loo Lin School of Medicine, the Global Conference on Gerophysics - “where physics meets aging biology” - aims to bridge statistical mechanics, complex systems theory, and dynamical modeling with the biological mechanisms of aging. This unique interdisciplinary approach has the potential to reshape our understanding of the aging process and revolutionize efforts to promote healthy longevity.A Collaborative Platform for InnovationThe conference will bring together leading scientists, researchers, and thought leaders from across the globe to:-Develop a shared scientific language and toolkit for aging research.-Explore novel frameworks for studying biological aging through the lens of physics.-Foster collaborations that could lead to breakthroughs in extending human healthspan.As a media partner, Aging (Aging-US) is committed to amplifying the impact of this pioneering initiative, ensuring that groundbreaking insights and discussions reach the global scientific community.Stay updated on the conference via LinkedIn: Centre for Healthy Longevity, X (formerly Twitter): @HealthyLongeviT or visit the official event page.Key Words: aging, gerophysics, longevity research, conference, physics, biology, meeting, collaboration, lifespan, healthspanPlease visit our website at www.Aging-US.com and connect with us:Facebook - www.facebook.com/AgingUS/X - twitter.com/AgingJrnlInstagram - www.instagram.com/agingjrnl/YouTube - www.youtube.com/@AgingJournalLinkedIn - www.linkedin.com/company/aging/Pinterest - www.pinterest.com/AgingUS/Spotify - open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- January 20, 2025 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) on December 5, 2024, Volume 16, Issue 22, titled “DNA-methylation age and accelerated epigenetic aging in blood as a tumor marker for predicting breast cancer susceptibility.”Researchers Su Yon Jung, Herbert Yu, Youping Deng, and Matteo Pellegrini from the University of California, Los Angeles and University of Hawaii Cancer Center have found that a simple blood test could help predict breast cancer (BC) risk in older women. Their study focuses on epigenetic aging, a process that reflects how fast the body’s cells age based on DNA methylation changes (DNAm).Breast cancer is one of the most common cancers worldwide, with the risk increasing significantly after menopause. The researchers analyzed blood samples from postmenopausal, non-Hispanic white women. They discovered that those with an “older” biological age had a significantly higher risk of being diagnosed with breast cancer. The risk was even greater in women who had their ovaries removed before natural menopause, likely due to reduced estrogen levels, a hormone that plays a key role in aging and breast health.“Of note, in women with bilateral oophorectomy before natural menopause experiencing shorter lifetime estrogen exposure than those with natural menopause, epigenetic age accel substantially influenced BC development, independent of obesity status and exogeneous estrogen use.”The study also found that lifestyle factors influence epigenetic aging and breast cancer risk. Women with obesity experienced faster biological aging, which increased their risk of developing cancer. Meanwhile, hormone replacement therapy had varying effects depending on the type and duration of treatment.Early detection of breast cancer is crucial for effective treatment and survival. Traditional risk assessments—such as age, family history, and lifestyle habits—may not provide the full picture. This study suggests that adding a blood test to measure biological aging could help clinicians identify high-risk women earlier and offer personalized prevention strategies.With further research, this blood test could become a routine screening tool in women’s health check-ups. It may empower women to take proactive steps to reduce their breast cancer risk through healthy lifestyle choices, including maintaining a balanced diet, staying physically active, and considering appropriate hormone therapies under medical supervision.In conclusion, further studies are needed to validate these findings and explore their applicability to a broader population of women. However, this research presents a promising, non-invasive, and cost-effective approach to predicting breast cancer risk.DOI - https://doi.org/10.18632/aging.206169Corresponding author - Su Yon Jung - sjung@sonnet.ucla.eduVideo short - https://www.youtube.com/watch?v=g1tHojirvI8Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- January 16, 2025 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 22 on December 2, 2024, entitled “Less frequent skin ulcers among patients with Werner syndrome treated with pioglitazone: findings from the Japanese Werner Syndrome Registry.”Scientists from Chiba University in Japan and other institutions have discovered that the drug pioglitazone, commonly used to treat diabetes, may help prevent painful skin ulcers in people with Werner syndrome. Werner syndrome is a rare genetic condition that causes people to age faster than normal, leading to early gray hair, cataracts, and other age-related health problems. One of the most serious complications is skin ulcers, which affect nearly 70% of people with the disorder and can lead to severe pain, infections, and even amputations.The study, led by first author Kazuto Aono and corresponding author Masaya Koshizaka, looked at 51 patients with Werner syndrome from the Japanese Werner Syndrome Registry. Over half of the patients had skin ulcers, and those with ulcers were generally older and had higher blood pressure. The research team found that patients who took pioglitazone were much less likely to have ulcers, even after accounting for age.The research suggests that pioglitazone's ability to reduce inflammation helps wounds heal faster and prevents ulcers from forming. However, since the drug can cause side effects, like weaker bones, scientists recommend further studies to explore safer options, such as creams or gels made from pioglitazone that can be applied directly to the skin.“Nanostructured hybrid materials loaded with pioglitazone are also being developed for clinical use and may be useful as wound dressings for ulcer treatment.” Although the study shows promising results, the authors emphasize that more long-term studies are needed to confirm how effective the treatment is besides the exploration of other factors, like diet and exercise, that may also help reduce the ulcers.In conclusion, this study presents pioglitazone as a potential option to prevent skin ulcers in Werner syndrome patients. While further studies are needed, these findings provide hope for better treatments.DOI - https://doi.org/10.18632/aging.206161Corresponding author - Masaya Koshizaka - overslope@chiba-u.jpSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206161Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, Werner syndrome, skin ulcer, metformin, pioglitazon, progeroid syndromeAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- January 15, 2025 – A new priority #review was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) on January 12, 2025, entitled “Mikhail ‘Misha’ Blagosklonny’s enduring legacy in geroscience: the hyperfunction theory and the therapeutic potential of rapamycin.”This review, written by Dr. David A. Barzilai, from Geneva College of Longevity Science and Healthspan Coaching LLC, summarizes the outstanding scientific contributions of the late Dr. Mikhail "Misha" Blagosklonny, Founding Editor-in-Chief of Aging. Dr. Blagosklonny’s research changed how researchers and scientists think about aging by introducing a new theory and promoting the use of rapamycin, an mTOR inhibitor, to slow aging and extend healthy life. Published shortly after his passing, this review honors Dr. Blagosklonny’s work and highlights how it challenged the traditional belief that aging is caused mainly by accumulated damage in the body.Instead of describing aging as an accumulation of cellular damage, Dr. Blagosklonny’s Hyperfunction Theory redefined it as an ongoing biological process that goes into "overdrive" and leads to age-related diseases such as cancer, cardiovascular problems, and memory loss.He identified the mTOR pathway—an important growth signal in the body—as a key driver of this process. His research showed that by using rapamycin, which slows down mTOR activity, it is possible to reduce aging-related diseases and promote longer, healthier lives.Research supports many of Dr. Blagosklonny’s predictions about rapamycin’s benefits. Studies show that it can improve immune responses in older adults, making vaccines more effective. Other studies suggest rapamycin may help protect the heart, reduce harmful brain inflammation, and prevent the buildup of proteins linked to Alzheimer’s disease. Dr. Blagosklonny also proposed that rapamycin could reduce cancer risk by preventing excessive growth signals that contribute to tumor development.Believing in rapamycin’s potential as a “longevity drug," Dr. Blagosklonny advocated for its careful use with medical supervision and precise dosing. He called for further research and even envisioned “longevity clinics” where personalized anti-aging treatments could be provided. The review also highlights ongoing scientific efforts to refine rapamycin therapies and explore new options with fewer side effects.In conclusion, Dr. Blagosklonny has inspired a global shift toward viewing aging as a condition that can be managed rather than an inevitable decline. His research has left a legacy in the fields of geroscience, aging, and cancer prevention.“This contribution will undoubtedly be remembered in the coming decades and beyond as an innovative contribution to our theoretical grasp of the aging process and a foundation for exploring effective therapeutic approaches.”DOI - https://doi.org/10.18632/aging.206189Corresponding author - David A. Barzilai - david.longevity@gmail.comVideo short - https://www.youtube.com/watch?v=3iOcIqfQdyISubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout Aging-USThe journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- January 14, 2025 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 22 on November 26, 2024, entitled “When do the pathological signs become evident? Study of human mesenchymal stem cells in MDPL syndrome.”Researchers from the University of Rome Tor Vergata, Fondazione Policlinico Tor Vergata, Roma Tre University, and Meyer Children’s Hospital IRCCS have identified early cellular changes associated with Mandibular Hypoplasia, Deafness, Progeroid Features, and Lipodystrophy (MDPL) syndrome, a rare genetic aging disorder caused by a mutation in the POLD1 gene. MDPL leads to fat loss, distinct facial features, and metabolic disturbances. This study aimed to better understand how MDPL progresses at the cellular level.MDPL syndrome is extremely rare, with only a few documented cases worldwide, making it difficult to study. To investigate the disease, researchers Spitalieri Paola, Guerrieri Lara, Murdocca Michela, Di Cesare Silvia, Maccaroni Serena, Pecorari Rosalba, Nardone Anna Maria, Candi Eleonora, Colasuonno Fiorella, Gori Giulia, Traficante Giovanna, Novelli Giuseppe, and Sangiuolo Federica, converted skin cells from three female MDPL patients and two healthy donors into human induced pluripotent stem cells (hiPSCs). These hiPSCs were then transformed into mesenchymal stem cells (MSCs), cells that can form tissues like bone and fat, which are primarily affected in MDPL syndrome.The study revealed that MSCs from MDPL patients exhibited signs of premature aging much earlier than expected. The cells had irregular shapes, grew at a slower rate, and showed higher levels of cellular stress.“These cells differentiate with lower efficiency, proliferate more slowly and have abnormal mitochondrial activity with increased production of ROS. Furthermore, the telomeres show evident shortening.” All the findings suggest that aging-related changes may occur long before patients display visible symptoms of the disease. This highlights the need for early diagnosis and intervention, which could delay or even prevent the most debilitating effects of MDPL syndrome.In summary, this study offers new perspectives on the initial cellular impacts of MDPL, opening the door for the creation of novel treatments. The findings highlight the potential for personalized therapies and emphasize the critical role of lab-created hiPSCs in advancing research on rare genetic diseases and age-related conditions.DOI - https://doi.org/10.18632/aging.206159Corresponding author - Sangiuolo Federica - sangiuolo@med.uniroma2.itVideo short - https://www.youtube.com/watch?v=DLXD2ztPTm0Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206159Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, MDPL syndrome, MSCs, hiPSCs, POLD1 geneAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- January 8, 2025 – A new #research perspective was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 22 on December 18, 2024, entitled “Brown adipose tissue enhances exercise performance and healthful longevity.”Researchers from Rutgers New Jersey Medical School, Dorothy E. Vatner, Jie Zhang, and Stephen F. Vatner, evaluated the role of brown adipose tissue (BAT), a special type of fat that burns calories to generate heat, in improving exercise endurance and supporting healthy aging. Unlike regular white fat, which stores energy, brown fat helps the body stay warm and boosts metabolism. According to the authors, this process may also help protect against health conditions such as obesity, diabetes, and cardiovascular disease.This research perspective highlights key findings from multiple studies on BAT. While most studies have shown that exercise regulates BAT activation and increases BAT density, relatively few have demonstrated that BAT itself can directly increase exercise performance. One notable example involves RGS14 knockout mice, a genetically modified group known for their longer lifespan. When BAT from these mice was transplanted into regular mice, the recipients displayed improved running endurance just three days after the transplant. In contrast, brown fat from non-modified mice took much longer to produce similar improvements.These findings highlight the unique properties of BAT in enhancing physical performance. The researchers emphasized also that BAT improves blood circulation and reduces cellular stress, which may help combat age-related muscle loss, fatigue, and metabolic decline.The authors suggest that treatments designed to mimic the benefits of brown fat could lead to innovative approaches for improving energy levels, maintaining a healthy weight, and supporting heart health.“In view of the ability of BAT to mediate healthful longevity and enhance exercise performance, it is likely that a pharmaceutical analog of BAT will become a novel therapeutic modality.”In conclusion, continued research on this topic may lead to the development of promising new therapies that help older adults live more active lives while reducing the risk of chronic age-related conditions.DOI - https://doi.org/10.18632/aging.206179Corresponding author - Stephen F. Vatner - vatnersf@njms.rutgers.eduVideo short - https://www.youtube.com/watch?v=n1DvuR7owJQSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206179Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, brown adipose tissue, white adipose tissue, healthful longevity, exercise, regulator of G protein signaling 14About Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- January 7, 2025 – A new #research perspective was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 22 on December 9, 2024, entitled “Nuclear lipid droplets: a novel regulator of nuclear homeostasis and ageing.”In this article, Dr. Konstantinos Palikaras from the National and Kapodistrian University of Athens and Dr. Nektarios Tavernarakis from the University of Crete explore how tiny fat droplets, known as nuclear lipid droplets (nLDs), accumulate in the nucleus of cells as we age. Unlike regular lipid droplets, which store energy in the cytoplasm, these nuclear droplets may weaken the nucleus by disrupting critical cellular processes.The authors suggest that excessive buildup of nLDs could lead to nuclear instability and may be linked to metabolic conditions such as fatty liver disease, obesity-related disorders, and premature aging. This highlights the potential role of nLDs in cellular aging and age-related diseases.Previous research by the authors using Caenorhabditis elegans (C. elegans), a model organism commonly used to study aging, revealed the role of ATGL-1, an enzyme that regulates fat storage in the nucleus. When functioning properly, ATGL-1 helps maintain a healthy lipid balance. However, when it becomes inactive or overwhelmed, fat droplets build up around the nuclear lamina, making it more difficult for the cell to function properly.“These findings establish excessive nuclear lipid deposition as a key hallmark of aging, with profound implications for nuclear processes such as chromatin organization, DNA repair, and gene regulation.”The authors emphasize that lifestyle interventions, such as caloric restriction and better insulin regulation, can significantly reduce harmful nLD buildup, reinforcing the role of healthy metabolism in slowing cellular aging. They also call for further studies to understand how nLDs behave in human experimental models, particularly in patients with conditions like metabolic syndrome and progeria. A deeper understanding of these processes could lead to treatments designed to preserve cell health and delay age-related diseases.In summary, by presenting nuclear lipid droplets as potential therapeutic targets, this research perspective presents a new path for exploring treatments aimed at combating age-related diseases driven by lipid dysregulation.DOI - https://doi.org/10.18632/aging.206175Corresponding authors - Konstantinos Palikaras - palikarask@med.uoa.gr, and Nektarios Tavernarakis - tavernarakis@imbb.forth.grVideo short - https://www.youtube.com/watch?v=vuSLuDk8XjkSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206175Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, ATGL-1, HLH-30/TFEB, lipid droplet, non-linear optical phenomena, nucleusAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- January 2, 2025 – A new priority #research paper, featured as the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 22, was #published on December 29, 2024. The paper is titled “Cell-type specific epigenetic clocks to quantify biological age at cell-type resolution.”Researchers from the Chinese Academy of Sciences and Monash University developed a new way to measure biological aging in individual cell types. This new tool offers a more detailed understanding of how cells age, providing insights into diseases such as Alzheimer’s and liver pathologies, leading the way for more precise health assessments and targeted therapies.Biological age refers to how old a person’s body is biologically, which may differ from their actual age in years. Typically, biological age is estimated using “epigenetic clocks,” which rely on DNA methylation patterns—chemical marks linked to aging. Standard methods analyze all the cells from a specific tissue at once, making it difficult to understand the aging processes in the different cell types that constitute the tissue.To address this, researchers Huige Tong, Xiaolong Guo, Macsue Jacques, Qi Luo, Nir Eynon,m and Andrew E Teschendorff analyzed DNA samples from human brain and liver tissues to create a new analysis tool. With the help of advanced computer models, they studied changes in DNA methylation in samples from healthy and diseased individuals. By isolating biological aging within specific cell types, the team could better understand how these changes contribute to diseases like Alzheimer’s or liver conditions. The study revealed that certain brain cells, like neurons and glia, age faster in people with Alzheimer’s disease, suggesting that the aging of specific cell types plays a critical role in neurodegeneration. In liver diseases, such as fatty liver disease and obesity, the clock for liver cells showed signs of accelerated aging, making it a better tool than previous methods for detecting liver problems."We find that neuron and glia specific clocks display biological age acceleration in Alzheimer’s Disease with the effect being strongest for glia in the temporal lobe.” This new approach distinguishes the aging process within individual cell types from changes in the overall composition of cells in a tissue, offering a clearer view of how aging affects each specific cell type. This is crucial for identifying which cells are most affected by aging in certain diseases, guiding the development of targeted therapies. In conclusion, this study highlights the critical importance of precision in aging research, allowing deeper insights into the aging process and significant advancements in the prevention, diagnosis, and treatment of age-related diseases.DOI - https://doi.org/10.18632/aging.206184Corresponding author - Andrew E. Teschendorff - andrew@sinh.ac.cnVideo short - https://www.youtube.com/watch?v=FjJa5U2-AqQSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Imagine being 15 years old but having a body that shows signs of aging as if you are decades older. For some young people with sickle cell disease (SCD), this is a reality. A new study published in Volume 16, Issue 21 of Aging shows that SCD causes the body to age much faster than normal. The research not only explains why this happens but also points to new ways to help people with the disease live healthier, longer lives.What Is Sickle Cell Disease?SCD is a genetic condition that changes the shape of red blood cells. Instead of being round, like a doughnut, the cells become curved like a sickle (a farming tool). These misshapen cells struggle to move through blood vessels, often blocking blood flow and leading to pain, organ damage, and other health problems. Even with modern treatments, they can experience complications like those seen in older adults, such as weaker bones, frailty, and organ failure. In the study “Adolescents and young adults with sickle cell disease exhibit accelerated aging with elevated T-cell p16INK4a expression,” researchers wanted to understand why this happens and what it means for people with the disease.Full blog - https://aging-us.org/?p=6372Paper DOI - https://doi.org/10.18632/aging.206152Corresponding author - Samuel R. Wilson - samuel.wilson@med.unc.eduVideo short - https://www.youtube.com/watch?v=QXVdxBikaqgSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206152Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, sickle cell disease, p16, adolescents, young adultsAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- December 19, 2024 – We are pleased to announce that Dr. Marco Demaria, a leading expert in aging and cellular senescence, will join Aging (Aging-US) as Editor-in-Chief, starting January 1, 2025. Dr. Demaria will work alongside an esteemed Editorial Board.Dr. Demaria has an impressive background in aging research. He earned his PhD in Molecular Medicine from the University of Torino, Italy. In 2010, he joined the laboratory of Aging Founding Editor, the late Dr. Judith Campisi, at the Buck Institute for Research on Aging. There he developed cellular and animal models for studying cellular aging, also known as cellular senescence, and its role in tissue repair, cancer, and aging.Currently, Dr. Demaria leads DemariaLab, whose mission is “to extend human healthspan by pioneering discoveries in molecular and cellular mechanisms that regulate the aging process.” His groundbreaking research has significantly advanced our understanding of cellular senescence and its role in aging and age-related diseases. Dr. Demaria aims to develop new therapeutic approaches to create more effective treatments that mitigate the diseases and extend the healthspan. His work specifically focuses on interfering with the mechanisms of cellular senescence using genetic, pharmacological, and nutraceutical strategies.“My research is focused on understanding the molecular basis of age-related dysfunctions and disorders, and to identify new molecular and cellular targets to improve health and longevity.” - Marco DemariaHe is also a Full Professor at the European Research Institute for the Biology of Ageing (ERIBA), Director of the Mechanisms of Health, Ageing and Disease (MoHAD) at the University Medical Center Groningen (UMCG), President of the International Cell Senescence Association (ICSA), and Co-Founder of Cleara Biotech. Dr. Demaria also brings valuable editorial experience from his former positions as Editor-in-Chief of npj Aging and Editorial Board member of Aging Cell.All the above, combined with Dr. Demaria’s academic contributions, commitment, and expertise, align perfectly with Aging’s mission to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. For more information about Marco Demaria, PhD, please visit www.demarialab.com and follow him on X (Twitter) @marc_dema or on Bluesky @marcdema.bsky.social.About Aging-USPlease visit our website at https://www.Aging-US.com and connect with us on social media at:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- December 18, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 21 on November 22, 2024, entitled, “Anti-aging effect of extracellular vesicles from mesenchymal stromal cells on senescence-induced chondrocytes in osteoarthritis.”The study, authored by Jérémy Boulestreau, Marie Maumus, Giuliana Bertolino Minani, Christian Jorgensen, and Danièle Noël from the Institute for Regenerative Medicine and Biotherapy and Centre Hospitalier Universitaire de Montpellier, introduces a potential new therapy for osteoarthritis. This therapy uses tiny particles called extracellular vesicles (EVs), derived from fat tissue, to repair damage caused by aging cells in the joints, slowing the progression of osteoarthritis and restoring joint health.Osteoarthritis, the most common joint disorder in older adults, occurs when cartilage breaks down, leading to inflammation, stiffness, and pain. One major contributor to it is cellular senescence, a process where cells stop dividing and release harmful substances that worsen inflammation and damage joint tissues.In this study, the researchers showed that EVs from fat-derived mesenchymal stromal cells (ASC-EVs) decreased the harmful effects of senescent cells. ASC-EVs showed strong therapeutic effects in both cellular and mouse preclinical studies. They reduced inflammation and DNA damage markers in cells derived from human joints and improved cellular health. In mice with osteoarthritis, the vesicles restored joint balance, reduced cartilage damage, and preserved joint function for weeks.The findings highlight the potential of regenerative medicine, which uses the body’s own mechanisms to repair damage. By targeting the aging process in joint cells, this therapy offers a breakthrough for osteoarthritis treatment. Millions of people suffering from joint pain, inflammation, and reduced mobility could benefit from this innovative approach.In the future, the researchers plan to explore ways to enhance the therapy, including whether repeated treatments could provide even longer-lasting benefits. These could lead to new options in treating osteoarthritis and other age-related conditions.“In addition to their anti-inflammatory and regenerative properties, our study confirms that ASC-EVs may be a relevant option for future clinical applications in degenerative diseases, such as OA, which are increasing with the population aging.”In conclusion, this research offers a promising regenerative therapy for osteoarthritis, with the potential to improve the quality of life for millions of older adults.DOI - https://doi.org/10.18632/aging.206158Corresponding author - Danièle Noël - daniele.noel@inserm.frVideo short - https://www.youtube.com/watch?v=06qw2nR3ovYSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206158Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- December 17, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 21 on November 29, 2024, entitled, “Thermotherapy has sexually dimorphic responses in APP/PS1 mice.”Researchers Samuel A. McFadden, Mackenzie R. Peck, Lindsey N. Sime, MaKayla F. Cox, Erol D. Ikiz, Caleigh A. Findley, Kathleen Quinn, Yimin Fang, Andrzej Bartke, Erin R. Hascup, and Kevin N. Hascup from Southern Illinois University School of Medicine, found that raising body temperature through heat therapy improved memory in male mice with Alzheimer’s disease but worsened memory in females. These findings emphasize the importance of personalized treatments based on sex-specific responses to therapy.Alzheimer’s disease (AD) is a progressive brain disorder characterized by memory loss and confusion. It is caused by the buildup of harmful proteins like beta-amyloid, which damages brain cells over time. In this study, genetically modified mice predisposed to develop Alzheimer disease (APP/PS1 mice) were kept in warmer environments for six months to explore the effects of heat therapy on memory and metabolism.The results revealed that male mice benefited from the therapy, with improved memory and reduced levels of beta-amyloid in their brains. Female mice, however, experienced a worsening of memory, likely due to increased inflammation triggered by the heat therapy. Inflammation, where the immune system is hyperactivated, can harm brain cells and worsen Alzheimer's disease symptoms.“Thermotherapy improved spatial navigation in male C57BL/6 and APP/PS1 mice, with the later attributed to reduced hippocampal soluble amyloid-β (Aβ)42. Female APP/PS1 mice exhibited worse spatial memory recall after chronic thermotherapy.”Heat therapy is already known to provide general health benefits, such as improving heart health and regulating blood sugar. This study suggests it could also offer a simple, non-drug approach to slowing Alzheimer’s progression, particularly for men. Unlike exercise, which offers similar benefits, heat therapy is accessible for people who are weak or unable to engage in physical activity.While these findings are promising, the researchers emphasize the need for more studies to understand why men and women respond so differently to heat therapy. Future research should also investigate whether the results can be replicated in humans and how the therapy can be tailored to individual needs.In conclusion, heat therapy could present a safe and practical option for managing Alzheimer’s disease, particularly in men. However, the observed gender differences highlight the importance of further research to refine its therapeutic potential and ensure it benefits everyone.DOI - https://doi.org/10.18632/aging.206156Corresponding author - Kevin N. Hascup - khascup49@siumed.eduVideo short - https://www.youtube.com/watch?v=IeMPHss4vj8Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- December 11, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 21 on November 14, 2024, entitled, “Adolescents and young adults with sickle cell disease exhibit accelerated aging with elevated T-cell p16INK4a expression.”Researchers Samuel R. Wilson, Natalia Mitin, Vanessa L. Ayer Miller, Andrew B. Smitherman, and Marcus A. Carden, from the University of North Carolina at Chapel Hill, Sapere Bio, Campbell University, and Cogent Biosciences have discovered that young people with sickle cell disease (SCD) exhibit signs of accelerated biological aging compared to those without the disease. By measuring levels of p16INK4a, a key marker of cellular aging, the team found significantly higher levels in individuals with SCD. Remarkably, some participants showed biological aging equivalent to an additional 43 years. These findings suggest that SCD may drive faster aging in the body, offering new insights into the disease's long-term impact.Sickle cell disease (SCD) is a genetic condition primarily affecting individuals of African or Mediterranean descent. While treatments have advanced, people with SCD often face significant health challenges, including complications that mimic the effects of aging.Cellular aging, or senescence, occurs when cells stop dividing yet continue to send harmful signals that damage surrounding tissues. Researchers believe this process happens at an accelerated rate in people with SCD, underscoring the importance of finding ways to slow it down and mitigate its impact.The study compared p16INK4a levels in 18 adolescents and young adults with SCD to 27 healthy people of the same age. The results showed that even the youngest participant with SCD had higher levels of this aging marker than anyone in the non-SCD group. “Our youngest participant, a 15-year-old with SCD, had a higher p16 expression than all the comparators, underscoring the early rise of p16 expression in this population.”The researchers believe this faster aging could be caused by the chronic inflammation, lack of oxygen, and stress on the body associated with SCD. Along with managing the symptoms of the disease, SCD patients also face a higher risk of aging-related problems like organ damage and physical decline much earlier in life.The findings suggest that measuring p16INK4a levels could help clinicians identify patients at risk for these problems earlier and offer targeted care. The study also opens the door to new treatments, such as drugs that aim to remove old, damaged cells. These therapies could potentially slow down the aging process.Further research is essential to confirm these findings and to gain a deeper understanding of how to support SCD patients effectively. Larger, long-term studies could investigate whether therapies targeting cell aging can help prevent complications and improve the quality of life for individuals with SCD.In conclusion, this study marks an important step in understanding how SCD accelerates aging and offers new ways to improve the lives of those living with the condition.DOI - https://doi.org/10.18632/aging.206152Corresponding author - Samuel R. Wilson - samuel.wilson@med.unc.eduVideo short - https://www.youtube.com/watch?v=QXVdxBikaqgAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com.MEDIA@IMPACTJOURNALS.COM
Sleep is essential for everyone, but for those living with dementia, it is vital for better health and quality of life. Addressing sleep problems in dementia care is a crucial step toward improving life for both patients and caregivers.Dementia and SleepSleep is critical for brain health and well-being, but it is often a struggle for people with dementia. Dementia, a condition that affects memory, thinking, and daily life, is frequently complicated by other health issues like heart disease, diabetes, and anxiety. On top of these challenges, sleep problems such as insomnia and sleep apnea are common, making life even harder for patients and their caregivers. Addressing sleep issues is key to improving the lives of people with dementia and easing the burden on their support systems. Recognizing this need, researchers Upasana Mukherjee, Ujala Sehar, Malcolm Brownell, and P. Hemachandra Reddy from Texas Tech University Health Sciences Center conducted an extensive review. Published in Aging, Volume 16, Issue 21, their work aims to update healthcare professionals on these issues and promote new practices in dementia care.The Study: Update on Sleep and Dementia’s Connection“Sleep deprivation in dementia comorbidities: focus on cardiovascular disease, diabetes, anxiety/depression and thyroid disorders” is a comprehensive review that explores the connections between sleep disturbances, dementia, and related conditions like heart disease, diabetes, and anxiety.Full blog - https://aging-us.org/2024/12/the-hidden-link-between-sleep-and-dementia-how-better-rest-can-improve-lives/Paper DOI - https://doi.org/10.18632/aging.206157Corresponding author - P. Hemachandra Reddy - hemachandra.reddy@ttuhsc.eduVideo short - https://www.youtube.com/watch?v=lrrrXabMjjMSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206157Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, dementia and comorbidities, sleep disturbances, cardiovascular disease, diabetes, thyroid disorders, anxiety, insomnia, sleep apneaAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- December 10, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 21 on November 18, 2024, entitled, “Prostaglandin E2 regulates senescence and post-senescence neoplastic escape in primary human keratinocytes.”Researchers Elise Srour, Nathalie Martin, Claire Drullion, Clémentine De Schutter, Joëlle Giroud, Adrien Pioger, Julie Deslé, Laure Saas, Joe Nassour, Julien Théry, Gauthier Decanter, Nicolas Penel, Chantal Vercamer, Clara Salazar-Cardozo, Corinne Abbadie, and Olivier Pluquet from CNRS, University of Lille, the Oscar Lambret Center, and the University of Colorado School of Medicine have revealed how a molecule called Prostaglandin E2 (PGE2) influences skin aging and cancer risk.Their study shows that PGE2 not only drives skin cells to age but also enables some of these aging cells to bypass natural limits and develop into pre-cancerous cells. This process provides insights into why older skin is more susceptible to cancer.The study focused on keratinocytes, the primary cells in the outer layer of the skin. As these cells age, they enter a state called senescence, where they stop dividing to prevent damaged cells from turning cancerous. While this process typically serves as a protective mechanism, the researchers found that, in certain cases, some senescent cells can escape this state, re-enter the cell cycle, and acquire characteristics of early cancer. By examining keratinocytes from donors of different ethnicities and ages, the researchers identified the PTGS2/PGE2/EP4 pathway as a key driver of this escape process.The researchers show that blocking PGE2 or its associated pathway reduced the chances of aged cells becoming precancerous. This suggests that drugs targeting this pathway, including some anti-inflammatory medications already in use, might be repurposed to slow skin aging and prevent early-stage skin cancers. Additionally, the study also found that PGE2 levels increase in the skin as it ages, further supporting its role in skin health and disease."These results indicate that the PTGS2/PGE2/EP4 pathway is required to induce and maintain the senescent phenotype of NHEKs, and that PGE2 level is a potential determinant of the initial steps of the age-related oncogenic process."The team also highlighted the broader implications of their work. The PTGS2/PGE2/EP4 pathway is not only linked to skin health but also to age-related inflammation, a condition that contributes to several diseases. By addressing this pathway, researchers hope to address not only skin aging but other health challenges linked to aging and chronic inflammation.In conclusion, this study reveals important molecular drivers of skin aging and early cancer, leading the way for new approaches that can promote healthier skin.DOI - https://doi.org/10.18632/aging.206149Corresponding author - Olivier Pluquet - olivier.pluquet@ibl.cnrs.frVideo short - https://www.youtube.com/watch?v=4aNf3X2RJSwAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- December 4, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 21 on November 22, 2024, entitled, “The effects of young and aged, male and female megakaryocyte conditioned media on angiogenic properties of endothelial cells.”Researchers Murad K. Nazzal, Hanisha L. Battina, Nikhil P. Tewari, Sarah L. Mostardo, Rohit U. Nagaraj, Donghui Zhou, Olatundun D. Awosanya, Saveda K. Majety, Sue Samson, Rachel J. Blosser, Ushashi C. Dadwal, Patrick L. Mulcrone, and Melissa A. Kacenaat from Indiana University School of Medicine and Richard L. Roudebush Veterans' Administration Medical Center, have uncovered how certain bone marrow cells, called megakaryocytes (MKs), promote the growth of new blood vessels (angiogenesis) to aid in bone healing. Their findings help explain why healing slows with age and offer insights into potential treatments to accelerate fracture recovery in older adults.Broken bones are common in older adults, and slower healing can lead to complications and longer hospital stays. Accelerating the healing process could significantly improve the quality of life for millions.In this study, researchers investigated the effects of substances secreted by MKs, collected from young and older male and female mice. These substances, known as conditioned media (CM), were tested for their ability to stimulate the growth and function of endothelial cells (EC), which form the building blocks of blood vessels. Blood vessels play a critical role in healing by delivering oxygen and nutrients to damaged areas, making angiogenesis a vital part of the recovery process.The results showed that CM from younger MKs mice was more effective at helping blood vessels grow. Interestingly, MKs from female mice performed better than those from males, regardless of age. For example, substances from female MKs mice boosted blood vessel growth by over 115% and significantly improved the movement of cells needed for healing. The researchers also studied changes in genes related to blood vessel growth, and found that aging affects how these genes work. These changes may explain why older people heal more slowly after breaking a bone. “An understanding of which factors regulate which mechanisms of EC functionality may allow for isolation of one or a few factors that influence EC migration changes with aging, resulting in the development of targeted therapy to improve EC migration, subsequent angiogenesis, and fracture healing.” In conclusion, this research paves the way for developing new therapies to help older individuals recover from fractures more quickly, reducing pain and improving mobility. One potential approach could involve creating treatments that replicate the effects of MKs from younger individuals or isolating the specific substances that promote blood vessel growth. This represents an important step toward addressing the growing challenge of delayed healing in an aging population.DOI - https://doi.org/10.18632/aging.206077Corresponding authors - Patrick L. Mulcrone - pamulcro@iu.edu, and Melissa A. Kacena - mkacena@iupui.eduAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com.MEDIA@IMPACTJOURNALS.COM
In the this episode of the Longevity & Aging Series, Dr. Meesha Dogan, CEO of Cardio Diagnostics, joined host Dr. Evgeniy Galimov to discuss her pioneering work in #artificialintelligence, #epigenetics, and #genetics in developing next-generation DNA-based tests for preventing and managing #cardiovasculardisease globally.Video interview - https://www.youtube.com/watch?v=9yPzl10vDlQVideo transcription - https://www.aging-us.com/interviews/longevity-aging-series-s2-e4-dr-meesha-doganCardio Diagnostics - https://cdio.ai/About Evgeniy GalimovEvgeniy Galimov, Ph.D., is a researcher and data scientist with experience in research in ageing and age-related diseases. He studied bioengineering and bioinformatics and received PhD from Lomonosov Moscow State University. Evgeniy’s early research was devoted to molecular mechanisms of cancer, atherosclerosis and neurodegeneration, later he switched to modelling the evolution of ageing and published several papers about it. Evgeniy also has start-up experience and applied machine learning to predict lifespan in model organisms and coronary heart disease in patients based on blood biomarkers. Additionally, Dr. Galimov developed a deep-learning model capable of classifying lifespan in C. elegans and identifying morphological features that influence the prediction. Currently, Dr. Galimov is engaged in Real World Evidence health data research focused on age-related pathologies.About Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- December 2, 2024 – A new #review was #published on the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 21, titled, “Sleep deprivation in dementia comorbidities: focus on cardiovascular disease, diabetes, anxiety/depression and thyroid disorders.”The review, authored by Upasana Mukherjee, Ujala Sehar, Malcolm Brownell, and P. Hemachandra Reddy from Texas Tech University Health Sciences Center, compiles findings from recent studies on how sleep problems—such as insomnia, sleep apnea, and disrupted sleep cycles—can worsen dementia and accelerate cognitive decline. It also emphasizes the profound impact of these sleep disorders on caregivers, who often face burnout and emotional stress. Dementia is a condition that significantly impairs the ability to think, remember, and make decisions, making everyday life increasingly difficult to manage. Sleep problems are a major challenge for individuals with dementia, with more than half experiencing disturbed sleep. These disturbances include difficulty falling asleep, staying asleep, or engaging in nighttime wandering.Such issues go beyond causing fatigue—they accelerate memory loss, increase confusion, and raise the risk of behavioral symptoms like agitation. Addressing sleep challenges is critical to improving quality of life for both patients and their caregivers. Caregivers, who often support loved ones around the clock, face significant stress when dealing with these sleep disorders.“This situation creates a vicious cycle where caregiver distress exacerbates patient symptoms, further increasing the burden on caregivers.”This review also explores how other illnesses, common in older adults with dementia, worsen sleep disturbances. Conditions such as diabetes, thyroid dysfunction, heart disease, and anxiety disrupt sleep, and poor sleep then worsens both the dementia and the underlying illnesses. For instance, untreated sleep apnea can significantly accelerate cognitive decline in people with dementia.To improve sleep for dementia patients, the authors recommend holistic approaches that address both sleep disturbances and related health conditions. Simple changes, such as establishing a regular bedtime routine, reducing nighttime noise, and encouraging daytime physical activity, can significantly enhance sleep quality.Non-pharmacological treatments, including light therapy and cognitive behavioral therapy for insomnia, have also shown promise. Managing coexisting conditions such as diabetes or anxiety can help reduce the severity of sleep issues. The authors emphasize the need for more research into targeted, multidisciplinary approaches to effectively manage sleep disturbances, improve patient well-being, and reduce caregiver stress.In conclusion, this review highlights the critical need for a more comprehensive approach to dementia care. Improving sleep could slow the progression of dementia, reduce caregiver stress, and enhance the quality of life for everyone involved. As dementia cases rise worldwide, addressing sleep issues will become an increasingly important aspect of care.DOI - https://doi.org/10.18632/aging.206157Corresponding author - P. Hemachandra Reddy - hemachandra.reddy@ttuhsc.eduVideo short - https://www.youtube.com/watch?v=lrrrXabMjjMSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.Please visit our website at https://www.Aging-US.com.MEDIA@IMPACTJOURNALS.COM
Dr. Fabienne Hershkowitz Sikron from the Meuhedet Health Maintenance Organization (HMO) in Tel-Aviv, discusses a #research paper she co-authored that was #published in Volume 16, Issue 20 of Aging, entitled “Development and validation of an electronic frailty index in a national health maintenance organization.”DOI - https://doi.org/10.18632/aging.206141Corresponding Author - Fabienne Hershkowitz Sikron - fabian_hershkowitz@meuhedet.co.ilVideo interview - https://www.youtube.com/watch?v=pc9_ByZ1_ewVideo transcription - https://www.aging-us.com/interviews/validating-electronic-frailty-index-in-national-health-systemAbstractBackground: Frailty constitutes a major factor that puts the elderly at risk of health and functional deterioration.Objectives: To develop and validate an Electronic Frailty Index based on electronic data routinely collected in the HMO.Study design and setting: A retrospective cohort of the HMO members.Participants: 120,986 patients, aged 65 years and over at the beginning of 2023.Predictors: A cumulative frailty index including 36 medical, functional, and social deficits.Outcomes: One-year all-cause mortality or hospitalization.Statistical analysis: One-year hazard ratios were estimated for composite outcome of mortality or hospitalization using multivariable hierarchical Cox regression.Results: The mean EFI score increased with the Social Security Nursing Benefit. Compared to fit patients, mild, moderate, and severe frailty patients had 2.07, 3.35, and 4.4-fold increased risks of mortality or hospitalization, after controlling for covariates.Conclusions: The findings showed that the Electronic Frailty Index version we created is valid in predicting mortality or hospitalization. In addition, the Electronic Frailty Index converged with an independent measurement produced by National Social Security.Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206141Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, frailty, older people, electronic frailty index, electronic health record, health maintenance organizationAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- November 26, 2024 – This #editorial was #published by Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) in Volume 16, Issue 17, titled, “The silent protector: Nucleoporin93’s role in vascular health.”Written by Julia Michalkiewicz, Tung D. Nguyen, and Monica Y. Lee from The University of Illinois at Chicago College of Medicine, this editorial highlights the critical role of a protein called Nucleoporin93 (Nup93) in maintaining blood vessel health as we age. The authors review new research suggesting that Nup93 could be a key target for treatments to prevent or reduce aging-related diseases, including heart disease and stroke.Cardiovascular diseases remain the leading causes of death worldwide, with aging identified as a major risk factor. Vascular health declines as endothelial cells (EC)—the protective lining of blood vessels—lose their functionality with age. This deterioration leads to inflammation, arterial stiffening, and reduced blood flow, significantly increasing the risk of life-threatening diseases. The authors underscore the urgent need to uncover the molecular mechanisms driving these changes.Nup93 plays an essential role within nuclear pore complexes (NPCs)—gateways that regulate molecular exchanges between the cell nucleus and cytoplasm. Age-related loss of Nup93 disrupts this delicate system, weakening endothelial cells function and accelerating vascular aging. Researchers identified Nup93 as a crucial protector of endothelial health, preventing harmful protein build-ups such as Yes-associated protein (Yap), a known driver of inflammation and cellular aging. Excitingly, scientists have discovered that restoring Nup93 levels in damaged endothelial cells can reverse some of these harmful effects. They also found that blocking Yap can prevent issues caused by low Nup93 levels. These findings highlight the potential for new medicines or therapies to protect blood vessels as people age. The authors propose that future treatments could involve delivering Nup93 directly to damaged blood vessels to restore their health and prevent cardiovascular diseases. They emphasize the importance of further research to uncover why Nup93 levels decrease with age and how restoring it might improve blood vessel function. “These latest discoveries provide a fresh and innovative perspective of EC biology, highlighting NPCs as major regulators of EC health that may underlie mechanisms of vascular aging and disease progression.”In conclusion, the editorial encourages scientists to focus on understanding how endothelial cells stay strong and the role of NPCs in keeping blood vessels healthy. This research could lead to important breakthroughs in slowing down aging and improving people's quality of life.DOI - https://doi.org/10.18632/aging.206097Corresponding author - Monica Y. Lee - monicaYL@uic.eduVideo short - https://www.youtube.com/watch?v=as6opv9_FYMSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Drs. Alex Zhavoronkov, Morten Scheibye-Knudsen, Evelyne Bischof and Dominika Wilczok discuss a research paper they co-authored that was published as the cover of Aging (Aging-US) Volume 16, Issue 20, entitled, “Longevity biotechnology: bridging AI, biomarkers, geroscience and clinical applications for healthy longevity.”DOI - https://doi.org/10.18632/aging.206135Corresponding Authors - Yu-Xuan Lyu - lvyx@sustech.edu.cn, Alex Zhavoronkov - alex@insilico.com, Morten Scheibye-Knudsen - mscheibye@sund.ku.dk, and Daniela Bakula - bakula@sund.ku.dkVideo interview - https://www.youtube.com/watch?v=2nqvJ8cn5FgVideo transcript - https://www.aging-us.com/interviews/longevity-biotechnology-ai-biomarkers-geroscience-for-healthy-agingSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206135Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, biotechnology, artificial intelligence, healthy longevityAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Aging (Aging-US) was a proud sponsor of the “Future of Aging Research Mixer 2024” hosted by the Aging Initiative at Harvard University on November 15 in Boston. This event united a vibrant community of students, researchers and technologists, all driven by a shared mission: advancing innovations in aging research and longevity science.Key Highlights from the Future of Aging Research Mixer 2024The event kicked off with inspiring opening remarks and a keynote by George Church, professor at Harvard Medical School, founding member of the Wyss Institute, and co-founder of over 50 biotech companies. He was joined by Kat Kajderowicz, an MIT PhD student and Principal at age1. Together, they highlighted the interdisciplinary nature of aging research and its immense potential to drive transformative advancements.Jesse Poganik, HMS Instructor in Medicine and Executive Co-Director of the Biomarkers of Aging Consortium, discussed the evolution of aging science and the critical role biomarkers play in understanding aging processes and assessing the effectiveness of interventions aimed at slowing or reversing age-related changes.Alex Colville, co-founder and general partner at age1, explained how venture capital can accelerate innovation in longevity biotechnology. He shared career advice for aspiring researchers and paid tribute to his mentor, Dr. David Sinclair, a pioneer in aging research.These talks highlighted the importance of mentorship, interdisciplinary collaboration, and investment in driving progress in the aging research field.Read the full summary - https://aging-us.org/2024/11/agings-commitment-to-advancing-research-sponsoring-the-future-of-aging-research-mixer/About Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- November 20, 2024 – This #review was #published by Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), in Volume 16, Issue 17, titled, “A systematic review of phenotypic and epigenetic clocks used for aging and mortality quantification in humans.”This systematic review by Brandon Warner, Edward Ratner, Anirban Datta and Amaury Lendasse from Verseon International Corporation, University of Houston and Missouri University of Science and Technology, explores how biological clocks measure aging and predict mortality. These clocks are tools scientists use to track the body's aging process by identifying specific changes over time.This review analyzes 33 biological clocks proposed over the last decade, offering key insights into their design, accuracy, and clinical applications. The study categorizes these clocks into two types: epigenetic clocks, which track cellular aging through DNA changes, and phenotypic clocks, which assess physical biomarkers like blood pressure and cholesterol. These findings highlight the transformative potential of biological clocks in aging research and preventive healthcare.Epigenetic clocks have demonstrated impressive precision in estimating chronological age by analyzing DNA methylation, a key marker of cellular aging. These tools are also linked to age-related diseases, offering valuable insights into the aging process. Phenotypic clocks, which rely on common clinical measures, have been shown to better predict mortality and health outcomes. As the study highlights: “Phenotypic clocks have shown to be better predictors of mortality than chronological age and do so using easily measurable clinical variables.” Their affordability and ease of implementation make them especially practical for healthcare settings.The review also explores how advancements in technology, such as artificial intelligence and machine learning, are enhancing the accuracy and utility of these clocks. For example, newer models now use neural networks to improve predictive performance and identify key aging biomarkers.Understanding biological age can help detect diseases earlier, tailor interventions, and encourage lifestyle changes to slow aging. By providing a clearer picture of individual aging processes, these clocks could lead the way toward personalized healthcare and improved health outcomes. The researchers call for further studies to make epigenetic clocks more affordable and expand the integration of phenotypic clocks into routine healthcare.In conclusion, this review underscores the transformative potential of biological clocks to redefine our understanding and management of aging. By addressing gaps in current research, it paves the way for future advancements in aging science and healthcare.DOI - https://doi.org/10.18632/aging.206098Corresponding author - Brandon Warner - bwarner@verseon.comVideo short - https://www.youtube.com/watch?v=rrqk5HrljQ0Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- November 19, 2024 – A new #review was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), on October 29, 2024, Volume 16, Issue 20, titled, ”Brain aging and Alzheimer’s disease, a perspective from non-human primates.“In the review, Ferrer Isidro from the University of Barcelona and Reial Acadèmia de Medicina de Catalunya, explores the differences in brain aging and Alzheimer’s disease between humans and their closest evolutionary relatives, such as chimpanzees, baboons, and macaques. The study highlights that while humans are uniquely susceptible to severe cognitive decline and memory loss caused by Alzheimer’s disease, non-human primates typically experience only mild changes as they age.Alzheimer’s affects over 50 million people worldwide, making it crucial to understand how aging impacts the brain. This review sheds light on the differences between humans and non-human primates and reveals that while brain aging in primates involves some structural and protein changes, it does not result in the toxic protein deposits that drive Alzheimer’s in humans.In humans, harmful tau protein deposits, known as tau tangles, appear early in life and spread widely through the brain, which damages cells and contributes to memory loss. In non-human primates, tau tangles are rare and typically confined to small regions. While primates may develop beta-amyloid deposits—fragments derived from amyloid precursor protein—these deposits are less toxic and do not interact with tau tangles to trigger Alzheimer’s-like symptoms. Aging primates experience only mild memory or behavioral changes, avoiding the severe cognitive decline and dementia often seen in humans.Humans’ unique vulnerability to Alzheimer’s may be linked to traits that emerged through evolution, including larger brains, longer lifespans, and higher cognitive abilities. These adaptations may have come at a cost, making human brains more susceptible to aging-related damage.This review also suggests that tau tangles play a more critical role in Alzheimer’s progression than previously thought. While traditional treatments focus on targeting beta-amyloid deposits, this research highlights the need to shift attention to tau pathology. The work challenges the widely accepted amyloid cascade hypothesis, which suggests that beta-amyloid is the main driver of Alzheimer’s. Instead, it points to tau tangles as the initial and most damaging change in human brains. This insight could encourage new treatments that focus on preventing or reducing tau deposits.The findings also emphasize the value of studying non-human primates to understand why their brains are more resistant to severe aging-related damage. By identifying protective mechanisms in primates, researchers may discover new strategies to delay or prevent Alzheimer’s in humans. “These observations show that human brain aging differs from brain aging in non-human primates, and humans constitute the exception among primates in terms of severity and extent of brain aging damage.”In conclusion, this review not only improves our understanding of why humans are uniquely vulnerable to Alzheimer’s disease but also opens new avenues for exploring innovative strategies to combat aging-related brain damage in humans.DOI - https://doi.org/10.18632/aging.206143Corresponding author - Ferrer Isidro - 8082ifa@gmail.comVideo short - https://www.youtube.com/watch?v=kUN88OSsJesAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.Please visit our website at https://www.Aging-US.com and connect with us on social media.MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- November 13, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), on October 25, 2024, Volume 16, Issue 20, titled, ”Canonical ligand-dependent and non-canonical ligand-independent EphA2 signaling in the eye lens of wild-type, knockout, and aging mice.“Researchers from the School of Optometry and Vision Science Program at Indiana University have uncovered important new insights into how the aging affects the eye lens and contributes to cataract formation, a condition impacting millions worldwide. This study focuses on the EphA2 protein, traditionally associated with cancer, which researchers have now identified as essential for maintaining the lens’s clarity and function as it ages.Cataracts are the leading cause of blindness worldwide, primarily affecting older adults, yet the precise biological mechanisms behind their formation remain unclear. This research sheds light on the role of the EphA2 protein receptor in the eye lens, revealing that it operates through two distinct signaling pathways: a canonical (ligand-dependent) and a non-canonical (ligand-independent) pathway. By studying various groups of mice, including those lacking the EphA2 protein receptor and its ligand partner ephrin-A5, scientists observed how these signaling pathways change with age, affecting the organization and maturation of lens cells.Researchers Jenna L. Horner, Michael P. Vu, Jackson T. Clark, Isaiah J. Innis, and Catherine Cheng observed that EphA2’s canonical signaling, which organizes lens cells, remains stable in aging lens tissue, particularly in epithelial cells. They found that the non-canonical signaling pathway—previously associated primarily with aggressive cancer cells—increases with age in normal lens cells. This increase suggests that non-canonical signaling plays a crucial role in helping lens fiber cells mature and maintain their structure over time.“Here, we report that canonical ligand-mediated EphA2 activation is restricted to the lens epithelial cells and show the first evidence of physiological non-canonical EphA2 activity in a normal tissue.”This understanding could lead to new therapies targeting EphA2 to delay or prevent cataracts.In conclusion, this study represents a significant advance in understanding the cellular mechanisms behind lens aging and cataract development, potentially paving the way for new non-surgical cataract treatments.DOI - https://doi.org/10.18632/aging.206144Corresponding author - Catherine Cheng - ckcheng@iu.eduVideo short - https://www.youtube.com/watch?v=3ScKLgOxQvASign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206144Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, fiber cells, epithelial cells, Y588, Y589, S897, phosphorylation, maturation, ephrinAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- November 12, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), on October 24, 2024, Volume 16, Issue 20, titled, "Development and validation of an electronic frailty index in a national health maintenance organization."The study, led by researchers Fabienne Hershkowitz Sikron, Rony Schenker, Yishay Koom, Galit Segal, Orit Shahar, Idit Wolf, Bawkat Mazengya, Maor Lewis, Irit Laxer and Dov Albukrek from Meuhedet Health Maintenance Organization (HMO) in collaboration with colleagues from the Joint-Eshel Organization and the Israeli Ministry of Health, introduces the Meuhedet Electronic Frailty Index (MEFI)—a digital tool designed to assess frailty in older people and identify those most at risk for serious health outcomes, such as hospitalization or death.As people live longer, identifying those at higher risk for health complications is essential to maintaining quality of life in older age. Frailty, a condition marked by increased vulnerability to adverse health outcomes, has emerged as a crucial predictor of health deterioration in older people. While frailty assessment tools exist, this study adapts and validates an Electronic Frailty Index (EFI) tailored specifically to Israeli data and healthcare infrastructure, enabling more targeted and culturally relevant assessments.The MEFI was developed using data from 120,986 individuals aged 65 and older, comprising different indicators, including physical, social, and cognitive deficits. The index classifies individuals as "fit," "mildly frail," "moderately frail," or "severely frail" and is integrated into Israel’s electronic health records system. Researchers found that patients with higher MEFI scores faced significantly increased risks of hospitalization or mortality within one year, with risk levels rising fourfold for the most frail compared to those classified as fit. According to the authors, “The findings also showed that the MEFI version we created is valid in predicting mortality or hospitalization and had better predictive accuracy compared to CCI,” underscoring its reliability in assessing health risks. This integration enables Meuhedet HMO to implement proactive and preventive care measures across its network.Beyond predicting hospitalization and mortality, the MEFI’s alignment with Israel’s National Social Security benefit system reinforces its validity and practical use. As the authors note, “As a health maintenance organization, our mandate is to help our patients live longer and better. Using the MEFI as part of routine primary care may help us achieve this goal.” By focusing on early intervention for those most at risk, MEFI could significantly impact health maintenance costs and enable clinicians to allocate resources more effectively.This new EFI version positions Israel at the forefront of frailty research, and its success could pave the way for other countries with similar healthcare systems to adopt or adapt the approach. Future steps include integrating MEFI as a routine part of primary care in Israel to ensure timely intervention and support as patients age.In summary, MEFI is a powerful tool that empowers Israel’s healthcare system to identify and support older adults most in need, marking a significant advancement in caring for an aging population.DOI - https://doi.org/10.18632/aging.206141Corresponding Author - Fabienne Hershkowitz Sikron - fabian_hershkowitz@meuhedet.co.ilVideo short - https://www.youtube.com/watch?v=HxIDuGI1cGcPlease visit our website at https://www.Aging-US.com.MEDIA@IMPACTJOURNALS.COM
Imagine a future where we not only live longer but stay healthy throughout those extra years. Thanks to recent breakthroughs in biotechnology and artificial intelligence (AI) in healthcare, this vision is closer to becoming a reality.Advancements in Aging ResearchAging research has made significant progress in recent years by combining disciplines like biology, technology, and medicine to tackle the challenges of extending healthspans and reducing age-related diseases. While people today live longer than ever before, extending our “healthspan”—the years we stay active and illness-free—remains challenging. AI and health biomarkers (biological indicators of our body’s condition) are now key tools in the pursuit of longer, healthier lives.In a recent paper, led by corresponding authors Yu-Xuan Lyu from Southern University of Science and Technology Shenzhen; Alex Zhavoronkov from Insilico Medicine AI Limited, Masdar City, Abu Dhabi; Morten Scheibye-Knudsen and Daniela Bakula from the Center for Healthy Aging, University of Copenhagen, along with numerous other collaborators, the transformative potential of AI in aging research was explored. The research paper, titled “Longevity biotechnology: bridging AI, biomarkers, geroscience and clinical applications for healthy longevity,” was published as the cover paper in Aging’s Volume 16, Issue 20.Full blog - https://aging-us.org/2024/11/how-ai-and-longevity-biotechnology-are-revolutionizing-healthcare-for-healthier-longer-lives/Paper DOI - https://doi.org/10.18632/aging.206135Corresponding authors - Yu-Xuan Lyu - lvyx@sustech.edu.cn, Alex Zhavoronkov - alex@insilico.com, Morten Scheibye-Knudsen - mscheibye@sund.ku.dk, and Daniela Bakula - bakula@sund.ku.dkVideo short - https://www.youtube.com/watch?v=Hpfe5WJ5g7ISign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206135Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, biotechnology, artificial intelligence, healthy longevityAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- November 6, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), Volume 16, Issue 20 on October 24, 2024, entitled “On the lifespan of Enchytraeus crypticus - impact of iron (nanomaterial and salt) on aging.”This recent study reveals important insights into how iron oxide nanoparticles (Fe3O4 NMs)—tiny particles with unique magnetic properties widely used in medicine and environmental procedures—may affect soil health over time. Led by Susana I.L. Gomes, Janeck J. Scott-Fordsmand, and Mónica J.B. Amorim from the University of Aveiro in Portugal and Aarhus University in Denmark, the research focuses on how these particles interact with the soil-dwelling worm Enchytraeus crypticus, which plays an essential role in breaking down organic matter and supporting soil structure. Iron oxide nanoparticles are increasingly used in applications like magnetic resonance imaging, drug delivery, and environmental cleanup. Their effects on soil ecosystems remain largely unexplored. In this study, the team selected Enchytraeus crypticus, a globally present soil-dwelling worm, as an indicator species to assess potential risks to soil health. Over a 202-day period, they examined how iron oxide nanoparticles and traditional iron salt (FeCl3) impact the worm’s lifespan, aging, and reproductive ability.Findings revealed that prolonged exposure to iron oxide nanoparticles reduced the lifespan, longevity, and reproductive success of Enchytraeus crypticus, particularly in isolated conditions. Worms in lower-density groups experienced greater harm, with shorter lifespans and fewer offspring, while those in larger groups faced less severe impacts. This suggests that population density and environmental factors may influence nanoparticle toxicity. Although iron chloride also showed toxic effects, iron oxide nanoparticles posed higher risks over time, likely due to a slower release of iron ions that extends exposure.In conclusion, this research highlights the importance of comprehensive studies on the long-term effects of nanoparticles on the environment. As iron oxide nanoparticles become more prevalent, understanding their impact on soil ecosystems is crucial to protecting biodiversity and ensuring the sustainability of natural resources.DOI - https://doi.org/10.18632/aging.206134Corresponding author - Mónica J.B. Amorim - mjamorim@ua.ptVideo short - https://www.youtube.com/watch?v=ElhbSAhMeXwSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206134Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, long-term, magnetite, nanobiomaterial, survivalAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- November 5, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), Volume 16, Issue 20 on October 17, 2024, entitled, “Werner syndrome RECQ helicase participates in and directs maintenance of the protein complexes of constitutive heterochromatin in proliferating human cells.”Researchers from the Department of Laboratory Medicine and Pathology at the University of Washington have discovered that the Werner syndrome gene (WRN), linked to premature aging, plays a crucial role in maintaining cellular organization and DNA stability. Their study shows that loss of WRN function disrupts essential protein interactions, potentially accelerating aging as cells lose structural integrity.Werner syndrome is a rare genetic disorder that causes accelerated aging due to mutations in the WRN gene, which disrupts normal cell functions. The WRN gene is typically responsible for essential tasks like DNA repair, replication, and maintaining telomeres—the protective caps on DNA that shorten with age. However, exactly how WRN loss leads to faster aging is still not fully understood.In this study, researchers Pavlo Lazarchuk, Matthew Manh Nguyen, Crina M. Curca, Maria N. Pavlova, Junko Oshima, and Julia M. Sidorova found that beyond its known roles, the WRN gene is also essential for maintaining a specialized structure in the cell nucleus called constitutive heterochromatin (CH). CH is a densely packed form of DNA that keeps certain parts of the genome stable and “switched off,” protecting against unwanted changes. In cells lacking WRN, the CH structure becomes disorganized, leading to DNA instability and accelerating cellular aging.Another important finding was that WRN loss affects the nuclear envelope, the membrane surrounding DNA, which houses essential proteins like Lamin B1 and Lamin B receptor (LBR). These proteins anchor constitutive heterochromatin (CH) to the nuclear membrane, helping keep DNA compact and stable. Without WRN, this anchoring weakens, and the cell’s internal structure begins to resemble that of aging cells.“Our study highlights WRN as a contributor to the integrity of CH and points at the altered levels and distribution of LBR as a mediating mechanism.” By identifying WRN’s role in organizing the cell’s interior, this study provides a new perspective on age-related genomic instability, where DNA becomes more prone to damage.In conclusion, this research highlights the importance of stable cell structures in slowing aging, potentially paving the way for future treatments targeting WRN pathways to protect DNA integrity and combat premature aging. This new insight may also inform therapies for age-related diseases.DOI - https://doi.org/10.18632/aging.206132Corresponding Author - Julia M. Sidorova - julias@uw.eduVideo short - https://www.youtube.com/watch?v=N4m6QFJhQNASign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206132Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, Werner progeria, heterochromatin, senescence, nuclear lamina, satellite repeatsAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- October 31, 2024 – A new #research paper was #published as the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), Volume 16, Issue 20, entitled, “Longevity biotechnology: bridging AI, biomarkers, geroscience and clinical applications for healthy longevity.”This paper summarizes recent advances in healthspan biotechnology discussed at the 2023 Aging Research and Drug Discovery Meeting (ARDD), where leading experts reviewed breakthroughs in artificial intelligence (AI), biomarkers, aging clocks, geroscience, and clinical trials that support healthier, longer lives. The authors present a comprehensive view of how these technologies are shaping research and industry approaches to aging, focusing on targeting aging itself to reduce multiple age-related diseases and extend the healthy years of life.With people living longer, addressing age-related health issues is more critical than ever. Traditional healthcare often treats age-related diseases individually, overlooking aging as a core issue. Longevity biotechnology seeks to change this by combining AI with biomarker analysis to detect early signs of aging, enabling targeted interventions that not only delay disease but also promote longer, healthier lives.Led by corresponding authors Yu-Xuan Lyu from Southern University of Science and Technology Shenzhen; Alex Zhavoronkov from Insilico Medicine AI Limited, Masdar City, Abu Dhabi; Morten Scheibye-Knudsen and Daniela Bakula from the Center for Healthy Aging, University of Copenhagen, this research synthesizes the potential of AI to identify precise biomarkers of aging, supporting the development of "aging clocks"—tools that use biological data to estimate a person’s biological age and health risks. These tools help clinicians tailor prevention and treatment to individual needs. Additionally, AI speeds up the discovery of drugs that target primary aging drivers, such as cellular damage and decreased cellular energy, offering the potential to slow, prevent, or even reverse certain effects of aging and enhance quality of life.“The fusion of AI with biomarker research has markedly revolutionized the way biomarkers are identified and validated in the field of ageing.”This approach not only promises to slow, prevent, or even reverse certain effects of aging but also emphasizes the potential for AI-driven methods to extend healthspans.In conclusion, the authors emphasize the need for continued investment in AI-driven therapies and biomarker research, which hold the potential to redefine aging care and improve health outcomes as people grow older.DOI - https://doi.org/10.18632/aging.206135Corresponding Authors - Yu-Xuan Lyu - lvyx@sustech.edu.cn, Alex Zhavoronkov - alex@insilico.com, Morten Scheibye-Knudsen - mscheibye@sund.ku.dk, and Daniela Bakula - bakula@sund.ku.dkVideo short - https://www.youtube.com/watch?v=Hpfe5WJ5g7ISign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206135Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, biotechnology, artificial intelligence, healthy longevityAbout Aging-USThe journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- October 29, 2024 – A new #editorial was #published in Aging (listed by MEDLINE/PubMed as “Aging (Albany NY)” and “Aging-US” by Web of Science) Volume 16, Issue 19 on October 14, 2024, entitled “Integrating cardiovascular risk biomarkers in the context of inflammaging.”Cardiovascular diseases (CVD) remain the leading cause of death worldwide, accounting for nearly one-third of all global mortalities. Risk assessment for CVD has traditionally focused on well-known factors linked to atherosclerosis, including demographics, lifestyle choices like smoking and physical activity, and conditions such as diabetes, hypertension, and obesity. Biomarkers, such as non-HDL cholesterol, have also played a key role in identifying those at risk.However, significant residual cardiovascular risk persists despite managing these established risk factors, suggesting additional, unaddressed contributors to cardiovascular health.In their paper, researchers Jacopo Sabbatinelli, Matilde Sbriscia, Fabiola Olivieri, and Angelica Giuliani from Università Politecnica delle Marche and IRCCS INRCA in Ancona, Italy, explore how integrating specific cardiovascular biomarkers could help assess this residual inflammatory risk, particularly in the context of aging-related inflammation, or “inflammaging.” The biomarkers investigated—high-sensitivity C-reactive protein (hs-CRP), high-sensitivity cardiac troponin (hs-cTn), and natriuretic peptides—serve as valuable indicators of both inflammatory burden and early cardiovascular risk.In conclusion, the authors demonstrate that combining markers of chronic inflammation with cardiac health indicators offers a more complete understanding of cardiovascular risk and reveals the impact of aging-related inflammation, or “inflammaging,” on heart health. Researchers suggest that this approach opens new avenues for targeted interventions in aging populations.DOI - https://doi.org/10.18632/aging.206136Corresponding author - Jacopo Sabbatinelli - j.sabbatinelli@staff.univpm.itVideo short - https://www.youtube.com/watch?v=yJJXbwHj6hsSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206136Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, cardiovascular disease, inflammaging, cardiac biomarkers, residual inflammatory riskAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- October 24, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), Volume 16, Issue 19 on October 3, 2024, entitled “A new model and precious tool to study molecular mechanisms of macrophage aging.”As highlighted in the abstract, the accumulation of senescent cells, marked by a senescence-associated secretory phenotype (SASP), plays a role in chronic inflammation and age-related diseases (ARD). During aging, macrophages can develop a senescent-like phenotype with altered functions, promoting the buildup of senescent cells. In the context of aging and ARD, controlling the resolution of inflammation and preventing chronic inflammation—particularly by targeting macrophages—should be a priority.In their paper, researchers Rémy Smith, Kévin Bassand, Ashok Dussol, Christophe Piesse, Eric Duplus, and Khadija El Hadri from Sorbonne Université in Paris and Université Sorbonne Paris Nord in Bobigny, France, developed an in vitro model of murine peritoneal macrophage aging. Using this model, they demonstrated that chronic treatment with CB3, a thioredoxin-1 mimetic anti-inflammatory peptide, completely prevents the increase of p21CIP1 and allows day 14 macrophages to maintain their proliferative activity."We describe a new model of macrophage aging with a senescence-like phenotype associated with inflammatory, metabolic and functional perturbations.”DOI - https://doi.org/10.18632/aging.206124Corresponding authors - Eric Duplus - eric.duplus@sorbonne-universite.fr, and Khadija El Hadri - khadija.zegouagh@sorbonne-universite.frVideo short - https://www.youtube.com/watch?v=LfN78LR-CYUSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206124Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, macrophage, inflammation, senescence, thioredoxin-1 mimetic peptideAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
In this installment of the Longevity & Aging Series, Dr. Jon Berner from the Woodinville Psychiatric Associates in Woodinville, WA, joined host Dr. Evgeniy Galimov to discuss a research paper he co-authored that was published in Volume 16, Issue 14 of Aging (Aging-US), entitled, “mTORC1 activation in presumed classical monocytes: observed correlation with human size variation and neuropsychiatric disease.”DOI - https://doi.org/10.18632/aging.206033Corresponding author - Jon Berner - jonbernermd@gmail.comVideo interview - https://www.youtube.com/watch?v=45L89MaJ7qAAbstractBackground: Gain of function disturbances in nutrient sensing are likely the largest component in human age-related disease. Mammalian target of rapamycin complex 1 (mTORC1) activity affects health span and longevity. The drugs ketamine and rapamycin are effective against chronic pain and depression, and both affect mTORC1 activity. Our objective was to measure phosphorylated p70S6K, a marker for mTORC1 activity, in individuals with psychiatric disease to determine whether phosphorylated p70S6K could predict medication response.Methods: Twenty-seven females provided blood samples in which p70S6K and phosphorylated p70S6K were analyzed. Chart review gathered biometric measurements, clinical phenotypes, and medication response. Questionnaires assessed anxiety, depression, autism traits, and mitochondrial dysfunction, to determine neuropsychiatric disease profiles. Univariate and multivariate statistical analyses were used to identify predictors of medication response.Results: mTORC1 activity correlated highly with both classical biometrics (height, macrocephaly, pupil distance) and specific neuropsychiatric disease profiles (anxiety and autism). Across all cases, phosphorylated p70S6K was the best predictor for ketamine response, and also the best predictor for rapamycin response in a single instance.Conclusions: The data illustrate the importance of mTORC1 activity in both observable body structure and medication response. This report suggests that a simple assay may allow cost-effective prediction of medication response.Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206033Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, ketamine, lithium, monocyte, mTORC1, rapamycinAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
It is with great sadness and heavy heart that we announce the recent passing of Dr. Mikhail (Misha) V. Blagosklonny, our beloved Editor-in-Chief. Misha succumbed to metastatic lung cancer after a courageous battle.Dr. Blagosklonny will be remembered as a brilliant and extraordinary scientist who dedicated his life to science. He was a visionary thinker, who made highly original contributions to cancer and aging research that were often ahead of their time. Dr. Blagosklonny was born into a family of scientists. His mother, Professor of Medicine Yanina V. Blagosklonnaya, specialized in endocrinology and was a talented teacher, mentoring several generations of medical students. His father, Professor Vladimir M. Dilman, was a brilliant gerontologist, endocrinologist and oncologist, known for being a very charismatic person. He was the first person to encourage Misha to think about nature, aging, and philosophy. Misha was a theorist by nature. While in school, he was deeply interested in physics and dreamed of becoming a theoretical physicist. Eventually, he chose biology, driven to study aging and age-related diseases, including cancer. He started as an experimentalist, but over the years, he became a theoretical biologist. In a way, his dream came true. The full tribute to Misha - https://www.aging-us.com/news-room/tribute-to-dr-mikhail-misha-blagosklonny
BUFFALO, NY- October 22, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), Volume 16, Issue 19 on September 26, 2024, entitled, “Use of the senolytics dasatinib and quercetin for prevention of pelvic organ prolapse in a mouse animal model.”Pelvic organ prolapse is a common condition among women in the U.S., with a 13% estimated risk of requiring surgery by age 80. Senolytic agents like dasatinib and quercetin (D+Q) target age-related cellular senescence and reduce senescent cell activity in various disease processes.In their paper, researchers Erryn Tappy, Haolin Shi, Jessica Pruszynski, and Maria Florian-Rodriguez from the University of Texas Southwestern Medical Center, Department of Obstetrics and Gynecology in Dallas, utilized a mouse model of pelvic organ prolapse, Fibulin-5 knockout (Fbln-5-/-) mice, to assess the ability of D+Q to prevent development of prolapse.The D+Q injections administered did not result in significant differences in prolapse development but did reduce cellular senescence markers in Fbln-5-/- mice. This suggests senolytic agents may help mitigate the role of cellular senescence in tissue dysfunction associated with prolapse. The researchers suggest that further studies are needed to determine optimal timing, dosage, and delivery of senolytics for prolapse prevention."This study represents one of the first to evaluate the impact of senolytic agents D+Q on the clinical development of pelvic organ prolapse and expression of proteins associated with cellular senescence in a mouse model.”DOI - https://doi.org/10.18632/aging.206120Corresponding author - Maria Florian-Rodriguez - Maria.Florian-Rodriguez@UTSouthwestern.eduVideo short - https://www.youtube.com/watch?v=kTQfjhubx_4Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206120Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, pelvic organ prolapse, cellular senescence, senolytic agents, animal modelAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Bone mass declines with age, and the anabolic effects of skeletal loading decrease. While much research has focused on gene transcription, how bone ages and loses its mechanoresponsiveness at the protein level remains unclear.Researchers Christopher J. Chermside-Scabbo, John T. Shuster, Petra Erdmann-Gilmore, Eric Tycksen, Qiang Zhang, R. Reid Townsend, Matthew J. Silva from Washington University School of Medicine and Washington University in St. Louis, MO, share their findings which underscore the need for complementary protein-level assays in skeletal biology research.On October 12, 2024, their research paper was published as the cover of Aging (listed by MEDLINE/PubMed as “Aging (Albany NY)” and “Aging-US” by Web of Science), Volume 16, Issue 19, entitled, “A proteomics approach to study mouse long bones: examining baseline differences and mechanical loading-induced bone formation in young-adult and old mice.”Full blog - https://aging-us.org/2024/10/exploring-baseline-variations-and-mechanical-loading-induced-bone-formation-in-young-adult-and-aging-mice-through-proteomics/Paper DOI - https://doi.org/10.18632/aging.206131Corresponding author - Christopher J. Chermside-Scabbo - ccherms@wustl.eduVideo short - https://www.youtube.com/watch?v=xm6o7gWH8p4Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206131Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, bone, mechanical loading, proteomics, RNA-seq/transcriptomicsAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- October 17, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), Volume 16, Issue 19 on September 18, 2024, entitled, “Fibroblast growth factor 21 inversely correlates with survival in elderly population – the results of the Polsenior2 study.”As noted in the abstract, fibroblast growth factor 21 (FGF21) is a liver-secreted hormone involved in regulating lipid, glucose, and energy metabolism. Its serum concentration increases with age and is elevated in various diseases. FGF21 is currently being investigated for its potential as a biomarker and therapeutic target.In their paper, Polish researchers Gabriela Handzlik, Aleksander J. Owczarek, Andrzej Więcek, Małgorzata Mossakowska, Tomasz Zdrojewski, Anna Chudek, Magdalena Olszanecka-Glinianowicz, and Jerzy Chudek from the Medical University of Silesia in Katowice, the International Institute of Molecular and Cell Biology in Warsaw, and the Medical University of Gdansk aimed to assess the prognostic value of FGF21 in an older, population-based cohort from the PolSenior2 study.The researchers report that in a sub-analysis of 3,512 individuals aged 60 and older, stratified into tertiles based on FGF21 levels, the survival estimate was worse in participants with middle and high FGF21 levels compared to those in the lowest tertile. These findings were supported by univariable Cox regression analysis, where participants in the middle and high FGF21 tertiles, after adjusting for age, had a 1.43-fold (HR 1.31; 95% CI, 1.05–1.62) and 2.56-fold (HR 1.94; 95% CI, 1.59–2.37) increased risk of mortality, respectively, compared to the lowest tertile. In multivariable Cox regression analysis, the highest FGF21 levels were independently associated with increased mortality (HR 1.53; 95% CI, 1.22–1.92), regardless of co-morbidities and blood parameters."These results indicate that higher serum FGF21 concentration is an independent predictor of all-cause mortality in the general population of older adults.”DOI - https://doi.org/10.18632/aging.206114Corresponding author - Gabriela Handzlik - ghandzlik@sum.edu.plVideo short - https://www.youtube.com/watch?v=QkPrI68nbLESign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206114Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, fibroblast growth factor 21, survival, population-based study, longevityAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- October 15, 2024 – A new #research paper was #published on the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), Volume 16, Issue 19 on October 12, 2024, entitled, “A proteomics approach to study mouse long bones: examining baseline differences and mechanical loading-induced bone formation in young-adult and old mice.”As noted in the abstract, bone mass declines with age, and the anabolic effects of skeletal loading decrease. While much research has focused on gene transcription, how bone ages and loses its mechanoresponsiveness at the protein level remains unclear.In their paper, researchers Christopher J. Chermside-Scabbo, John T. Shuster, Petra Erdmann-Gilmore, Eric Tycksen, Qiang Zhang, R. Reid Townsend, and Matthew J. Silva from Washington University School of Medicine and Washington University in St. Louis, Missouri, describe how they developed a novel proteomics approach and conducted paired mass spectrometry and RNA-seq analyses on tibias from young-adult (5-month) and old (22-month) mice.The researchers report the first correlation estimate between the bone proteome and transcriptome (Spearman ρ = 0.40). While this is consistent with findings from other tissues, it suggests that only a relatively low amount of variation in protein levels is explained by variation in transcript levels.Of the 71 shared targets that differed with age, eight were associated with bone mineral density in previous GWAS, including the understudied targets Asrgl1 and Timp2. Using complementary RNA in situ hybridization, the researchers confirmed that Asrgl1 and Timp2 showed reduced expression in osteoblasts/osteocytes in aged bones. Additionally, they found evidence of reduced TGF-beta signaling with aging, particularly Tgfb2. The researchers also identified proteomic changes following mechanical loading, noting that at the protein level, bone differed more with age than with loading, and aged bone exhibited fewer loading-induced changes."Overall, our findings underscore the need for complementary protein-level assays in skeletal biology research.”DOI - https://doi.org/10.18632/aging.206131Corresponding author - Christopher J. Chermside-Scabbo - ccherms@wustl.eduVideo short - https://www.youtube.com/watch?v=xm6o7gWH8p4Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206131Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, bone, mechanical loading, proteomics, RNA-seq/transcriptomicsAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
In this installment of the Longevity & Aging Series, Dr. Ming Yu and Namita Hattangady from the Fred Hutchinson Cancer Center in Seattle, join host Dr. Evgeniy Galimov to discuss a research paper they co-authored that was published as the cover for Volume 16, Issue 4 of Aging (Aging-US), entitled, “Mapping the core senescence phenotype of primary human colon fibroblasts.”DOI - https://doi.org/10.18632/aging.205577Corresponding authors - William M. Grady - wgrady@fredhutch.org, and Ming Yu - myu@fredhutch.orgVideo interview - https://www.youtube.com/watch?v=eqSa7My_a7wInterview transcription - https://www.aging-us.com/interviews/longevity-aging-series-s2-e2-dr-ming-yu-and-namita-hattangadyAbstractAdvanced age is the largest risk factor for many diseases and several types of cancer, including colorectal cancer (CRC). Senescent cells are known to accumulate with age in various tissues, where they can modulate the surrounding tissue microenvironment through their senescence associated secretory phenotype (SASP). Recently, we showed that there is an increased number of senescent cells in the colons of CRC patients and demonstrated that senescent fibroblasts and their SASP create microniches in the colon that are conducive to CRC onset and progression. However, the composition of the SASP is heterogenous and cell-specific, and the precise senescence profile of colon fibroblasts has not been well-defined. To generate a SASP atlas of human colon fibroblasts, we induced senescence in primary human colon fibroblasts using various in vitro methods and assessed the resulting transcriptome. Using RNASequencing and further validation by quantitative RT-PCR and Luminex assays, we define and validate a ‘core senescent profile’ that might play a significant role in shaping the colon microenvironment. We also performed KEGG analysis and GO analyses to identify key pathways and biological processes that are differentially regulated in colon fibroblast senescence. These studies provide insights into potential driver proteins involved in senescence-associated diseases, like CRC, which may lead to therapies to improve overall health in the elderly and to prevent CRC.Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205577Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, senescence, senescence associated secretory phenotype, SASP, colorectal cancer, cancerAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- October 8, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), Volume 16, Issue 18 on September 18, 2024, entitled, “Determinants of cerebral blood flow and arterial transit time in healthy older adults.”This research paper highlights that brain health deteriorates with age, particularly in terms of cerebral blood flow (CBF) and arterial transit time (ATT), key markers of brain vascular health. This decline can impair cognitive function and limit independence in later life—an issue that will affect many as the global population continues to age rapidly.In their paper, researchers Jack Feron, Katrien Segaert, Foyzul Rahman, Sindre H. Fosstveit, Kelsey E. Joyce, Ahmed Gilani, Hilde Lohne-Seiler, Sveinung Berntsen, Karen J Mullinger, and Samuel J. E. Lucas from the University of Birmingham, University of Agder, and University of Nottingham aimed to identify modifiable determinants of CBF and ATT in healthy older adults (n = 78, aged 60–81 years). They also investigated the relationship between CBF, ATT, and cognitive function in older adults. The researchers hypothesized that markers of superior general health—such as higher cardiorespiratory fitness, handgrip strength, and grey matter volume, or lower age, BMI, and blood pressure—would be associated with greater CBF and shorter ATT.Results from multiple linear regressions revealed that a higher BMI was associated with lower global cerebral blood flow (CBF) (β = −0.35, P = 0.008) and longer global arterial transit time (ATT) (β = 0.30, P = 0.017). Additionally, global ATT increased with age (β = 0.43, P = 0.004), while higher cardiorespiratory fitness was linked to longer ATT in the parietal (β = 0.44, P = 0.004) and occipital (β = 0.45, P = 0.003) regions. However, neither global nor regional CBF or ATT were associated with processing speed, working memory, or attention.“In conclusion, preventing excessive weight gain may help attenuate age-related declines in brain vascular health.”DOI - https://doi.org/10.18632/aging.206112Corresponding author - Jack Feron - j.feron@bham.ac.ukVideo short - https://www.youtube.com/watch?v=QpS4kK273osSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206112Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Nadiyeh Rouhi, PhD student in Medical Physiology and Biophysics, Department of Physiology at the University of Mississippi Medical Center (UMMC), Jackson, MS, discusses an editorial she co-authored that was published by Aging (Aging-US) in Volume 16, Issue 16, titled “Cardiac Metabolism in the Elderly: Effects and Consequences."DOI - https://doi.org/10.18632/aging.206071Corresponding author - Ji Li - jli3@umc.eduVideo interview - https://www.youtube.com/watch?v=tr-ngN3rl38Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206071Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, metabolism, heart failure, Pdk4About Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- August 27, 2024 – A new #research perspective was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), Volume 16, Issue 15 on July 25, 2024, entitled, “Trioxidized cysteine and aging: a molecular binomial that extends far beyond classical proteinopathic paradigms.”Oxidative stress (OS) - characterized by an imbalance between oxidants and antioxidants - leads to the formation of oxidative posttranslational modifications (PTMs), including those involving cysteine (Cys) residues in aging proteomes. Specifically, the formation of trioxidized Cys (t-Cys) results in permanent protein damage. Recent findings in rodents have revealed that irregular regulation of t-Cys residues in the aging proteome disrupts homeostatic phosphorylation signaling, leading to alterations in proteins similar to those caused by phosphorylated serine (p-Ser) residues.In this perspective, researchers José Antonio Sánchez Milán, María Mulet, Aida Serra and Xavier Gallart-Palau from University Hospital Arnau de Vilanova (HUAV) and University of Lleida (UdL), present novel data, validating the increase of specific t-Cys sites associated with aging in a blood-related circulating human proteome."The scope and findings included here support the hypothesis that t-Cys residues may serve as important mechanistic and biological markers, warranting further exploration in the context of unhealthy aging and age-related major diseases.”DOI - https://doi.org/10.18632/aging.206036Corresponding authors - Aida Serra - aida.serra@udl.cat, and Xavier Gallart-Palau - xgallart@irblleida.catVideo short - https://www.youtube.com/watch?v=roO_8WMGak8Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206036Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, oxidative stress, unhealthy aging, t-Cys, aging diseases, aging proteomeAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
In this #review, #researchers explore the intricate relationship between various cell death pathways and host immunological responses.Kuo-Cheng Lu, Kuo-Wang Tsai, Yu-Kuen Wang, and Wan-Chung Hufrom Taipei Tzu Chi Hospital, Fu Jen Catholic University, Taoyuan Armed Forces General Hospital, Tri-Service General Hospital and Ming Chuan University, have delved into the literature surrounding cell death pathways and their connections to host immunological pathways. Their review was published as the cover paper of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), Volume 16, Issue 15, entitled, “Types of Cell Death and Their Relations to Host Immunological Pathways.”Full blog - https://aging-us.org/2024/08/exploring-links-between-cell-death-pathways-and-immune-responses/Paper DOI - https://doi.org/10.18632/aging.206035Corresponding author - Wan-Chung Hu - Wanchung.Hu09@tzuchi.com.twVideo short - https://www.youtube.com/watch?v=oPaevm0vpR8Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206035Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, apoptosis, autophagy, ferroptosis, necroptosis, NETosis, pyroptosisAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- August 21, 2024 – A new #editorial was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), Volume 16, Issue 15 on August 8, 2024, entitled, “The benefits of exercise on aging: focus on muscle biomarkers.”The focus on maintaining health and vitality (e.g., good healthspan) in later life has become increasingly important as the world’s population ages. Over the past few decades, groundbreaking research in the field of aging has deepened our understanding of the molecular basis of this process. In the last decade, advances in aging research have identified biomarkers such as DNA methylation (DNAm) and gene expression, offering insights into both chronological and biological aging.Researchers Robin Grolaux, Bernadette Jones-Freeman, Macsue Jacques, and Nir Eynon from the Australian Regenerative Medicine Institute at Monash University in Melbourne, explore the impact of exercise on these biomarkers in human skeletal muscle—a critical tissue for metabolism, thermogenesis, and movement—revealing its potential to foster healthier aging.This study represents the first quantitative and qualitative analysis of the effects of exercise on age-related biomarkers in human skeletal tissues. Future research could explore the global effects of exercise on various molecular pathways and differentiate between exercise types to develop more effective personalized therapies.“We have the opportunity to uncover functional therapies that effectively impact aging.”DOI - https://doi.org/10.18632/aging.206064Corresponding Author - Nir Eynon - nir.eynon@monash.eduVideo short - https://www.youtube.com/watch?v=Dhiq2I0sW1USign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206064Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, skeletal muscle, exercise, epigenetics, OMICs, biomarkersAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- August 20, 2024 – A new #editorial was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), Volume 16, Issue 15 on July 19, 2024, entitled, “Physical fitness and lifestyles associated with biological aging”.Given the growing aging population worldwide, it is crucial to develop interventional strategies that target aging itself, rather than focusing solely on organ- or disease-based medicine. The geroscience hypothesis, which suggests that delaying aging can prevent the onset of diseases, is gaining traction due to advancements in aging biomarkers, driven by improvements in both measurement techniques (e.g., omics) and analytical technologies (e.g., bioinformatics).In their editorial, researchers Takuji Kawamura, Radak Zsolt, Mitsuru Higuchi, and Kumpei Tanisawa from the Faculty of Sport Sciences at Waseda University and the Research Center for Molecular Exercise Science at Hungarian University of Sports Science, emphasize the importance of investigating the relationship between cardiorespiratory fitness (CRF) and the DNA methylation (DNAm) aging clock. Their goal is to establish fitness reference values that could help delay aging. They also discuss their recent report on the "Associations between cardiorespiratory fitness and lifestyle-related factors with DNA methylation-based aging clocks in older men: WASEDA’S Health Study.""Our study reinforces the geroscience concept that active lifestyle choices may impact quantifiable molecular biomarkers that capture biological aging.”DOI - https://doi.org/10.18632/aging.206031Corresponding author - Takuji Kawamura - takuji3@aoni.waseda.jpVideo short - https://www.youtube.com/watch?v=-j_MaL8G4eoSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206031Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, DNA methylation, epigenetic clock, physical fitness, anthropometry, blood biochemical parameters, nutritional intakeAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- August 16, 2024 – A new #review was #published as the #cover paper of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), Volume 16, Issue 15, entitled, “Types of cell death and their relations to host immunological pathways”.Various immune pathways in the host, such as TH1, TH2, TH3, TH9, TH17, TH22, TH1-like, and THαβ, have been identified. While TH2 and TH9 responses primarily target multicellular parasites, host immune pathways against viruses, intracellular microorganisms (like bacteria, protozoa, and fungi), and extracellular microorganisms utilize programmed cell death mechanisms to initiate immune responses and effectively eliminate pathogens.In their review, researchers Kuo-Cheng Lu, Kuo-Wang Tsai, Yu-Kuen Wang, and Wan-Chung Hu from Taipei Tzu Chi Hospital, Fu Jen Catholic University, Taoyuan Armed Forces General Hospital, Tri-Service General Hospital and Ming Chuan University, reviewed these cell death pathways associated with the host immunological pathways."These relationships can help us understand the host defense mechanisms against invading pathogens and provide new insights for developing better therapeutic strategies against infections or autoimmune disorders.”DOI - https://doi.org/10.18632/aging.206035Corresponding authors - Wan-Chung Hu - Wanchung.Hu09@tzuchi.com.twVideo short - https://www.youtube.com/watch?v=oPaevm0vpR8Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206035Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, apoptosis, autophagy, ferroptosis, necroptosis, NETosis, pyroptosisAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- August 14, 2024 – A new #editorial was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), Volume 16, Issue 14 on July 17, 2024, entitled, “Recalibrate concepts of epigenetic aging clocks in human health.”As detailed in the opening of this editorial, DNA methylation-based epigenetic clocks are used as biomarkers of biological age in human health. Multiple epigenetic clocks have rapidly emerged in the past decade by modeling DNA methylation changes with age in large cohorts, primarily using peripheral blood samples. Despite efforts to understand the functional implications of features used to estimate biological age, the underlying mechanisms of these clocks remain poorly understood, leading to potential misinterpretations of their associations with health outcomes.Researchers Ze Zhang, Brock C. Christensen, and Lucas A. Salas from the Divisions of Population Sciences and Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, the Department of Epidemiology, Geisel School of Medicine, Dartmouth College, Dartmouth Cancer Center, Dartmouth-Hitchcock Medical Center, and the Department of Molecular and Systems Biology, Geisel School of Medicine, Dartmouth College explored the association of 12 immune cell types with epigenetic age acceleration (EAA) in both healthy and diseased populations. Their work sheds light on the complex interplay between immune cell composition and epigenetic aging, utilizing high-resolution methylation cytometry in blood samples.“In this editorial, we aim to address the key implications of our study on epigenetic aging clocks in human health from a broader perspective. While epigenetic clocks are widely hyped as aging biomarkers today, it's essential to recalibrate some fundamental concepts in this field.”DOI - https://doi.org/10.18632/aging.206027Corresponding author - Lucas A. Salas - lucas.a.salas@dartmouth.eduVideo short - https://www.youtube.com/watch?v=9lV-pkYm22MSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206027Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, epigenetics, DNA methylation, epigenetic clock, epigenetic age acceleration, methylation cytometryAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- August 13, 2024 – A new #research perspective was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), Volume 16, Issue 14 on July 19, 2024, entitled, “Lipid accumulation drives cellular senescence in dopaminergic neurons.”As highlighted in the Abstract of this perspective, Parkinson’s disease (PD) is an age-related movement disorder caused by the loss of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc) of the midbrain. However, the underlying causes of this DA neuron loss in PD are unknown, and there are currently no effective treatments to prevent or slow neuronal loss or the progression of related symptoms. In their perspective, researchers Taylor Russo and Markus Riessland from Stony Brook University found that artificially inducing GluCer accumulation leads to cellular senescence of DA neurons. This suggests that lipid aggregation plays a crucial role in the pathology of PD by driving senescence in these vulnerable neurons.“Here, we discuss the relevance of the age-related aggregation of lipids as well as the direct functional link between general lipid aggregation, cellular senescence, and inflammaging of DA neurons.”Additionally, they propose that the expression of a cellular senescence phenotype in the most vulnerable neurons in PD can be triggered by lysosomal impairment and lipid aggregation. “Importantly, we highlight additional data that perilipin (PLIN2) is significantly upregulated in senescent DA neurons, suggesting an overall enrichment of lipid droplets (LDs) in these cells.”DOI - https://doi.org/10.18632/aging.206030Corresponding author - Markus Riessland - markus.riessland@stonybrook.eduVideo short - https://www.youtube.com/watch?v=CsBthdwpdGgSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206030Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, lipids, cellular senescence, Parkinson’s disease, glucosylceramides, lysosomes, neuroinflammationAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- August 7, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), Volume 16, Issue 14 on July 26, 2024, entitled, “mTORC1 activation in presumed classical monocytes: observed correlation with human size variation and neuropsychiatric disease.”In this new study, researchers Karl Berner, Naci Oz, Alaattin Kaya, Animesh Acharjee, and Jon Berner from Woodinville Psychiatric Associates, Virginia Commonwealth University, University of Birmingham, University Hospitals Birmingham, and MRC Health Data Research UK, aimed to measure phosphorylated p70S6K, a marker for mTORC1 activity, in individuals with psychiatric disease to determine whether phosphorylated p70S6K could predict medication response.Their results showed that mTORC1 activity correlated highly with classical biometrics (height, macrocephaly, pupil distance) and specific neuropsychiatric disease profiles (anxiety and autism).“Our data suggest that human variability of mTORC1 gain of function observed during the differentiation of stem-like monocytes into vascular tissue-resident macrophages correlates with physical size, subsets of neuropsychiatric disease, and clinical ketamine or rapamycin response.”DOI - https://doi.org/10.18632/aging.206033Corresponding author - Jon Berner - jonbernermd@gmail.comVideo short - https://www.youtube.com/watch?v=EXzX6CjtAHcSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206033Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, ketamine, lithium, monocyte, mTORC1, rapamycinAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- August 6, 2024 – On July 28, 2024, Mikhail V. Blagosklonny M.D., Ph.D., from Roswell Park Comprehensive Cancer Center #published a new #editorial in Volume 16, Issue 14 of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), entitled, “Targeted cancer therapy: the initial high concentration may slow down the selection for resistance.”“Unfortunately, any targeted therapy is, always, started with low levels of the drug in the organism, selecting for drug resistance. One should propose that initial drug levels must be maximized, and durations may be minimized, ideally, as portions of preemptive combination of targeted drugs.”Read the full paper: DOI: https://doi.org/10.18632/aging.206046Corresponding Author: Mikhail V. Blagosklonny - Blagosklonny@oncotarget.com, Blagosklonny@rapalogs.comVideo short - https://www.youtube.com/watch?v=6gQWkymimSwSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206046Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, lung cancer, resistance, brain metastases, METex14, capmatinib, rapamycinAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- August 5, 2024 – A new #research paper was #published on the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 14, entitled, “Association between osteoporosis and the rate of telomere shortening.”A shorter leukocyte telomere length (LTL) is reported to be associated with age-related diseases, including osteoporosis. Many studies have tried identifying the association between LTL and osteoporosis, although it remains controversial. In this current study, researchers Myung-Hoon Han , Hyuk Sung Kwon, Mina Hwang, Hyun-Hee Park, Jee Hyang Jeong, Kyung Won Park, Eun-Joo Kim, Soo Jin Yoon, Bora Yoon, Jae-Won Jang, Jin Yong Hong, Seong Hye Choi, and Seong-Ho Koh from Hanyang University Guri Hospital, Hanyang University Graduate School of Biomedical Science and Engineering, Ewha Womans University College of Medicine, Dong-A University College of Medicine, Pusan National University Hospital, Eulji University Hospital, Eulji University School of Medicine, Konyang University College of Medicine, Kangwon National University School of Medicine, Yonsei University Wonju College of Medicine, and Inha University College of Medicine, aimed to determine whether osteoporosis is independently associated with LTL shortening in a prospective longitudinal cohort.“We compared the LTL values for each participant at baseline and over a 2-year follow-up period.” Multivariable linear regression was conducted to identify whether osteoporosis is independently associated with the rate of telomere shortening. A total of 233 subjects (from 55 to 88 years) from the KBASE cohort were finally enrolled in the study. Multivariable linear regression analysis indicated that only osteoporosis was independently associated with rapid LTL shortening over 2 years (B, -8.08; p = 0.038).“We sought to identify an association between osteoporosis and LTL shortening in an independent prospective cohort.”DOI - https://doi.org/10.18632/aging.206034Corresponding authors - Seong Hye Choi - seonghye@inha.ac.kr, and Seong-Ho Koh - ksh213@hanyang.ac.krVideo short - https://www.youtube.com/watch?v=SGdkAYfA4-ASign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206034Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, leukocyte telomere length, osteoporosis, interleukin-6, prospective cohortAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- July 23, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 13, entitled, “Co-analysis of methylation platforms for signatures of biological aging in the domestic dog reveals previously unexplored confounding factors.”Chronological age reveals the number of years an individual has lived since birth. By contrast, biological age varies between individuals of the same chronological age at a rate reflective of physiological decline. Differing rates of physiological decline are related to longevity and result from genetics, environment, behavior, and disease. The creation of methylation biological age predictors is a long-standing challenge in aging research due to the lack of individual pre-mortem longevity data. In this new study, researchers Aitor Serres Armero, Reuben M. Buckley, Lajoyce Mboning, Gabriella J. Spatola, Steve Horvath, Matteo Pellegrini, and Elaine A. Ostrander from the National Human Genome Research Institute, the University of California Los Angeles, and Altos Labs ask whether dogs experience changes in their epigenetic age at a rate predicted by breed longevity.“The consistent differences in longevity between domestic dog breeds enable the construction of biological age estimators which can, in turn, be contrasted with methylation measurements to elucidate mechanisms of biological aging.”The researchers drew on three flagship methylation studies using distinct measurement platforms and tissues to assess the feasibility of creating biological age methylation clocks in the dog. They expanded epigenetic clock building strategies to accommodate phylogenetic relationships between individuals, thus controlling for the use of breed standard metrics. The team observed that biological age methylation clocks are affected by population stratification and require heavy parameterization to achieve effective predictions. “Finally, we observe that methylation-related markers reflecting biological age signals are rare and do not colocalize between datasets.”DOI - https://doi.org/10.18632/aging.206012Corresponding author - Elaine A. Ostrander - eostrand@mail.nih.govVideo short - https://www.youtube.com/watch?v=Rr2gA8bpJwkSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206012Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, biological age, methylation, dog, lifespan, penalized regressionAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Over the human lifespan, our cells encounter numerous stressors that can trigger an intrinsic defense mechanism called cellular senescence. Cellular senescence is characterized by irreversible growth arrest and can act as a safeguard against cancer. However, when senescent cells accumulate in various tissues as we age, it can contribute to tissue degeneration and chronic diseases. The senescence-associated secretory phenotype (SASP), a hallmark of senescent cells, plays a critical role by secreting inflammatory factors, proteases, and growth factors, disrupting tissue balance and fueling pathological conditions. Consequently, selectively eliminating senescent cells has emerged as a promising therapeutic strategy, potentially restoring tissue function and mitigating age-related disorders.Full blog - https://aging-us.org/2024/07/links-between-exercise-senescence-and-lung-health/Research Paper DOI - https://doi.org/10.18632/aging.205976Corresponding author - Masataka Sugimoto - msugimot@tmig.or.jpVideo short - https://www.youtube.com/watch?v=Bzgb2PEiV9cSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205976Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, senescence, exercise, PEDF, myokine, COPDAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- July 17, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 13, entitled, “Modulating in vitro lung fibroblast activation via senolysis of senescent human alveolar epithelial cells.”Idiopathic pulmonary fibrosis (IPF) is an age-related disease with poor prognosis and limited therapeutic options. Activation of lung fibroblasts and differentiation to myofibroblasts are the principal effectors of disease pathology, but damage and senescence of alveolar epithelial cells, specifically type II (ATII) cells, has recently been identified as a potential trigger event for the progressive disease cycle. Targeting ATII senescence and the senescence-associated secretory phenotype (SASP) is an attractive therapeutic strategy; however, translatable primary human cell models that enable mechanistic studies and drug development are lacking.In this new study, researchers Joseph S. Spina, Tracy L. Carr, Lucy A. Phillips, Heather L. Knight, Nancy E. Crosbie, Sarah M. Lloyd, Manisha A. Jhala, Tony J. Lam, Jozsef Karman, Meghan E. Clements, Tovah A. Day, Justin D. Crane, and William J. Housley from AbbVie Bioresearch Center and Northeastern University describe a novel system of conditioned medium (CM) transfer from bleomycin-induced senescent primary alveolar epithelial cells (AEC) onto normal human lung fibroblasts (NHLF) that demonstrates an enhanced fibrotic transcriptional and secretory phenotype compared to non-senescent AEC CM treatment or direct bleomycin damage of the NHLFs. “In the current study, we confirm the presence of senescent cell populations within the human IPF lung, as well as assess primary cell reagents for sensitivity to senescent cell targeting therapies.”In this system, the bleomycin-treated AECs exhibited classical hallmarks of cellular senescence, including SASP and a gene expression profile that resembles aberrant epithelial cells of the IPF lung. Fibroblast activation by CM transfer was attenuated by pre-treatment of senescent AECs with the senolytic Navitoclax and AD80, but not with the standard of care agent Nintedanib or senomorphic JAK-targeting drugs (e.g., ABT-317, ruxolitinib). This model provided a relevant human system for profiling novel senescence-targeting therapeutics for IPF drug development.“Taken together, the model described herein provides a physiologically relevant, primary human cell system to study the effects of alveolar epithelial cell senescence on lung fibroblasts in the context of chronic fibrotic lung disease.”DOI - https://doi.org/10.18632/aging.205994Corresponding author - Tovah A. Day - t.day@northeastern.eduVideo short - https://www.youtube.com/watch?v=rpmo2PlGDKcSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205994Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- July 15, 2024 – A new #research paper was #published on the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 13, entitled, “Roles of pigment epithelium-derived factor in exercise-induced suppression of senescence and its impact on lung pathology in mice.”Senescent cells contribute to tissue aging and underlie the pathology of chronic diseases. The benefits of eliminating senescent cells have been demonstrated in several disease models, and the efficacy of senolytic drugs is currently being tested in humans. Exercise training has been shown to reduce cellular senescence in several tissues; however, the mechanisms responsible remain unclear.In this new study, researchers Hiromichi Tsushima, Hirobumi Tada, Azusa Asai, Mikako Hirose, Tohru Hosoyama, Atsushi Watanabe, Taro Murakami, and Masataka Sugimoto from Tokyo Metropolitan Institute for Geriatrics and Gerontology, Shigakkan University, and National Center for Geriatrics and Gerontology investigated myocyte-secreted factors with the potential to suppress cellular senescence, aiming to explore their protective effects against lung disease. “We found that myocyte-derived factors significantly extended the replicative lifespan of fibroblasts, suggesting that myokines mediate the anti-senescence effects of exercise.”A number of proteins within myocyte-derived factors were identified by mass spectrometry. Among these, pigment epithelium-derived factor (PEDF) exerted inhibitory effects on cellular senescence. Eight weeks of voluntary running increased PEDF levels in skeletal muscles and suppressed senescence markers in the lungs. The administration of PEDF reduced senescence markers in multiple tissues and attenuated the decline in respiratory function in the pulmonary emphysema mouse model. The researchers also showed that blood levels of PEDF inversely correlated with the severity of COPD in patients. “Collectively, these results strongly suggest that PEDF contributes to the beneficial effects of exercise, potentially suppressing cellular senescence and its associated pathologies.”DOI - https://doi.org/10.18632/aging.205976Corresponding authors - Masataka Sugimoto - msugimot@tmig.or.jpVideo short - https://www.youtube.com/watch?v=Bzgb2PEiV9cSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205976Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, senescence, exercise, PEDF, myokine, COPDAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- July 10, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 12, entitled, “Aging exacerbates oxidative stress and liver fibrosis in an animal model of Down Syndrome.”Down Syndrome (DS) is a common genetic disorder characterized by an extra copy of chromosome 21, leading to dysregulation of various metabolic pathways. Oxidative stress in DS is associated with neurodevelopmental defects, neuronal dysfunction, and a dementia onset resembling Alzheimer's disease. Additionally, chronic oxidative stress contributes to cardiovascular diseases and certain cancers prevalent in DS individuals.In this new study, researchers Sebastiano Giallongo, Jessica Ferrigno, Rosario Caltabiano, Giuseppe Broggi, Amer M. Alanazi, Alfio Distefano, Emanuela Tropea, Antonella Tramutola, Marzia Perluigi, Giovanni Li Volti, Eugenio Barone, and Ignazio Alberto Barbagallo from the University of Catania, King Saud University, and Sapienza University of Rome investigated the impact of aging on oxidative stress and liver fibrosis using a DS murine model (Ts2Cje mice). “Our results show that DS mice show increased liver oxidative stress and impaired antioxidant defenses, as evidenced by reduced glutathione levels and increased lipid peroxidation.” DS liver exhibited an altered inflammatory response and mitochondrial fitness as the researchers showed by assaying the expression of HMOX1, CLPP, and the heat shock proteins Hsp90 and Hsp60. DS liver also displayed dysregulated lipid metabolism, indicated by altered expression of PPARα, PPARγ, FATP5, and CTP2. Consistently, these changes might contribute to non-alcoholic fatty liver disease development, a condition characterized by liver fat accumulation. Consistently, histological analysis of DS liver revealed increased fibrosis and steatosis, as showed by Col1a1 increased expression, indicative of potential progression to liver cirrhosis. Therefore, their findings suggest an increased risk of liver pathologies in DS individuals, particularly when combined with the higher prevalence of obesity and metabolic dysfunctions in DS patients.“These results shed a light on the liver's role in DS-associated pathologies and suggest potential therapeutic strategies targeting oxidative stress and lipid metabolism to prevent or mitigate liver-related complications in DS individuals.”DOI - https://doi.org/10.18632/aging.205970Corresponding author - Giovanni Li Volti - livolti@unict.itVideo short - https://www.youtube.com/watch?v=8GlAruy0xfkSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205970Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, Down Syndrome, oxidative stress, liverAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- July 9, 2024 – A new #editorial paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 12, entitled, “Aging retinal pigmented epithelium: omics-based insights into vision decline.”In this new editorial, researchers Ioan V. Matei and Luminita Paraoan from Edge Hill University discuss vision decline with aging. Of all senses affected by aging, vision decline arguably has the most impactful relationship with overall wellbeing, health and personal autonomy. However, while the ensuing importance of vision loss has long been recognised from a public health perspective given an increasingly aging population, understanding the molecular and cellular mechanisms driving age-related pathological changes is still in its infancy. “This matter is, therefore, critical for tackling sensory impairment and ensuring healthy aging.” The retinal pigmented epithelium (RPE), the cellular monolayer located between the neuroretina and the highly vascularized choroid, from which it is separated by Bruch’s membrane (BrM), has a critical role in human vision and performs essential functions throughout life for maintaining the retinal homeostasis. RPE is a specialised, fully differentiated tissue that is mitotically inactive, with no regenerative potential. Unsurprisingly, given all its characteristics, functions and metabolic demands, the RPE is particularly susceptible to aging, sustaining significant morphologic and physiologic changes. “Aging is recognised as the highest risk factor for age-related macular degeneration (AMD), the leading cause of adult visual impairment and blindness in the Northern Hemisphere, which is directly linked to specific pathological changes of the RPE located in the macula, i.e., the central part of retina; these changes, therefore, affect central vision required for reading, driving, and discerning details of pictures, faces, shapes and colors.”DOI - https://doi.org/10.18632/aging.205914Corresponding author - Luminita Paraoan - Luminita.Paraoan@edgehill.ac.ukVideo short - https://www.youtube.com/watch?v=_-zhhFjlQ4YSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205914Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, RPE, vision, omicsAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- July 1, 2024 – A new #review paper was #published on the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 12, entitled, “Senescent cell-derived vaccines: a new concept towards an immune response against cancer and aging?”Two recent seminal works have untangled the intricate role of tumor-associated senescent cells in cancer progression, or regression, by guiding our immune system against cancer cells. The characterization of these unique, yet diverse cell populations, should be considered, particularly when contemplating the use of senolytics, which are drugs that selectively eliminate senescent cells, in a cancer framework. In this new review, researchers João Pessoa, Sandrina Nóbrega-Pereira, and Bruno Bernardes de Jesus from the University of Aveiro describe the current knowledge in this field. “In particular, we will discuss how the presence of senescent cells in tumors could be used as a therapeutic target in immunogenic cancers and how we may hypothetically design an adaptive anti-aging vaccine.”DOI - https://doi.org/10.18632/aging.205975Corresponding authors - Bruno Bernardes de Jesus - brunob.jesus@ua.ptVideo short - https://www.youtube.com/watch?v=hbhkSu1kX5YSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205975Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, cancer, immunotherapy, tumor-associated senescent cells, senescence, antigen, vaccineAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
Cellular quality control mechanisms like mitophagy, a specialized form of autophagy that eliminates dysfunctional mitochondria, play a pivotal role in various physiological processes. Defects in mitophagy have been linked to neurodegeneration, heart failure, cancer, and aging.A recent study, by researchers Marta Mauro-Lizcano, Federica Sotgia, and Michael P. Lisanti from the University of Salford, has shed light on the intricate link between mitophagy and cancer stem cells (CSCs). In this study, the researchers developed an innovative fluorescence-based approach to enrich subpopulations of cancer cells exhibiting high basal levels of mitophagy. Their findings reveal that elevated mitophagy activity enhances CSC properties, including self-renewal, ATP production, proliferation, and cell migration, underscoring the potential of targeting mitophagy as a therapeutic strategy for cancer treatment. On June 4, 2024, their research paper was published on the cover of Aging’s Volume 16, Issue 11, entitled, “Mitophagy and cancer: role of BNIP3/BNIP3L as energetic drivers of stemness features, ATP production, proliferation, and cell migration.”Full blog - https://aging-us.org/2024/06/targeting-mitophagy-as-a-therapeutic-strategy-for-cancer-treatment/Paper DOI - https://doi.org/10.18632/aging.205939Corresponding authors - Federica Sotgia - fsotgia@gmail.com, and Michael P. Lisanti - michaelp.lisanti@gmail.comVideo short - https://www.youtube.com/watch?v=n872jCkc-q8Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205939Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, mitophagy, BNIP3, BNIP3L(NIX), cancer stem cells (CSCs), flow cytometry (FACS)About Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- June 26, 2024 – A new editorial paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 11, entitled, “Global consensus for sarcopenia.”In this new editorial, researchers Ben Kirk, Peggy M. Cawthon, and Alfonso J. Cruz-Jentoft from the University of Melbourne and Western Health discuss the global societal issue of skeletal muscle loss and weakness, termed Sarcopenia. Low muscle mass or low strength/function increases the susceptibility to poor outcomes such as fragility, hip fractures, disability, and low quality of life in older people [1–4]. Skeletal muscle also acts as an endocrine organ and interacts with local and distal tissues; for instance, muscle cells secrete molecules involved in bone fracture healing and the same molecules help regulate distal tissues such as the brain, heart, and kidneys [5, 6]. This may partially explain why low muscle mass is a strong predictor of disease-specific mortality (dementia, cancer, heart failure, kidney/liver disease) as well as all-cause mortality in aging [7]. “Until now, there has been no universal agreement on a definition for Sarcopenia.”Previous definitions were continent- and region-specific: Asia, Europe, North America, and Australia/New Zealand [8]. These definitions were certainly important in drawing attention to, and understanding of, this muscle disease. However, these definitions led to wide estimates in disease prevalence/incidence as well as heterogeneity when comparing treatments results of randomised trials [9]. The lack of a single definition likely impacted the identification of or treatment for sarcopenia in research and clinical practice (i.e., caused confusion for scientists, physicians and health care professionals on which definition, cutpoints, and muscle assessment tools to employ). “To address this, the Global Leadership Initiative in Sarcopenia (GLIS) [9] was formed to create a unified global definition for use in research and clinical settings.”DOI - https://doi.org/10.18632/aging.205919Corresponding author - Ben Kirk - ben.kirk@unimelb.edu.auVideo short - https://www.youtube.com/watch?v=NnhM3y6qi5USign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205919Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, sarcopenia, global definition, GLIS, skeletal muscleAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- June 25, 2024 – A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 11, entitled, “Associations of childhood, adolescence, and midlife cognitive function with DNA methylation age acceleration in midlife.”Prior studies showed increased age acceleration (AgeAccel) is associated with worse cognitive function among old adults. In this new study, researchers Junyu Chen, Leah Moubadder, Elizabeth S. Clausing, Katrina L. Kezios, Karen N. Conneely, Anke Hüls, Andrea Baccarelli, Pam Factor-Litvak, Piera Cirrillo, Rachel C. Shelton, Bruce G. Link, and Shakira F. Suglia from Emory University, University of Nebraska, Columbia University, Public Health Institute, Washington, DC, and the University of California Riverside examined the associations of childhood, adolescence and midlife cognition with AgeAccel based on DNA methylation (DNAm) in midlife.“To the best of our knowledge, this is the first study to show the association of cognition at younger age with midlife age acceleration, and associations between midlife age acceleration measures and cognitive function that are independent of childhood and adolescent cognition.”Data are from 359 participants who had cognition measured in childhood and adolescence in the Child Health and Development study, and had cognition, blood based DNAm measured during midlife in the Disparities study. Childhood cognition was measured by Raven’s Progressive Matrices and Peabody Picture Vocabulary Test (PPVT). Adolescent cognition was measured only by PPVT. Midlife cognition included Wechsler Test of Adult Reading (WTAR), Verbal Fluency (VF), Digit Symbol (DS). AgeAccel measures including Horvath, Hannum, PhenoAge, GrimAge and DunedinPACE were calculated from DNAm. Linear regressions adjusted for potential confounders were utilized to examine the association between each cognitive measure in relation to each AgeAccel.There are no significant associations between childhood cognition and midlife AgeAccel. A 1-unit increase in adolescent PPVT, which measures crystalized intelligence, is associated with 0.048-year decrease of aging measured by GrimAge and this association is attenuated after adjustment for adult socioeconomic status. Midlife crystalized intelligence measure WTAR is negatively associated with PhenoAge and DunedinPACE, and midlife fluid intelligence measure (DS) is negatively associated with GrimAge, PhenoAge and DunedinPACE. AgeAccel is not associated with VF in midlife.“In conclusion, our study showed the potential role of cognitive functions at younger ages in the process of biological aging. We also showed a potential relationship of both crystalized and fluid intelligence with aging acceleration.”DOI - https://doi.org/10.18632/aging.205943Corresponding author - Junyu Chen - junyu.chen@emory.eduVideo short - https://www.youtube.com/watch?v=v7xiVCqVwPwSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout Aging-USThe mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- June 19, 2024 – A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 11, entitled, “Dietary sucrose determines the regulatory activity of lithium on gene expression and lifespan in Drosophila melanogaster.”The amount of dietary sugars and the administration of lithium both impact the lifespan of the fruit fly Drosophila melanogaster. It is noteworthy that lithium is attributed with insulin-like activity as it stimulates protein kinase B/Akt and suppresses the activity of glycogen synthase kinase-3 (GSK-3). However, its interaction with dietary sugar has largely remained unexplored. In this new study, researchers Katharina Jans, Kai Lüersen, Jakob von Frieling, Thomas Roeder, and Gerald Rimbach from the University of Kiel investigated the effects of lithium supplementation on known lithium-sensitive parameters in fruit flies, such as lifespan, body composition, GSK-3 phosphorylation, and the transcriptome, while varying the dietary sugar concentration. “Based on this proposed overlapping bioactivity of dietary sugar and lithium in the female fruit fly, we decided to investigate the extent of these similarities and whether a joint mechanism lies at their root.”For all these parameters, the researchers observed that the efficacy of lithium was significantly influenced by the sucrose content in the diet. Overall, they found that lithium was most effective in enhancing longevity and altering body composition when added to a low-sucrose diet. Whole-body RNA sequencing revealed a remarkably similar transcriptional response when either increasing dietary sucrose from 1% to 10% or adding 1 mM LiCl to a 1% sucrose diet, characterized by a substantial overlap of nearly 500 differentially expressed genes. “Hence, dietary sugar supply is suggested as a key factor in understanding lithium bioactivity, which could hold relevance for its therapeutic applications.”DOI - https://doi.org/10.18632/aging.205933Corresponding author - Katharina Jans - jans@foodsci.uni-kiel.deVideo short - https://www.youtube.com/watch?v=HaxZU4Gd5Z4Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205933Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, lithium, longevity, glycogen synthase kinase 3, fruit fly, trace elementAbout Aging (Aging-US):Aging aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed Central, Web of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- June 17, 2024 – A new research paper was published on the cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 11, entitled, “Mitophagy and cancer: role of BNIP3/BNIP3L as energetic drivers of stemness features, ATP production, proliferation, and cell migration.”Mitophagy is a selective form of autophagy which permits the removal of dysfunctional or excess mitochondria. This occurs as an adaptative response to physiological stressors, such as hypoxia, nutrient deprivation, or DNA damage. Mitophagy is promoted by specific mitochondrial outer membrane receptors, among which are BNIP3 and BNIP3L. The role of mitophagy in cancer is being widely studied, and more specifically in the maintenance of cancer stem cell (CSC) properties, such as self-renewal. Given that CSCs are responsible for treatment failure and metastatic capacity, targeting mitophagy could be an interesting approach for CSC elimination. In this new study, researchers Marta Mauro-Lizcano, Federica Sotgia, and Michael P. Lisanti from the University of Salford describe a new model system to enrich sub-populations of cancer cells with high basal levels of mitophagy, based on the functional transcriptional activity of BNIP3 and BNIP3L. “Briefly, we employed a BNIP3(L)-promoter-eGFP-reporter system to isolate cancer cells with high BNIP3/BNIP3L transcriptional activity by flow cytometry (FACS).” The model was validated by using complementary lysosomal and mitophagy-specific probes, as well as the mitochondrially-targeted red fluorescent protein (RFP), namely mt-Keima. High BNIP3/BNIP3L transcriptional activity was accompanied by increases in i) BNIP3/BNIP3L protein levels, ii) lysosomal mass, and iii) basal mitophagy activity. Furthermore, cancer cells with increased BNIP3/BNIP3L transcriptional activity exhibited CSC features, such as greater mammosphere-forming ability and high CD44 levels. “To further explore the model, we also analysed other stemness characteristics in MCF7 and MDA-MB-231 breast cancer cell lines, directly demonstrating that BNIP3(L)-high cells were more metabolically active, proliferative, migratory, and drug-resistant, with elevated anti-oxidant capacity. Therefore, high levels of basal mitophagy appear to enhance CSC features.”DOI - https://doi.org/10.18632/aging.205939Corresponding authors - Federica Sotgia - fsotgia@gmail.com, and Michael P. Lisanti - michaelp.lisanti@gmail.comVideo short - https://www.youtube.com/watch?v=n872jCkc-q8Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205939Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout Aging-USAging publishes research papers in all fields of aging research, including but not limited to aging processes (from yeast to mammals), cellular senescence, age-related diseases (such as cancer and Alzheimer’s disease) and their prevention and treatment, anti-aging strategies and drug development, and, importantly, the role of signal transduction pathways in aging (such as mTOR) and potential approaches to modulate these signaling pathways to extend lifespan.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Werner syndrome (WS) is a rare genetic disorder marked by the premature onset of features typically associated with normal aging. This autosomal recessive condition manifests in individuals who generally develop normally until adolescence. As the syndrome progresses, affected individuals are predisposed to age-related diseases much earlier in life. These conditions include cataracts, type 2 diabetes, atherosclerosis, osteoporosis, and various cancers. The underlying cause of Werner syndrome is believed to be mutations in the WRN gene, which encodes a RecQ helicase crucial for DNA repair and replication.Despite the accelerated aging, cognitive function remains unaffected in individuals with WS, providing a unique model for studying the mechanisms of aging and exploring potential therapeutic interventions. Although extensive research has been conducted, the precise mechanisms underlying these effects remain elusive.On May 24, 2024, researchers Lucie Aumailley, Marie Julie Dubois, André Marette, and Michel Lebel from Université Laval published research paper chosen as the cover of Aging’s Volume 16, Issue 10, entitled, “Integrated liver and serum proteomics uncover sexual dimorphism and alteration of several immune response proteins in an aging Werner syndrome mouse model.” Recognizing the limitations of traditional investigative approaches, Aumailley et al. utilized advanced proteomics in their study. Proteomics allows the simultaneous identification and quantification of hundreds of proteins, providing a comprehensive analysis of liver and serum proteome profiles from wild-type and WRN mutant mice at different ages to uncover biological processes influenced by age and genotype.Full blog - https://aging-us.org/2024/06/werner-syndrome-and-the-power-of-proteomics/Paper DOI - https://doi.org/10.18632/aging.205866Corresponding author - Michel Lebel - michel.lebel@crchudequebec.ulaval.caVideo short - https://www.youtube.com/watch?v=uP6deANWgP4Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205866Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, proteomics, Werner syndrome, fatty liver, sexual dimorphism, immunoglobulinsAbout Aging-USAging publishes research papers in all fields of aging research, including but not limited to aging processes (from yeast to mammals), cellular senescence, age-related diseases (such as cancer and Alzheimer’s disease) and their prevention and treatment, anti-aging strategies and drug development, and, importantly, the role of signal transduction pathways in aging (such as mTOR) and potential approaches to modulate these signaling pathways to extend lifespan.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- June 12, 2024 – A new review paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 10, entitled, “Peripheral vascular dysfunction and the aging brain.”Aging is the greatest non-modifiable risk factor for most diseases, including cardiovascular diseases (CVD), which remain the leading cause of mortality worldwide. In their new review, researchers Devin Wahl and Zachary S. Clayton from Colorado State University and the University of Colorado note that robust evidence indicates that CVD are a strong determinant for reduced brain health and all-cause dementia with advancing age. “CVD are also closely linked with peripheral and cerebral vascular dysfunction, common contributors to the development and progression of all types of dementia, that are largely driven by excessive levels of oxidative stress (e.g., reactive oxygen species [ROS]).”Emerging evidence suggests that several fundamental aging mechanisms (e.g., “hallmarks” of aging), including chronic low-grade inflammation, mitochondrial dysfunction, cellular senescence and deregulated nutrient sensing contribute to excessive ROS production and are common to both peripheral and cerebral vascular dysfunction. Therefore, targeting these mechanisms to reduce ROS-related oxidative stress and improve peripheral and/or cerebral vascular function may be a promising strategy to reduce dementia risk with aging. Investigating how certain lifestyle strategies (e.g., aerobic exercise and diet modulation) and/or select pharmacological agents (natural and synthetic) intersect with aging “hallmarks” to promote peripheral and/or cerebral vascular health represent a viable option for reducing dementia risk with aging. “Therefore, the primary purpose of this review is to explore mechanistic links among peripheral vascular dysfunction, cerebral vascular dysfunction, and reduced brain health with aging. Such insight and assessments of non-invasive measures of peripheral and cerebral vascular health with aging might provide a new approach for assessing dementia risk in older adults.”DOI - https://doi.org/10.18632/aging.205877Corresponding authors - Devin Wahl - devin.wahl@colostate.edu, and Zachary S. Clayton - zachary.clayton@colorado.eduVideo short - https://www.youtube.com/watch?v=0gx9DklNZVMSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205877Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, peripheral vascular health, cerebrovascular health, cognitive function, dementiaAbout Aging-USAging publishes research papers in all fields of aging research, including but not limited to aging processes (from yeast to mammals), cellular senescence, age-related diseases (such as cancer and Alzheimer’s disease) and their prevention and treatment, anti-aging strategies and drug development, and, importantly, the role of signal transduction pathways in aging (such as mTOR) and potential approaches to modulate these signaling pathways to extend lifespan.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- June 11, 2024 – A new editorial paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 10, entitled, “CCR4-NOT complex in stress resistance and longevity in C. elegans.”The ability to mount an adaptive response to environmental stress is crucial in organismal survival and overall fitness. In the context of aging, many genes that mediate resistance to stressors are also important in longevity, and aging has been shown to cause a decline in stress resistance. In their new editorial, researchers Cheng-Wei Wu and Hadi Tabarraei from the University of Saskatchewan wrote that recently, during a screening for genes that are required for the transcriptional response to heavy metal and oxidative stress in C. elegans, they found that depletion of subunits within the evolutionarily conserved CCR4-NOT protein complex compromises stress resistance and decreases lifespan.“The CCR4-NOT (Carbon Catabolite Repression 4 – Negative On TATA-less) is a multi-protein complex tasked with regulating RNA metabolism across multiple steps including mRNA decay, transcription initiation and elongation, mRNA quality control and export, and mRNA translatability (reviewed in [3]).”Studies in yeast have shown that CCR4-NOT is required for transcriptional elongation of stress responsive genes and that loss of function mutants of this protein complex have increased sensitivity to replication stress caused by DNA damaging agents [4, 5]. An expansive role for the CCR4-NOT complex in stress-induced transcriptional programming was demonstrated in C. elegans via whole-transcriptome sequencing analysis [2]. “Together, while the CCR4-NOT complex has been extensively studied for the past 3 decades, new studies in the model organism C. elegans have revealed an important new role for this protein complex in regulating normal aging as well as a requirement for many well-characterized and evolutionarily conserved pro-longevity pathways including reduced insulin signaling, mitochondrial suppression, enhanced stress response, and dietary restriction.”DOI - https://doi.org/10.18632/aging.205918Corresponding author - Cheng-Wei Wu - michael.wu@usask.caVideo short - https://www.youtube.com/watch?v=UFi7Dq5JXJ4Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205918Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, oxidative stress, C. elegans, CCR4-NOTAbout Aging-USAging publishes research papers in all fields of aging research, including but not limited to aging processes (from yeast to mammals), cellular senescence, age-related diseases (such as cancer and Alzheimer’s disease) and their prevention and treatment, anti-aging strategies and drug development, and, importantly, the role of signal transduction pathways in aging (such as mTOR) and potential approaches to modulate these signaling pathways to extend lifespan.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.).Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- June 11, 2024 – The Ride for Roswell is one of the nation’s largest cycling events—hosted by Roswell Park Comprehensive Cancer Center—to raise awareness and funds for cancer research and patient care. This charity bike ride, based out of Buffalo, New York, has brought people together for 28 years to celebrate cancer survivors, pay tribute to lives that have been lost, and to work together to support research and find a cure.THE ORIGIN OF THE RIDEThe Ride for Roswell started in 1989 when Mitch Flynn, owner of the advertising agency Flynn & Friends, met Katherine Gioia. Katherine was a four-year-old patient battling a rare form of cancer. After Katherine’s death (less than a year after her diagnosis), Katherine’s mother, Anne Gioia, and aunt, Donna Gioia, founded the Roswell Park Alliance Foundation in her memory to raise money for cancer research and treatment. On June 29, 1996, Mitch and Alliance Foundation staff launched the first Ride for Roswell.In the 28 years since then, thanks to over 135,000 riders and thousands of volunteers, the Ride for Roswell has raised over $72 million to fund cancer research. The event has become one of the largest charity rides in the United States. THIS YEARThis year, Ride Day is on Saturday, June 22, 2024, and will once again begin at the University at Buffalo North Campus. There are nine routes to choose from, ranging from five to 100 mile distances. All riders are encouraged to check in on the Thursday or Friday before Ride Day. Learn more about The Ride, check in, and routes: https://www.rideforroswell.org/routes/JOIN A TEAM: TEAM OPEN ACCESSImpact Journals has been a part of this event since 2018 and continues to sponsor captain Sergei Kurenov’s peloton, Team Open Access. Team Open Access was named in honor of all open-source online medical journals, such as Aging, Oncotarget, Genes & Cancer, and Oncoscience. Sergei works at Roswell Park Comprehensive Cancer Center to create, develop, and implement innovative diagnostic and surgical pre-planning software used in cancer treatment. He has been riding in the event since 2016.“I am proud to [say] that our team is supported again by open source cancer-related scientific journals: Oncotarget and Aging! Both of these journals publish high-impact research papers of general interest and biological significance in all fields of cancer research,” Sergei said.There is still time to join Team Open Access in the Ride for Roswell. You can also support the team by giving a donation of any size. Any avenue of support you may choose to donate to the Ride for Roswell will make a difference and change lives.“Finding a cure for cancer is something we are all incredibly passionate about, and we are so thankful and grateful for your support. Together, we can make a difference!” Sergei said. “Thank you so much for your donations, your support, and well wishes!”Visit the Open Access team page to join or donate today: https://give.roswellpark.org/site/TR/SpecialEvents/General?team_id=19666&pg=team&fr_id=1940For media requests, please contact media@impactjournals.com.
BUFFALO, NY- June 10, 2024 – A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 10, entitled, “Relationships of depression and antidepressant use with epigenetic age acceleration and all-cause mortality among postmenopausal women.”In this new study, researchers May A. Beydoun, Hind A. Beydoun, Jason Ashe, Michael F. Georgescu, Steve Horvath, Ake Lu, Anthony S. Zannas, Aladdin H. Shadyab, Su Yon Jung, Sylvia Wassertheil-Smoller, Ramon Casanova, Alan B. Zonderman, and Robert L. Brunner from the National Institute on Aging, U.S. Department of Veterans Affairs (Washington, DC), University of Texas Health Science Center at Houston, University of California Los Angeles, University of North Carolina at Chapel Hill, University of California San Diego, Albert Einstein College of Medicine, Wake Forest University School of Medicine, and University of Nevada Reno investigated relations of depressive symptoms, antidepressant use, and epigenetic age acceleration with all-cause mortality risk among postmenopausal women. “Frequently under-recognized depression is a major contributor to the Global Burden of Diseases [1, 2] while being the most prevalent mental illness among geriatric populations [2].”Data were analyzed from ≤1,900 participants in the Women's Health Initiative study testing four-way decomposition models. After a median 20.4y follow-up, 1,161 deaths occurred. Approximately 11% had elevated depressive symptoms (EDS+), 7% were taking antidepressant medication at baseline (ANTIDEP+), while 16.5% fell into either category (EDS_ANTIDEP+). Baseline ANTIDEP+, longitudinal transition into ANTIDEP+ and accelerated epigenetic aging directly predicted increased mortality risk. GrimAge DNA methylation age acceleration (AgeAccelGrim) partially mediated total effects of baseline ANTIDEP+ and EDS_ANTIDEP+ on all-cause mortality risk in socio-demographic factors-adjusted models (Pure Indirect Effect >0, P < 0.05; Total Effect >0, P < 0.05). Thus, higher AgeAccelGrim partially explained the relationship between antidepressant use and increased all-cause mortality risk, though only prior to controlling for lifestyle and health-related factors. “Antidepressant use and epigenetic age acceleration independently predicted increased all-cause mortality risk. Further studies are needed in varying populations.”DOI - https://doi.org/10.18632/aging.205868Corresponding author - May A. Beydoun - baydounm@mail.nih.govSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205868Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, depressive symptoms, epigenetic age acceleration, mortalityAbout Aging-USAging publishes research papers in all fields of aging research, including but not limited to aging processes (from yeast to mammals), cellular senescence, age-related diseases (such as cancer and Alzheimer’s disease) and their prevention and treatment, anti-aging strategies and drug development, and, importantly, the role of signal transduction pathways in aging (such as mTOR) and potential approaches to modulate these signaling pathways to extend lifespan.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- June 5, 2024 – A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 10, entitled, “Serine racemase expression profile in the prefrontal cortex and hippocampal subregions during aging in male and female rats.”Aging is associated with a decrease in N-methyl-D-aspartate (NMDA) receptor function, which is critical for maintaining synaptic plasticity, learning, and memory. Activation of the NMDA receptor requires binding of the neurotransmitter glutamate and also the presence of co-agonist D-serine at the glycine site. The enzymatic conversion of L-serine to D-serine is facilitated by the enzyme serine racemase (SR). Subsequently, SR plays a pivotal role in regulating NMDA receptor activity, thereby impacting synaptic plasticity and memory processes in the central nervous system. As such, age-related changes in the expression of SR could contribute to decreased NMDA receptor function. However, age-associated changes in SR expression levels in the medial and lateral prefrontal cortex (mPFC, lPFC), and in the dorsal hippocampal subfields, CA1, CA3, and dentate gyrus (DG), have not been thoroughly elucidated. In this new study, researchers Linda Bean, Prodip K. Bose, Asha Rani, and Ashok Kumar from Indiana University School of Medicine, North Florida/South Georgia Veterans Health System, and the University of Florida aimed to determine the SR expression profile, including protein levels and mRNA, for these regions in aged and young male and female Fischer-344 rats. Their results demonstrate a significant reduction in SR expression levels in the mPFC and all hippocampal subfields of aged rats compared to young rats. No sex differences were observed in the expression of SR. “These findings suggest that the decrease in SR levels may play a role in the age-associated reduction of NMDA receptor function in brain regions crucial for cognitive function and synaptic plasticity.”DOI - https://doi.org/10.18632/aging.205841Corresponding author - Ashok Kumar - kash@ufl.eduSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205841Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, serine racemase, hippocampus, medial prefrontal cortex (mPFC), NMDA receptorAbout Aging-USAging publishes research papers in all fields of aging research, including but not limited to aging processes (from yeast to mammals), cellular senescence, age-related diseases (such as cancer and Alzheimer’s disease) and their prevention and treatment, anti-aging strategies and drug development, and, importantly, the role of signal transduction pathways in aging (such as mTOR) and potential approaches to modulate these signaling pathways to extend lifespan.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- June 3, 2024 – A new research paper was published on the cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 10, entitled, “Integrated liver and serum proteomics uncover sexual dimorphism and alteration of several immune response proteins in an aging Werner syndrome mouse model.”Werner syndrome (WS) is a progeroid disorder caused by mutations in a protein containing both a DNA exonuclease and DNA helicase domains. Previous studies indicated that males lacking the helicase domain of the Wrn protein orthologue exhibited hepatic transcriptomic and metabolic alterations. In this new study, researchers Lucie Aumailley, Marie Julie Dubois, André Marette, and Michel Lebel from Université Laval used a label-free liquid chromatography-tandem mass spectrometry approach to uncover proteins abundance associated with specific biological processes that differed depending on the age (four or ten months) and/or the genotype (wild type or Wrn mutant) in the serum and liver of mice. Principal component analysis of the proteomic data from both serum and hepatic tissue revealed a sexual dimorphism regardless of the age and the genotype of the mice. “Moreover, although all Wrn mutant mice exhibited fatty liver by the age of ten months, a significant age and genotype dependent enrichment of proteins involved in lipid and fatty acid metabolic processes were uncovered only in males.”Also, a genotype dependent increase in serum oxidant detoxification processes was observed in the serum of Wrn mutant males. Despite these sexual differences, several aspects of the immune system were affected in both females and males. Finally, an increase of specific immunoglobulin molecules was common in the liver and serum of both older Wrn mutant females and males. “Such results suggest that specific immunoglobulin variants maybe associated with fatty liver progression in WS.”DOI - https://doi.org/10.18632/aging.205866Corresponding author - Michel Lebel - michel.lebel@crchudequebec.ulaval.caSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205866Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, proteomics, Werner syndrome, fatty liver, sexual dimorphism, immunoglobulinsAbout Aging-USAging publishes research papers in all fields of aging research, including but not limited to aging processes (from yeast to mammals), cellular senescence, age-related diseases (such as cancer and Alzheimer’s disease) and their prevention and treatment, anti-aging strategies and drug development, and, importantly, the role of signal transduction pathways in aging (such as mTOR) and potential approaches to modulate these signaling pathways to extend lifespan.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- May 22, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 9, entitled, “Cell type-dependent modulation of senescence features using Weo electrolyzed water.”Electrolyzed-reduced water has powerful antioxidant properties with constituents that scavenge reactive oxygen species (ROS), which are known to be produced by several intrinsic and extrinsic processes. When there is an imbalance between ROS production and antioxidant defenses, oxidative stress occurs. Persistent oxidative stress leads to cellular senescence, an important hallmark of aging, and is involved in several age-related conditions and illnesses. In this new study, researchers Brenda L. Court-Vazquez, Shirley A. Arroyo-Vizcarrondo, Jonathan A. Poli, Lara Nyman, Kelly Halderman, Anthony Ginter, and Pierre-Yves Desprez from Weo LLC and California Pacific Medical Center investigated whether Weo electrolyzed water (WEW) could modulate the phenotype of senescent cells. “The focus of this study was to utilize two different cell types, human normal fibroblasts and human breast cancer cells, to investigate the impact of Weo electrolyzed water (WEW) on markers of cellular senescence, inflammation, and stress response genes.”The researchers compared normal human lung fibroblasts (BJ) and breast cancer cells (T47D) treated with hydrogen peroxide (H2O2) to induce senescence. They assessed the molecular impact of WEW on markers of cellular senescence, senescence-associated secretory phenotype (SASP) factors, and stress response genes. Treatment with WEW modulated markers of cellular senescence, such as the senescence-associated β-galactosidase (SA-β-gal) activity, EdU incorporation and p21 expression, similarly in both cell types. However, WEW modulated the expression of SASP factors and stress response genes in a cell type-dependent and opposite fashion, significantly decreasing them in BJ cells, while stimulating their expression in T47D cells. Reduction in the expression of SASP factors and stress-related genes in BJ cells suggests that WEW acts as a protective factor, thereby reducing oxidative stress in normal cells, while making cancer cells more sensitive to the effects of cellular stress, thus increasing their elimination and consequently reducing their deleterious effects. “In conclusion, we have shown here that the new technology developed by Weo, WEW, could attenuate the overall process of cellular senescence in both normal BJ fibroblasts and cancer T47D cells.”DOI - https://doi.org/10.18632/aging.205789Corresponding authors - Brenda L. Court-Vazquez - bco@we-o.com, and Pierre-Yves Desprez - pydesprez@cpmcri.orgSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, cellular senescence, senescence-associated secretory phenotype, oxidative stress, lung fibroblasts, breast cancer cells, senomorphicAbout Aging-USAging publishes research papers in all fields of aging research, including but not limited to aging processes (from yeast to mammals), cellular senescence, age-related diseases (such as cancer and Alzheimer’s disease) and their prevention and treatment, anti-aging strategies and drug development, and, importantly, the role of signal transduction pathways in aging (such as mTOR) and potential approaches to modulate these signaling pathways to extend lifespan.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Dr. Leonid Peshkin from the Department of Systems Biology at Harvard Medical School details a research perspective he co-authored that was published by Aging (Aging-US) in Volume 16, Issue 4, entitled, “On standardization of controls in lifespan studies.”#aging #author #interview #researcher#data #standardization #lifespan #longevity #study #perspective #openaccess #openscience #peerreview #journal #publication #publishing #meded #spotlight #agingshort #videoDOI - https://doi.org/10.18632/aging.205604Corresponding author - Leonid Peshkin - pesha@hms.harvard.eduVideo interview - https://www.youtube.com/watch?v=N_tL2aTN2JwInterview transcript - https://aging-us.net/2024/05/22/behind-the-study-on-standardization-of-controls-in-lifespan-studies/AbstractThe search for interventions to slow down and even reverse aging is a burgeoning field. The literature cites hundreds of supposedly beneficial pharmacological and genetic interventions in model organisms: mice, rats, flies and worms, where research into physiology is routinely accompanied by lifespan data. However, when experimental animals from one article live as long as controls from another article, comparing the results of interventions across studies can yield misleading outcomes. Theoretically, all lifespan data are ripe for re-analysis: we could contrast the molecular targets and pathways across studies and help focus the further search for interventions. Alas, the results of most longevity studies are difficult to compare. This is in part because there are no clear, universally accepted standards for conducting such experiments or even for reporting such data. The situation is worsened by the fact that the authors often do not describe experimental conditions completely. As a result, works on longevity make up a set of precedents, each of which might be interesting in its own right, yet incoherent and incomparable at least for the reason that in a general context, it may indicate, for example, not prolonging the life of an average organism, but compensating for any genetic abnormalities of a particular sample or inappropriate living conditions. Here we point out specific issues and propose solutions for quality control by checking both inter- and intra-study consistency of lifespan data.Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205604Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, animal disease models, survival modeling, data standardizationAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- May 21, 2024 – A new research #paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 9, entitled, “Germicidal lamps using UV-C radiation may pose health safety issues: a biomolecular analysis of their effects on apoptosis and senescence.”The battle against the COVID-19 pandemic has spurred a heightened state of vigilance in global healthcare, leading to the proliferation of diverse sanitization methods. Among these approaches, germicidal lamps utilizing ultraviolet (UV) rays, particularly UV-C (wavelength ranging from 280 to 100 nm), have gained prominence for domestic use. These light-emitting diode (LED) lamps are designed to sanitize the air, objects, and surfaces. However, the prevailing concern is that these UV lamps are often introduced into the market without adequate accompanying information to ensure their safe utilization. Importantly, exposure to absorbed UV light can potentially trigger adverse biological responses, encompassing cell death and senescence.In this new study, researchers Nicola Alessio, Alessia Ambrosino, Andrea Boggi, Domenico Aprile, Iole Pinto, Giovanni Galano, Umberto Galderisi, and Giovanni Di Bernardo from the University of Campania Luigi Vanvitelli, Regional Public Health Laboratory in Siena, Italy, ASL Napoli 1 Centro P.S.I. Napoli Est-Barra, and Temple University performed a series of investigations aimed at comprehending the biological repercussions of UV-C radiation exposure from readily available domestic lamps. “Our focus centered on epithelial retinal cells, keratinocytes, and fibroblasts, components of the skin and ocular targets frequently exposed to UV irradiation.”Their findings underscore the potential harm associated with even brief exposure to UV, leading to irreversible and detrimental alterations in both skin cells and retinal cells of the eye. Notably, epithelial retinal cells exhibited heightened sensitivity, marked by substantial apoptosis. In contrast, keratinocytes demonstrated resilience to apoptosis even at elevated UV doses, though they were prone to senescence. Meanwhile, fibroblasts displayed a gradual amplification of both senescence and apoptosis as radiation doses escalated.“In summary, despite the potential benefits offered by UV-C in deactivating pathogens like SARS-CoV-2, it remains evident that the concurrent risks posed by UV-C to human health cannot be ignored.”DOI - https://doi.org/10.18632/aging.205787Corresponding authors - Umberto Galderisi - umberto.galderisi@unicampania.it, and Giovanni Di Bernardo - gianni.dibernardo@unicampania.itSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205787Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, senescence, apoptosis, UV light, public healthAbout Aging-USAging publishes research papers in all fields of aging research, including but not limited to aging processes (from yeast to mammals), cellular senescence, age-related diseases (such as cancer and Alzheimer’s disease) and their prevention and treatment, anti-aging strategies and drug development, and, importantly, the role of signal transduction pathways in aging (such as mTOR) and potential approaches to modulate these signaling pathways to extend lifespan.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- May 20, 2024 – Aging is a contributor at the 2024 Systems Aging Gordon Research Conference (GRC) on “Systems Modeling, Aging Biomarkers, and Longevity Interventions” — taking place from June 2–7, 2024, in Castelldefels, Barcelona, Spain.“The conference will present recent advances in systemic rejuvenation, multi-omics approaches, applications of machine learning/artificial intelligence, and approaches for enhancing the chance of successfully translating basic research results to the clinic.” – GRC.orgAdditionally, many Aging authors have been invited to speak and lead discussions at the 2024 Systems Aging GRC. Among them are distinguished members of Aging’s Editorial Board, including Steve Horvath, David Sinclair, Vera Gorbunova, Vadim Gladyshev, Guido Kroemer, and Anne Brunet.“The program will include speakers from diverse fields who are united in their pursuit of pioneering longevity and rejuvenating interventions. The 2024 Systems Aging GRC also aims to present advanced approaches for identifying comprehensive interventions that alleviate age-related pathology.” – GRC.orgAbout Aging:Aging publishes research papers in all fields of aging research, including but not limited to aging processes (from yeast to mammals), cellular senescence, age-related diseases (such as cancer and Alzheimer’s disease) and their prevention and treatment, anti-aging strategies and drug development, and, importantly, the role of signal transduction pathways in aging (such as mTOR) and potential approaches to modulate these signaling pathways to extend lifespan.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed Central, Web of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
For centuries, the question of when human life commences has perplexed philosophers, theologians, and scientists alike. With the advent of modern reproductive technologies and groundbreaking scientific advancements, this profound inquiry has taken on renewed urgency and complexity. In a fascinating new review paper, researchers Polina A. Loseva and Vadim N. Gladyshev from Harvard Medical School delved into this intricate subject, exploring the multifaceted perspectives that have shaped our understanding of life’s origins. On May 6, 2024, their review was published on the cover of Aging’s Volume 16, Issue 9, entitled, “The beginning of becoming a human.” Below, this article breaks down their chronological review of the various ways life has been defined: movement, fusion, self-sufficiency, uniqueness, and now, aging.Full blog - https://aging-us.org/2024/05/when-does-human-life-truly-begin/Paper DOI - https://doi.org/10.18632/aging.205824Corresponding authors - Polina A. Loseva - polina.loseva89@gmail.com, and Vadim N. Gladyshev - vgladyshev@rics.bwh.harvard.eduSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205824Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, human, life, 14-day ruleAbout Aging-USAging publishes research papers in all fields of aging research, including but not limited to aging processes (from yeast to mammals), cellular senescence, age-related diseases (such as cancer and Alzheimer’s disease) and their prevention and treatment, anti-aging strategies and drug development, and, importantly, the role of signal transduction pathways in aging (such as mTOR) and potential approaches to modulate these signaling pathways to extend lifespan.The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.).Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- May 14, 2024 – A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 8, entitled, “Characterization of age-associated gene expression changes in mouse sweat glands.”Evaporation of sweat on the skin surface is the major mechanism for dissipating heat in humans. The secretory capacity of sweat glands (SWGs) declines during aging, leading to heat intolerance in the elderly, but the mechanisms responsible for this decline are poorly understood. In this new study, researchers Alexandra G. Zonnefeld, Chang-Yi Cui, Dimitrios Tsitsipatis, Yulan Piao, Jinshui Fan, Krystyna Mazan-Mamczarz, Yutong Xue, Fred E. Indig, Supriyo De, and Myriam Gorospe from the National Institutes of Health’s National Institute on Aging investigated the molecular changes accompanying SWG aging in mice, where sweat tests confirmed a significant reduction of active SWGs in old mice relative to young mice. “We first identified SWG-enriched mRNAs by comparing the skin transcriptome of Eda mutant Tabby male mice, which lack SWGs, with that of wild-type control mice by RNA-sequencing analysis.”This comparison revealed 171 mRNAs enriched in SWGs, including 47 mRNAs encoding ‘core secretory’ proteins such as transcription factors, ion channels, ion transporters, and trans-synaptic signaling proteins. Among these, 28 SWG-enriched mRNAs showed significantly altered abundance in the aged male footpad skin, and 11 of them, including Foxa1, Best2, Chrm3, and Foxc1 mRNAs, were found in the ‘core secretory’ category. Consistent with the changes in mRNA expression levels, immunohistology revealed that higher numbers of secretory cells from old SWGs express the transcription factor FOXC1, the protein product of Foxc1 mRNA. “In sum, our study identified mRNAs enriched in SWGs, including those that encode core secretory proteins, and altered abundance of these mRNAs and proteins with aging in mouse SWGs.”DOI - https://doi.org/10.18632/aging.205776Corresponding authors - Chang-Yi Cui - cuic@mail.nih.gov, and Myriam Gorospe - gorospem@grc.nia.nih.govAuthor interview - https://www.youtube.com/watch?v=7A_TREuSv54Video abstract - https://www.youtube.com/watch?v=yJEphCaMhK8Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205776Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, FOXA1, BEST2, FOXC1, ectodysplasin/Eda, TabbyAbout Aging-USAging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- May 13, 2024 – Impact Journals publishes scholarly journals in the biomedical sciences, with a focus on all areas of cancer and aging research. Aging is one of the most prominent journals published by Impact Journals. Impact Journals is proud to participate at the Society for Scholarly Publishing (SSP) 46th Annual Meeting, which convenes in Boston, Massachusetts, at the Westin Boston Seaport District from May 29–31, 2024. This year, the SSP Annual Meeting theme is “Inflection Point: Setting the Course for the Future of Scholarly Communication.”Visit booth #212 at the SSP 46th Annual Meeting 2024 to connect with members of the Aging team.About Aging-US:Aging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed Central, Web of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
Dr. Chang-Yi Cui and Alexandra G. Zonnefeld from the Laboratory of Genetics and Genomics, National Institute on Aging in Baltimore, MD, discuss a research paper they co-authored that was published by Aging (Aging-US) in Volume 16, Issue 8, entitled, “Characterization of age-associated gene expression changes in mouse sweat glands.”DOI - https://doi.org/10.18632/aging.205776Corresponding authors - Chang-Yi Cui - cuic@mail.nih.gov, and Myriam Gorospe - gorospem@grc.nia.nih.govVideo interview - https://www.youtube.com/watch?v=7A_TREuSv54AbstractEvaporation of sweat on the skin surface is the major mechanism for dissipating heat in humans. The secretory capacity of sweat glands (SWGs) declines during aging, leading to heat intolerance in the elderly, but the mechanisms responsible for this decline are poorly understood. We investigated the molecular changes accompanying SWG aging in mice, where sweat tests confirmed a significant reduction of active SWGs in old mice relative to young mice. We first identified SWG-enriched mRNAs by comparing the skin transcriptome of Eda mutant Tabby male mice, which lack SWGs, with that of wild-type control mice by RNA-sequencing analysis. This comparison revealed 171 mRNAs enriched in SWGs, including 47 mRNAs encoding ‘core secretory’ proteins such as transcription factors, ion channels, ion transporters, and trans-synaptic signaling proteins. Among these, 28 SWG-enriched mRNAs showed significantly altered abundance in the aged male footpad skin, and 11 of them, including Foxa1, Best2, Chrm3, and Foxc1 mRNAs, were found in the ‘core secretory’ category. Consistent with the changes in mRNA expression levels, immunohistology revealed that higher numbers of secretory cells from old SWGs express the transcription factor FOXC1, the protein product of Foxc1 mRNA. In sum, our study identified mRNAs enriched in SWGs, including those that encode core secretory proteins, and altered abundance of these mRNAs and proteins with aging in mouse SWGs.Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205776Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, FOXA1, BEST2, FOXC1, ectodysplasin/Eda, TabbyAbout Aging-USAging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed Central, Web of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- May 9, 2024 – A new review #paper was #published in advance by Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), entitled, “The beginning of becoming a human.”According to birth certificates, the life of a child begins once their body comes out of the mother’s womb. In this new review, researchers Polina A. Loseva and Vadim N. Gladyshev from Harvard Medical School pose the controversial question: when does their organismal life begin? Science holds a palette of answers—depending on how one defines a human life.In 1984, a commission on the regulatory framework for human embryo experimentation opted not to answer this question, instead setting a boundary, 14 days post-fertilization, beyond which any experiments were forbidden. Recently, as the reproductive technologies developed and the demand for experimentation grew stronger, this boundary may be set aside leaving the ultimate decision to local oversight committees. While science has not come closer to setting a zero point for human life, there has been significant progress in our understanding of early mammalian embryogenesis. It has become clear that the 14-day stage does in fact possess features, which make it a foundational time point for a developing human. Importantly, this stage defines the separation of soma from the germline and marks the boundary between rejuvenation and aging. “We explore how different levels of life organization emerge during human development and suggest a new meaning for the 14-day stage in organismal life that is grounded in recent mechanistic advances and insights from aging studies.”DOI - https://doi.org/10.18632/aging.205824Corresponding authors - Polina A. Loseva - polina.loseva89@gmail.com, and Vadim N. Gladyshev - vgladyshev@rics.bwh.harvard.eduVideo short - https://www.youtube.com/watch?v=8LYjXYaePaMSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205824Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, human, life, 14-day ruleAbout Aging-USAging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- May 8, 2024 – A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 8, entitled, “The association between neighborhood deprivation and DNA methylation in an autopsy cohort.”Previous research has found that living in a disadvantaged neighborhood is associated with poor health outcomes. Living in disadvantaged neighborhoods may alter inflammation and immune response in the body, which could be reflected in epigenetic mechanisms such as DNA methylation (DNAm). In this new study, researchers Lindsay Pett, Zhenjiang Li, Sarina Abrishamcar, Kenyaita Hodge, Todd Everson, Grace Christensen, Marla Gearing, Michael S. Kobor, Chaini Konwar, Julia L. MacIsaac, Kristy Dever, Aliza P. Wingo, Allan Levey, James J. Lah, Thomas S. Wingo, and Anke Hüls from Emory University, University of British Columbia, BC Children’s Hospital Research Institute, Centre for Molecular Medicine and Therapeutics, and Atlanta VA Medical Center used robust linear regression models to conduct an epigenome-wide association study examining the association between neighborhood deprivation (Area Deprivation Index; ADI), and DNAm in brain tissue from 159 donors enrolled in the Emory Goizueta Alzheimer’s Disease Research Center (Georgia, USA). “We found one CpG site (cg26514961, gene PLXNC1) significantly associated with ADI after controlling for covariates and multiple testing (p-value=5.0e-8).”Effect modification by APOE ε4 was statistically significant for the top ten CpG sites from the EWAS of ADI, indicating that the observed associations between ADI and DNAm were mainly driven by donors who carried at least one APOE ε4 allele. Four of the top ten CpG sites showed a significant concordance between brain tissue and tissues that are easily accessible in living individuals (blood, buccal cells, saliva), including DNAm in cg26514961 (PLXNC1). This study identified one CpG site (cg26514961, PLXNC1 gene) that was significantly associated with neighborhood deprivation in brain tissue. PLXNC1 is related to immune response, which may be one biological pathway how neighborhood conditions affect health. “The concordance between brain and other tissues for our top CpG sites could make them potential candidates for biomarkers in living individuals.”DOI - https://doi.org/10.18632/aging.205764Corresponding author - Anke Hüls - anke.huels@emory.eduSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205764Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout Aging-USAging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- May 7, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 8, entitled, “Associations among NMR-measured inflammatory and metabolic biomarkers and accelerated aging in cardiac catheterization patients.”Research into aging has grown substantially with the creation of molecular biomarkers of biological age that can be used to determine age acceleration. Concurrently, nuclear magnetic resonance (NMR) assessment of biomarkers of inflammation and metabolism provides researchers with new ways to examine intermediate risk factors for chronic disease.In this new study, researchers Henry Raab, Elizabeth R. Hauser, Lydia Coulter Kwee, Svati H. Shah, William E. Kraus, and Cavin K. Ward-Caviness from the U.S. Environmental Protection Agency and Duke University used data from a cardiac catheterization cohort to examine associations between biomarkers of cardiometabolic health and accelerated aging assessed using both gene expression (Transcriptomic Age) and DNA methylation (Hannum Age, GrimAge, Horvath Age, and Phenotypic Age). “This study utilizes the CATHGEN cohort from the Jiang et al. study to investigate associations between multiple epigenetic and transcriptomic aging biomarkers and a broad array of NMR-based measures of inflammation, lipid homeostasis, and diabetes risk.”Linear regression models were used to associate accelerated aging with each outcome (cardiometabolic health biomarkers) while adjusting for chronological age, sex, race, and neighborhood socioeconomic status. Their study shows a robust association between GlycA and GrimAge (5.71, 95% CI = 4.36, 7.05, P = 7.94 × 10−16), Hannum Age (1.81, 95% CI = 0.65, 2.98, P = 2.30 × 10−3), and Phenotypic Age (2.88, 95% CI = 1.91, 3.87, P = 1.21 × 10−8). The researchers also saw inverse associations between apolipoprotein A-1 and aging biomarkers. “These associations provide insight into the relationship between aging and cardiometabolic health that may be informative for vulnerable populations.”DOI - https://doi.org/10.18632/aging.205758Corresponding authors - Cavin K. Ward-Caviness - ward-caviness.cavin@epa.govSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205758Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, biological aging, NMR, biomarkers, cardiac catheterizationAbout Aging-USAging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
With an ever-increasing global population grappling with age-related ocular ailments like cataracts, dry eyes, glaucoma, and macular degeneration, the need for new research in this domain is more pressing than ever. In a new study, researchers Kohsaku Numa, Sandip Kumar Patel, Zhixin A. Zhang, Jordan B. Burton, Akifumi Matsumoto, Jun-Wei B. Hughes, Chie Sotozono, Birgit Schilling, Pierre-Yves Desprez, Judith Campisi (1948-2024), and Koji Kitazawa from the Buck Institute for Research on Aging, Kyoto Prefectural University of Medicine, University of Cambridge, and California Pacific Medical Center shed light on a pivotal aspect of corneal health – the impact of ultraviolet-A (UV-A) radiation on corneal endothelial cells. Their research paper was published on the cover of Aging’s Volume 16, Issue 8, entitled, “Senescent characteristics of human corneal endothelial cells upon ultraviolet-A exposure.”“The objective of this study was to investigate the senescent phenotypes of human corneal endothelial cells (hCEnCs) upon treatment with ultraviolet (UV)-A.”Full blog - https://aging-us.org/2024/05/uv-a-exposure-cellular-senescence-and-vision-impairment/Paper DOI - https://doi.org/10.18632/aging.205761Corresponding author - Koji Kitazawa - kkitazaw@koto.kpu-m.ac.jpSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205761Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, cellular senescence, senescence-associated secretory phenotype, RNA-Seq, proteomics, gene ontology analysisAbout Aging-USAging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed Central, Web of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- May 1, 2024 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 8, entitled, “A novel deep proteomic approach in human skeletal muscle unveils distinct molecular signatures affected by aging and resistance training.”The skeletal muscle proteome alterations to aging and resistance training have been reported in prior studies. However, conventional proteomics in skeletal muscle typically yields wide protein abundance ranges that mask the detection of lowly expressed proteins.In this new study, researchers Michael D. Roberts, Bradley A. Ruple, Joshua S. Godwin, Mason C. McIntosh, Shao-Yung Chen, Nicholas J. Kontos, Anthony Agyin-Birikorang, Max Michel, Daniel L. Plotkin, Madison L. Mattingly, Brooks Mobley, Tim N. Ziegenfuss, Andrew D. Fruge, and Andreas N. Kavazis from Auburn University, Seer, Inc., and The Center for Applied Health Sciences adopted a novel deep proteomics approach whereby myofibril (MyoF) and non-MyoF fractions were separately subjected to protein corona nanoparticle complex formation prior to digestion and Liquid Chromatography Mass Spectrometry (LC-MS). “Specifically, we investigated MyoF and non-MyoF proteomic profiles of the vastus lateralis muscle of younger (Y, 22±2 years old; n=5) and middle-aged participants (MA, 56±8 years old; n=6). Additionally, MA muscle was analyzed following eight weeks of resistance training (RT, 2d/week).” Across all participants, the number of non-MyoF proteins detected averaged to be 5,645±266 (range: 4,888–5,987) and the number of MyoF proteins detected averaged to be 2,611±326 (range: 1,944–3,101). Differences in the non-MyoF (8.4%) and MyoF (2.5%) proteomes were evident between age cohorts, and most differentially expressed non-MyoF proteins (447/543) were more enriched in MA versus Y. Biological processes in the non-MyoF fraction were predicted to be operative in MA versus Y including increased cellular stress, mRNA splicing, translation elongation, and ubiquitin-mediated proteolysis. RT in MA participants only altered ~0.3% of MyoF and ~1.0% of non-MyoF proteomes. “In summary, aging and RT predominantly affect non-contractile proteins in skeletal muscle. Additionally, marginal proteome adaptations with RT suggest more rigorous training may stimulate more robust effects or that RT, regardless of age, subtly alters basal state skeletal muscle protein abundances.”DOI - https://doi.org/10.18632/aging.205751Corresponding author - Michael D. Roberts - mdr0024@auburn.eduSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205751Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout AgingAging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- April 30, 2024 – A new #researchpaper was #published on the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 8, entitled, “Senescent characteristics of human corneal endothelial cells upon ultraviolet-A exposure.”In this new study, researchers Kohsaku Numa, Sandip Kumar Patel, Zhixin A. Zhang, Jordan B. Burton, Akifumi Matsumoto, Jun-Wei B. Hughes, Chie Sotozono, Birgit Schilling, Pierre-Yves Desprez, Judith Campisi (1948-2024), and Koji Kitazawa from Buck Institute for Research on Aging, Kyoto Prefectural University of Medicine, University of Cambridge, and California Pacific Medical Center investigated the senescent phenotypes of human corneal endothelial cells (hCEnCs) upon treatment with ultraviolet (UV)-A.“We assessed cell morphology, senescence-associated β-galactosidase (SA-β-gal) activity, cell proliferation and expression of senescence markers (p16 and p21) in hCEnCs exposed to UV-A radiation, and senescent hCEnCs induced by ionizing radiation (IR) were used as positive controls.”The researchers performed RNA sequencing and proteomics analyses to compare gene and protein expression profiles between UV-A- and IR-induced senescent hCEnCs — they also compared the results to non-senescent hCEnCs. Cells exposed to 5 J/cm2 of UV-A or to IR exhibited typical senescent phenotypes, including enlargement, increased SA-β-gal activity, decreased cell proliferation and elevated expression of p16 and p21. RNA-Seq analysis revealed that 83.9% of the genes significantly upregulated and 82.6% of the genes significantly downregulated in UV-A-induced senescent hCEnCs overlapped with the genes regulated in IR-induced senescent hCEnCs. Proteomics also revealed that 93.8% of the proteins significantly upregulated in UV-A-induced senescent hCEnCs overlapped with those induced by IR. In proteomics analyses, senescent hCEnCs induced by UV-A exhibited elevated expression levels of several factors part of the senescence-associated secretory phenotype.“In this study, where senescence was induced by UV-A, a more physiological stress for hCEnCs compared to IR, we determined that UV-A modulated the expression of many genes and proteins typically altered upon IR treatment, a more conventional method of senescence induction, even though UV-A also modulated specific pathways unrelated to IR.”DOI - https://doi.org/10.18632/aging.205761Corresponding author - Koji Kitazawa - kkitazaw@koto.kpu-m.ac.jpSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205761Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout Aging-USAging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- April 24, 2024 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 7, entitled, “Using genetics and proteomics data to identify proteins causally related to COVID-19, healthspan and lifespan: a Mendelian randomization study.”The COVID-19 pandemic poses a heavy burden on public health and accounts for substantial mortality and morbidity. Proteins are building blocks of life, but specific proteins causally related to COVID-19, healthspan and lifespan, have not been systematically examined. In this new study, researchers Jie V. Zhao, Minhao Yao, and Zhonghua Liu from The University of Hong Kong and Columbia University conducted a Mendelian randomization study to assess the effects of 1,361 plasma proteins on COVID-19, healthspan and lifespan, using large GWAS of severe COVID-19 (up to 13,769 cases and 1,072,442 controls), COVID-19 hospitalization (32,519 cases and 2,062,805 controls) and SARS-COV2 infection (122,616 cases and 2,475,240 controls), healthspan (n = 300,477) and parental lifespan (~0.8 million of European ancestry).“We included both COVID-19 and healthspan and lifespan in the outcome, because COVID-19 which occurred in recent years reflects a new threat to longevity, whilst healthspan and lifespan reflect overall morbidity and mortality.”The researchers identified 35, 43, and 63 proteins for severe COVID, COVID-19 hospitalization, and SARS-COV2 infection, and 4, 32, and 19 proteins for healthspan, father’s attained age, and mother’s attained age. In addition to some proteins reported previously, such as SFTPD related to severe COVID-19, the team identified novel proteins involved in inflammation and immunity (such as ICAM-2 and ICAM-5 which affect COVID-19 risk, CXCL9, HLA-DRA and LILRB4 for healthspan and lifespan), apoptosis (such as FGFR2 and ERBB4 which affect COVID-19 risk and FOXO3 which affect lifespan) and metabolism (such as PCSK9 which lowers lifespan). They found 2, 2, and 3 proteins shared between COVID-19 and healthspan/lifespan, such as CXADR and LEFTY2, shared between severe COVID-19 and healthspan/lifespan. Three proteins affecting COVID-19 and seven proteins affecting healthspan/lifespan are targeted by existing drugs.“Our study provided novel insights into protein targets affecting COVID-19, healthspan and lifespan, with implications for developing new treatment and drug repurposing.”DOI - https://doi.org/10.18632/aging.205711Corresponding authors - Jie V. Zhao - janezhao@hku.hk, and Zhonghua Liu - zl2509@cumc.columbia.eduSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout Aging-USAging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- April 23, 2024 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 7, entitled, “The coupling between healthspan and lifespan in Caenorhabditis depends on complex interactions between compound intervention and genetic background.”Aging is characterized by declining health that results in decreased cellular resilience and neuromuscular function. The relationship between lifespan and health, and the influence of genetic background on that relationship, has important implications in the development of pharmacological anti-aging interventions. In this new study, researchers Stephen A. Banse, E. Grace Jackson, Christine A. Sedore, Brian Onken, David Hall, Anna Coleman-Hulbert, Phu Huynh, Theo Garrett, Erik Johnson, Girish Harinath, Delaney Inman, Suzhen Guo, Mackenzie Morshead, Jian Xue, Ron Falkowski, Esteban Chen, Christopher Herrera, Allie J. Kirsch, Viviana I. Perez, Max Guo, Gordon J. Lithgow, Monica Driscoll, and Patrick C. Phillips from the University of Oregon, The State University of New Jersey (Rutgers), The Buck Institute for Research on Aging, and National Institute on Aging assessed swimming performance as well as survival under thermal and oxidative stress across a nematode genetic diversity test panel to evaluate health effects for three compounds previously studied in the Caenorhabditis Intervention Testing Program and thought to promote longevity in different ways – NP1 (nitrophenyl piperazine-containing compound 1), propyl gallate, and resveratrol. “Overall, we find the relationships among median lifespan, oxidative stress resistance, thermotolerance, and mobility vigor to be complex.” The researchers showed that oxidative stress resistance and thermotolerance vary with compound intervention, genetic background, and age. The effects of tested compounds on swimming locomotion, in contrast, are largely species-specific. In this study, thermotolerance, but not oxidative stress or swimming ability, correlates with lifespan. Notably, some compounds exert strong impact on some health measures without an equally strong impact on lifespan. “Our results demonstrate the importance of assessing health and lifespan across genetic backgrounds in the effort to identify reproducible anti-aging interventions, with data underscoring how personalized treatments might be required to optimize health benefits.”DOI - https://doi.org/10.18632/aging.205743Corresponding authors - Gordon J. Lithgow - glithgow@buckinstitute.org, Monica Driscoll - driscoll@dls.rutgers.edu, and Patrick C. Phillips - pphil@uoregon.eduAbout Aging-USAging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY - April 22, 2024 – The Longevity & Aging Series is an enlightening and progressive video interview series presented by Aging, featuring esteemed researchers discussing the latest in aging research, with a focus on their studies published by Aging.In the premiere episode of the second season of the Longevity & Aging Series, Dr. Irina Conboy and Xiaoyue (Serafina) Mei from the Department of Bioengineering and QB3 at the University of California, Berkeley, discuss a priority research paper they co-authored and published in Aging’s Volume 15, Issue 17, entitled, “Fail-tests of DNA methylation clocks, and development of a noise barometer for measuring epigenetic pressure of aging and disease.”DOI - https://doi.org/10.18632/aging.205046Corresponding Author - Irina M. Conboy - iconboy@berkeley.eduVideo - https://www.youtube.com/watch?v=aYhUPpEPVv4Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205046Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, DNA methylation, epigenetics, clocks’ fail-test, biological noiseAbout Aging-USAging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed Central, Web of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
In the season 2 premiere episode of the Longevity & Aging Series, Dr. Irina Conboy and Xiaoyue (Serafina) Mei from the Department of Bioengineering and QB3 at the University of California, discuss a research paper they co-authored that was published in Volume 15, Issue 17, of Aging (Aging-US), entitled, “Fail-tests of DNA methylation clocks, and development of a noise barometer for measuring epigenetic pressure of aging and disease.”DOI - https://doi.org/10.18632/aging.205046Corresponding Author - Irina M. Conboy - iconboy@berkeley.eduVideo interview - https://www.youtube.com/watch?v=aYhUPpEPVv4Transcript - https://aging-us.net/2024/04/22/longevity-aging-series-s2-e1-dr-irina-conboy-and-xiaoyue-serafina-mei/Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205046Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, DNA methylation, epigenetics, clocks’ fail-test, biological noiseAbout Longevity & Aging SeriesIn its second season, the Longevity & Aging Series is a monthly video series that features esteemed researchers discussing the latest in aging research with a focus on their studies published by Aging (Aging-US).Learn more - https://www.aging-us.com/longevityAbout Aging-USAging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed Central, Web of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
Aging is still shrouded in proverbial darkness. But, some researchers hypothesize that aging may be linked to stem cell exhaustion. Stemness, the ability of a cell to differentiate into various cell types, is an essential characteristic defining the functionality of stem cells. It has been observed that stem cells seem to diminish with age, although the precise role of stem cells in human aging remains to be elucidated. “Among the biological pathways associated with aging, we can highlight stem cell exhaustion, which argues that during normal aging, the decrease in the number or activity of these cells contributes to physiological dysfunction in aged tissues [4].”In a new study, researchers Gabriel Arantes dos Santos, Gustavo Daniel Vega Magdaleno and João Pedro de Magalhães from the Universidade de Sao Paulo, University of Birmingham and the University of Liverpool applied a machine learning method to detect stemness signatures from transcriptome data of healthy human tissues. Their research paper was published on April 4, 2024, and chosen as the cover of Aging’s Volume 16, Issue 7, entitled, “Evidence of a pan-tissue decline in stemness during human aging.”Full blog - https://aging-us.org/2024/04/first-evidence-of-a-pan-tissue-decline-in-stemness-during-human-aging/Paper DOI - https://doi.org/10.18632/aging.205717Corresponding author - João Pedro de Magalhães - jp@senescence.infoSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205717Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, longevity, stem cells, transcriptomics, senescenceAbout Aging-USAging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed Central, Web of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- April 17, 2024 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 7, entitled, “The impact of continuous and intermittent ketogenic diets on cognitive behavior, motor function, and blood lipids in TgF344-AD rats.”Studies suggest that ketogenic diets (KD) may improve memory in mouse models of aging and Alzheimer’s disease (AD). In this new study, researchers Jennifer M. Rutkowsky, Zabrisky Roland, Anthony Valenzuela, An B. Nguyen, Heui Hye Park, Natalie Six, Ilknur Dursun, Kyoungmi Kim, Pamela J. Lein, and Jon J. Ramsey from the University of California Davis and Istinye University determined whether a continuous or intermittent KD (IKD) enhanced cognitive behavior in the TgF344-AD rat model of AD. “[...] it remains to be determined whether long-term consumption of a ketogenic diet can mitigate declines in cognitive or motor behavior in a rat model of AD. Therefore, the current study aimed to determine whether a KD improves cognitive or motor behavior in the TgF344-AD rat.”At 6 months-old, TgF344-AD and wild-type (WT) littermates were placed on a control (CD), KD, or IKD (morning CD and afternoon KD) provided as two meals per day for 2 or 6 months. Cognitive and motor behavior and circulating β-hydroxybutyrate (BHB), AD biomarkers and blood lipids were assessed. Animals on a KD diet had elevated circulating BHB, with IKD levels intermediate to CD and KD. TgF344-AD rats displayed impaired spatial learning memory in the Barnes maze at 8 and 12 months of age and impaired motor coordination at 12 months of age. Neither KD nor IKD improved performance compared to CD. At 12 months of age, TgF344-AD animals had elevated blood lipids. IKD reduced lipids to WT levels with KD further reducing cholesterol below WT levels. “[...] the IKD or KD did not improve motor coordination or spatial learning memory compared to the control diet. However, KD, and to a lesser extent IKD, mitigated elevations in plasma lipids in the TgF344-AD rats. Furthermore, the KD diet decreased plasma levels of total Tau in females.”DOI - https://doi.org/10.18632/aging.205741Corresponding author - Jennifer M. Rutkowsky - jrutkowsky@ucdavis.eduSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205741Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, ketogenic diet, Alzheimer’s disease, cognitive behavior, motor function, lipidsAbout Aging-USAging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- April 15, 2024 – A new #researchpaper was #published on the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 7, entitled, “Evidence of a pan-tissue decline in stemness during human aging.”Despite their biological importance, the role of stem cells in human aging remains to be elucidated. In a new study, researchers Gabriel Arantes dos Santos, Gustavo Daniel Vega Magdaleno and João Pedro de Magalhães from the Universidade de Sao Paulo, University of Birmingham and the University of Liverpool applied a machine learning method to detect stemness signatures from transcriptome data of healthy human tissues.“In this work, we applied a machine learning methodology to GTEx transcriptome data and assigned stemness scores to 17,382 healthy samples from 30 human tissues aged between 20 and 79 years.”The team found that ~60% of the studied tissues exhibit a significant negative correlation between the subject's age and stemness score. The only significant exception was the uterus, where they observed an increased stemness with age. Moreover, the researchers observed that stemness is positively correlated with cell proliferation and negatively correlated with cellular senescence. Finally, they also observed a trend that hematopoietic stem cells derived from older individuals might have higher stemness scores. “In conclusion, we assigned stemness scores to human samples and show evidence of a pan-tissue loss of stemness during human aging, which adds weight to the idea that stem cell deterioration may contribute to human aging.”DOI - https://doi.org/10.18632/aging.205717Corresponding author - João Pedro de Magalhães - jp@senescence.infoSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205717Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, longevity, stem cells, transcriptomics, senescenceAbout Aging-USAging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed Central, Web of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- April 10, 2024 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 6, entitled, “Geraniol attenuates oxidative stress and neuroinflammation-mediated cognitive impairment in D galactose-induced mouse aging model.”D-galactose (D-gal) administration was proven to induce cognitive impairment and aging in rodents’ models. Geraniol (GNL) belongs to the acyclic isoprenoid monoterpenes. GNL reduces inflammation by changing important signaling pathways and cytokines, and thus it is plausible to be used as a medicine for treating disorders linked to inflammation. In this new study, researchers Peramaiyan Rajendran, Fatma J. Al-Saeedi, Rebai Ben Ammar, Basem M. Abdallah, Enas M. Ali, Najla Khaled Al Abdulsalam, Sujatha Tejavat, Duaa Althumairy, Vishnu Priya Veeraraghavan, Sarah Abdulaziz Alamer, Gamal M. Bekhet, and Emad A. Ahmed from King Faisal University, Kuwait University, Center of Biotechnology of Borj-Cedria, Saveetha University, Alexandria University, and Assiut University examined the therapeutic effects of GNL on D-gal-induced oxidative stress and neuroinflammation-mediated memory loss in mice. “Life expectancy in the 21st century is rising, resulting in more age-related illnesses, such as memory impairment and Alzheimer’s disease. In this study, GNL was studied for its protective effect on D-gal-induced aging in mice.”The study was conducted using six groups of mice (6 mice per group). The first group received normal saline, then D-gal (150 mg/wt) dissolved in normal saline solution (0.9%, w/v) was given orally for 9 weeks to the second group. In the III group, from the second week until the 10th week, mice were treated orally (without anesthesia) with D-gal (150 mg/kg body wt) and GNL weekly twice (40 mg/kg body wt) four hours later. Mice in Group IV were treated with GNL from the second week up until the end of the experiment. For comparison of young versus elderly mice, 4 month old (Group V) and 16-month-old (Group VI) control mice were used. “We evaluated the changes in antioxidant levels, PI3K/Akt levels, and Nrf2 levels. We also examined how D-gal and GNL treated pathological aging changes.”Administration of GNL induced a significant increase in spatial learning and memory with spontaneously altered behavior. Enhancing anti-oxidant and anti-inflammatory effects and activating PI3K/Akt were the mechanisms that mediated this effect. Further, GNL treatment upregulated Nrf2 and HO-1 to reduce oxidative stress and apoptosis. This was confirmed using 99mTc-HMPAO brain flow gamma bioassays. “Thus, our data suggested GNL as a promising agent for treating neuroinflammation-induced cognitive impairment.”DOI - https://doi.org/10.18632/aging.205677Corresponding authors - Peramaiyan Rajendran - prajendran@kfu.edu.sa, and Fatma J. Al-Saeedi - fatma.alsaeedi@ku.edu.kwAbout Aging-USAging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.Please visit our website at https://www.Aging-US.com and connect with us on social media.MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- April 9, 2024 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 6, entitled, “CMS121: a novel approach to mitigate aging-related obesity and metabolic dysfunction.”Modulated by differences in genetic and environmental factors, laboratory mice often show progressive weight gain, eventually leading to obesity and metabolic dyshomeostasis. The geroneuroprotector CMS121 has a positive effect on energy metabolism in a mouse model of type 2 diabetes. In this new study, researchers Alcir L. Dafre, Saadia Zahid, Jessica Jorge Probst, Antonio Currais, Jingting Yu, David Schubert, and Pamela Maher from Salk Institute for Biological Studies, National University of Sciences and Technology (NUST) and Federal University of Santa Catarina investigated the potential of CMS121 to counteract the metabolic changes observed during the ageing process of wild type mice.“This comprehensive analysis aimed to further understand how CMS121 influences the metabolic landscape, paving the way for potential therapeutic applications beyond its established geroneuroprotective benefits.”Control or CMS121-containing diets were supplied ad libitum for 6 months, and mice were sacrificed at the age of 7 months. Blood, adipose tissue, and liver were analyzed for glucose, lipids, and protein markers of energy metabolism. The CMS121 diet induced a 40% decrease in body weight gain and improved both glucose and lipid indexes. Lower levels of hepatic caspase 1, caspase 3, and NOX4 were observed with CMS121 indicating a lower liver inflammatory status. Adipose tissue from CMS121-treated mice showed increased levels of the transcription factors Nrf1 and TFAM, as well as markers of mitochondrial electron transport complexes, levels of GLUT4 and a higher resting metabolic rate. Metabolomic analysis revealed elevated plasma concentrations of short chain acylcarnitines and butyrate metabolites in mice treated with CMS121.“The diminished de novo lipogenesis, which is associated with increased acetyl-CoA, acylcarnitine, and butyrate metabolite levels, could contribute to safeguarding not only the peripheral system but also the aging brain. By mimicking the effects of ketogenic diets, CMS121 holds promise for metabolic diseases such as obesity and diabetes, since these diets are hard to follow over the long term.”DOI - https://doi.org/10.18632/aging.205673Corresponding authors - Pamela Maher - pmaher@salk.edu and Alcir L. Dafre - alcir.dafre@ufsc.brSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205673Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout Aging-USAging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Menopause marks the beginning of the next biological chapter in a woman’s life. Characterized by the natural ebb of reproductive hormones (particularly estrogen), menopause ushers in a new season of aging. This hormonal shift not only signifies a transition in fertility but also influences systemic health. The menopause-associated decline in estrogen has been associated with various health issues, including alterations in brain structure and function. However, the mechanics of this phenomenon are still poorly understood. A greater understanding of how menopause alters the brain could aid in the early detection, and possible prevention, of neurodegenerative disease.In a new study, researchers Gwang-Won Kim, Kwangsung Park, Yun-Hyeon Kim, and Gwang-Woo Jeong from Chonnam National University used neuroimaging to shed light on how menopause alters brain morphology and functional connectivity in postmenopausal women. On March 23, 2024, their research paper was published as the cover of Aging’s Volume 16, Issue 6, entitled, "Altered brain morphology and functional connectivity in postmenopausal women: automatic segmentation of whole-brain and thalamic subnuclei and resting-state fMRI."Full blog - https://aging-us.org/2024/04/how-menopause-changes-brain-structure-and-connectivity/Paper DOI - https://doi.org/10.18632/aging.205662Corresponding author - Gwang-Woo Jeong - gwjeong@jnu.ac.krSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205662Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, brain morphology, functional connectivity, sex hormones, thalamic subnucleiAbout Aging-USAging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed Central, Web of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- April 3, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 6, entitled, “Targeting mitochondrial dysfunction using methylene blue or mitoquinone to improve skeletal aging.”Methylene blue (MB) is a well-established antioxidant that has been shown to improve mitochondrial function in both in vitro and in vivo settings. Mitoquinone (MitoQ) is a selective antioxidant that specifically targets mitochondria and effectively reduces the accumulation of reactive oxygen species. In this new study, researchers Sher Bahadur Poudel, Dorra Frikha-Benayed, Ryan R. Ruff, Gozde Yildirim, Manisha Dixit, Ron Korstanje, Laura Robinson, Richard A. Miller, David E. Harrison, John R. Strong, Mitchell B. Schaffler, and Shoshana Yakar from New York University College of Dentistry, City College of New York, The Jackson Laboratory, University of Michigan, South Texas Veterans Health Care System, and The University of Texas Health Science Center investigated the effect of long-term administration of MB or MitoQ on skeletal morphology during the aging process.“[...] we administered MB to aged (18 months old) female C57BL/J6 mice, as well as to adult male and female mice with a genetically diverse background (UM-HET3). Additionally, we used MitoQ as an alternative approach to target mitochondrial oxidative stress during aging in adult female and male UM-HET3 mice.”Although the researchers observed some beneficial effects of MB and MitoQ in vitro, the administration of these compounds in vivo did not alter the progression of age-induced bone loss. Specifically, treating 18-month-old female mice with MB for 6 or 12 months did not have an effect on age-related bone loss. Similarly, long-term treatment with MB from 7 to 22 months or with MitoQ from 4 to 22 months of age did not affect the morphology of cortical bone at the mid-diaphysis of the femur, trabecular bone at the distal-metaphysis of the femur, or trabecular bone at the lumbar vertebra-5 in UM-HET3 mice.“Based on our findings, it appears that long-term treatment with MB or MitoQ alone, as a means to reduce skeletal oxidative stress, is insufficient to inhibit age-associated bone loss. This supports the notion that interventions solely with antioxidants may not provide adequate protection against skeletal aging.”DOI - https://doi.org/10.18632/aging.205147Corresponding author - Shoshana Yakar - sy1007@nyu.eduSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205147Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout Aging-USAging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- April 1, 2024 – A new #research paper was #published on the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 6, entitled, “Altered brain morphology and functional connectivity in postmenopausal women: automatic segmentation of whole-brain and thalamic subnuclei and resting-state fMRI.”The transition to menopause is associated with various physiological changes, including alterations in brain structure and function. However, menopause-related structural and functional changes are poorly understood. In this new study, researchers Gwang-Won Kim, Kwangsung Park, Yun-Hyeon Kim, and Gwang-Woo Jeong from Chonnam National University not only compared the brain volume changes between premenopausal and postmenopausal women, but also evaluated the functional connectivity between the targeted brain regions associated with structural atrophy in postmenopausal women. “To the best of our knowledge, no comparative neuroimaging study on alterations in the brain volume and functional connectivity, especially focusing on the thalamic subnuclei in premenopausal vs. postmenopausal women has been reported.”Each of the 21 premenopausal and postmenopausal women underwent magnetic resonance imaging (MRI). T1-weighted MRI and resting-state functional MRI data were used to compare the brain volume and seed-based functional connectivity, respectively. In statistical analysis, multivariate analysis of variance, with age and whole brain volume as covariates, was used to evaluate surface areas and subcortical volumes between the two groups. Postmenopausal women showed significantly smaller cortical surface, especially in the left medial orbitofrontal cortex (mOFC), right superior temporal cortex, and right lateral orbitofrontal cortex, compared to premenopausal women (p < 0.05, Bonferroni-corrected) as well as significantly decreased functional connectivity between the left mOFC and the right thalamus was observed (p < 0.005, Monte-Carlo corrected). Although postmenopausal women did not show volume atrophy in the right thalamus, the volume of the right pulvinar anterior, which is one of the distinguished thalamic subnuclei, was significantly decreased (p < 0.05, Bonferroni-corrected). “Postmenopausal women showed significantly lower left mOFC, right lOFC, and right STC surface areas, reduced right PuA volume, and decreased left mOFC-right thalamus functional connectivity compared to premenopausal women. If replicated in an independent sample, these findings will be helpful for understanding the effects of menopause on the altered brain volume and functional connectivity in postmenopausal women.”DOI - https://doi.org/10.18632/aging.205662Corresponding author - Gwang-Woo Jeong - gwjeong@jnu.ac.krAbout Aging-USAging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.Please visit our website at https://www.Aging-US.com.MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- March 26, 2024 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 5, entitled, “Chlorogenic acid prevents ovariectomized-induced bone loss by facilitating osteoblast functions and suppressing osteoclast formation.”Osteoporosis is a common bone disease in aging populations, principally in postmenopausal women. Anti-resorptive and anabolic drugs have been applied to prevent and cure osteoporosis and are associated with different adverse effects. Du-Zhong is usually applied in Traditional Chinese Medicine to strengthen bone, regulate bone metabolism, and treat osteoporosis. Chlorogenic acid is a major polyphenol in Du-Zhong. In this new study, researchers Chien-Yi Ho, Chih-Hsin Tang, Trung-Loc Ho, Wen-Ling Wang, and Chun-Hsu Yao from China Medical University, China Medical University Hospital and Asia University found chlorogenic acid to enhance osteoblast proliferation and differentiation. Chlorogenic acid also inhibited RANKL-induced osteoclastogenesis. Notably, ovariectomy significantly decreased bone volume and mechanical properties in the ovariectomized (OVX) rats. Administration of chlorogenic acid antagonized OVX-induced bone loss. “Taken together, chlorogenic acid seems to be a hopeful molecule for the development of novel anti-osteoporosis treatment.”DOI - https://doi.org/10.18632/aging.205635Corresponding authors - Wen-Ling Wang - supercocono1@mail.cmu.edu.tw, and Chun-Hsu Yao - chyao@mail.cmu.edu.twSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205635Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, chlorogenic acid, osteoporosis, ovariectomized, osteoclast, osteoblastAbout Aging-USAging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed Central, Web of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
The human brain is a complex organ, and its aging process is influenced by a plethora of factors, both genetic and environmental. Aging-related changes in the brain can lead to cognitive decline and susceptibility to neurodegenerative diseases. Therefore, understanding the molecular mechanisms underlying these changes is crucial for developing therapeutic strategies to delay or prevent age-related cognitive decline.Over the past few years, a myriad of scientific studies have been conducted to understand the intricate relationship between our genes and the aging process. In a new study, researchers Joseph A. Zarrella and Amy Tsurumi from Harvard T.H. Chan School of Public Health, Massachusetts General Hospital, Harvard Medical School, and Shriner’s Hospitals for Children-Boston explored the concept of genome brain age prediction, a groundbreaking area of study that employs advanced bioinformatics tools to analyze changes in gene expression associated with aging. On February 28, 2024, their research paper was published and chosen as the cover paper for Aging’s Volume 16, Issue 5, entitled, “Genome-wide transcriptome profiling and development of age prediction models in the human brain.”“[…] we aimed to profile transcriptome changes in the aging PFC [prefrontal cortex] overall and compare females and males, and develop prediction models for age.”Full blog - https://aging-us.org/2024/03/predicting-brain-age-with-machine-learning-and-transcriptome-profiling/Paper DOI - https://doi.org/10.18632/aging.205609Corresponding author - Amy Tsurumi - atsurumi@mgh.harvard.eduSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205609Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, machine learning, prediction model, biomarker, transcriptomeAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- March 20, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 5, entitled, “FoxO6-mediated ApoC3 upregulation promotes hepatic steatosis and hyperlipidemia in aged rats fed a high-fat diet.”FoxO6, an identified factor, induces hyperlipidemia and hepatic steatosis during aging by activating hepatic lipoprotein secretion and lipogenesis leading to increased ApoC3 concentrations in the bloodstream. However, the intricate mechanisms underlying hepatic steatosis induced by elevated FoxO6 under hyperglycemic conditions remain intricate and require further elucidation.In this new study, researchers Dae Hyun Kim, Seulah Lee, Sang Gyun Noh, Jaewon Lee, and Hae Young Chung from Pusan National University aimed to delineate the regulatory pathway involving ApoC3 controlled by FoxO6 and its resultant functional impacts.“[...] we employed a spectrum of models including liver cell cultures, aged rats subjected to HFD, transgenic mice overexpressing FoxO6 (FoxO6-Tg), and FoxO6 knockout mice (FoxO6-KO).”Their findings indicate that FoxO6 triggered ApoC3-driven lipid accumulation in the livers of aged rats on an HFD and in FoxO6-Tg, consequently leading to hepatic steatosis and hyperglycemia. Conversely, the absence of FoxO6 attenuated the expression of genes involved in lipogenesis, resulting in diminished hepatic lipid accumulation and mitigated hyperlipidemia in murine models. Additionally, the upregulation of FoxO6 due to elevated glucose levels led to increased ApoC3 expression, consequently instigating cellular triglyceride mediated lipid accumulation. The transcriptional activation of FoxO6 induced by both the HFD and high glucose levels resulted in hepatic steatosis by upregulating ApoC3 and genes associated with gluconeogenesis in aged rats and liver cell cultures.“Our conclusions indicate that the upregulation of ApoC3 by FoxO6 promotes the development of hyperlipidemia, hyperglycemia, and hepatic steatosis in vivo, and in vitro. Taken together, our findings underscore the significance of FoxO6 in driving hyperlipidemia and hepatic steatosis specifically under hyperglycemic states by enhancing the expression of ApoC3 in aged rats.”DOI - https://doi.org/10.18632/aging.205610Corresponding author - Hae Young Chung - hyjung@pusan.ac.krSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205610Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, HFD-feeding aging, forkhead transcription factor O6, ApoC3, lipid accumulation, hepatic steatosisAging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- March 19, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 5, entitled, “PR55α-controlled protein phosphatase 2A inhibits p16 expression and blocks cellular senescence induction by γ-irradiation.”Cellular senescence is a permanent cell cycle arrest that can be triggered by both internal and external genotoxic stressors, such as telomere dysfunction and DNA damage. The execution of senescence is mainly by two pathways, p16/RB and p53/p21, which lead to CDK4/6 inhibition and RB activation to block cell cycle progression. While the regulation of p53/p21 signaling in response to DNA damage and other insults is well-defined, the regulation of the p16/RB pathway in response to various stressors remains poorly understood. In this new study, researchers Chitra Palanivel, Lepakshe S. V. Madduri, Ashley L. Hein, Christopher B. Jenkins, Brendan T. Graff, Alison L. Camero, Sumin Zhou, Charles A. Enke, Michel M. Ouellette, and Ying Yan from the University of Nebraska Medical Center report a novel function of PR55α, a regulatory subunit of PP2A Ser/Thr phosphatase, as a potent inhibitor of p16 expression and senescence induction by ionizing radiation (IR), such as γ-rays. “During natural aging, there is a gradual accumulation of p16-expressing senescent cells in tissues [76]. To investigate the significance of PR55α in this up-regulation of p16, we compared levels of the p16 and PR55α proteins in a panel of normal tissue specimens derived from young (≤43 y/o) and old (≥68 y/o) donors.”The results show that ectopic PR55α expression in normal pancreatic cells inhibits p16 transcription, increases RB phosphorylation, and blocks IR-induced senescence. Conversely, PR55α-knockdown by shRNA in pancreatic cancer cells elevates p16 transcription, reduces RB phosphorylation, and triggers senescence induction after IR. Furthermore, this PR55α function in the regulation of p16 and senescence is p53-independent because it was unaffected by the mutational status of p53. Moreover, PR55α only affects p16 expression but not p14 (ARF) expression, which is also transcribed from the same CDKN2A locus but from an alternative promoter. In normal human tissues, levels of p16 and PR55α proteins were inversely correlated and mutually exclusive. “Collectively, these results describe a novel function of PR55α/PP2A in blocking p16/RB signaling and IR-induced cellular senescence.”DOI - https://doi.org/10.18632/aging.205619Corresponding authors - Michel M. Ouellette - mouellet@unmc.edu, and Ying Yan - yyan@unmc.eduAbout Aging-US:Aging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed Central, Web of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).Please visit our website at https://www.Aging-US.com.MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- March 15, 2024 – A new #research paper was #published on the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 5, entitled, “Genome-wide transcriptome profiling and development of age prediction models in the human brain.”Aging-related transcriptome changes in various regions of the healthy human brain have been explored in previous works, however, a study to develop prediction models for age based on the expression levels of specific panels of transcripts is lacking. Moreover, studies that have assessed sexually dimorphic gene activities in the aging brain have reported discrepant results, suggesting that additional studies would be advantageous. The prefrontal cortex (PFC) region was previously shown to have a particularly large number of significant transcriptome alterations during healthy aging in a study that compared different regions in the human brain. In this new study, researchers Joseph A. Zarrella and Amy Tsurumi from the Harvard T.H. Chan School of Public Health, Massachusetts General Hospital, Harvard Medical School, and Shriner's Hospitals for Children-Boston aimed to profile PFC transcriptome changes during healthy human aging overall and comparing potential differences between female and male samples, as well as developing chronological age prediction models by various methods.“We harmonized neuropathologically normal PFC transcriptome datasets obtained from the Gene Expression Omnibus (GEO) repository, ranging in age from 21 to 105 years, and found a large number of differentially regulated transcripts in the old and elderly, compared to young samples overall, and compared female and male-specific expression alterations.” The team assessed the genes that were associated with age by employing ontology, pathway, and network analyses. Furthermore, they applied various established (least absolute shrinkage and selection operator (Lasso) and Elastic Net (EN)) and recent (eXtreme Gradient Boosting (XGBoost) and Light Gradient Boosting Machine (LightGBM)) machine learning algorithms to develop accurate prediction models for chronological age and validated them. Studies to further validate these models in other large populations and molecular studies to elucidate the potential mechanisms by which the transcripts identified may be related to aging phenotypes would be advantageous.“Our results support the notions that specific gene expression changes in the PFC are highly correlated with age, that some transcripts show female and male-specific differences, and that machine learning algorithms are useful tools for developing prediction models for age based on transcriptome information.”DOI - https://doi.org/10.18632/aging.205609Corresponding author - Amy Tsurumi - atsurumi@mgh.harvard.eduSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
Dr. Azra Frkatović-Hodžić from Genos Glycoscience Research Laboratory in Zagreb, Croatia, discusses a #research paper she co-authored that was #published by Aging (Aging-US) in Volume 15, Issue 24, entitled, “Mapping of the gene network that regulates glycan clock of ageing.”DOI - https://doi.org/10.18632/aging.205106Corresponding authors - Azra Frkatović-Hodžić - afrkatovic@genos.hr, and Gordan Lauc - glauc@genos.hrVideo - https://www.youtube.com/watch?v=5ExLCMDhpdEVideo transcription - https://aging-us.net/2024/03/13/behind-the-study-mapping-of-gene-network-that-regulates-glycan-clock-of-aging/AbstractGlycans are an essential structural component of immunoglobulin G (IgG) that modulate its structure and function. However, regulatory mechanisms behind this complex posttranslational modification are not well known. Previous genome-wide association studies (GWAS) identified 29 genomic regions involved in regulation of IgG glycosylation, but only a few were functionally validated. One of the key functional features of IgG glycosylation is the addition of galactose (galactosylation), a trait which was shown to be associated with ageing. We performed GWAS of IgG galactosylation (N=13,705) and identified 16 significantly associated loci, indicating that IgG galactosylation is regulated by a complex network of genes that extends beyond the galactosyltransferase enzyme that adds galactose to IgG glycans. Gene prioritization identified 37 candidate genes. Using a recently developed CRISPR/dCas9 system we manipulated gene expression of candidate genes in the in vitro IgG expression system. Upregulation of three genes, EEF1A1, MANBA and TNFRSF13B, changed the IgG glycome composition, which confirmed that these three genes are involved in IgG galactosylation in this in vitro expression system.Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205106Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, genome-wide association study, glycosylation, glycan clock, immunoglobulin G, CRISPR/dCas9About Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- March 13, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 4, entitled, “Single-Cell RNA-seq reveals transcriptomic modulation of Alzheimer’s disease by activated protein C.”Single-Cell RNA sequencing reveals changes in cell population in Alzheimer’s disease (AD) model 5xFAD (5x Familial AD mutation) versus wild type (WT) mice. In this new study, researchers Mohammad Kasim Fatmi, Hao Wang, Lily Slotabec, Changhong Wen, Blaise Seale, Bi Zhao, and Ji Li from the University of South Florida, University of Mississippi Medical Center and the G.V. (Sonny) Montgomery VA Medical Center used single-cell RNA sequencing and bioinformatic analysis to analyze the effects of APC [Activated Protein C] treatment on AD transgenic mice.“In our investigation, we utilized transgenic mice that contain expression for five major amyloid pathologies that allow for rapid progression of AD and Aβ deposition known as 5xFAD mice.”The returned sequencing data was processed through the 10x Genomics CellRanger platform to perform alignment and form corresponding matrix to perform bioinformatic analysis. Alterations in glial cells occurred in 5xFAD versus WT, especially increases in microglia proliferation were profound in 5xFAD. Differential expression testing of glial cells in 5xFAD versus WT revealed gene regulation. Globally, the critical genes implicated in AD progression are upregulated such as Apoe, Ctsb, Trem2, and Tyrobp. Using this differential expression data, GO term enrichment was completed to observe possible biological processes impacted by AD progression. Utilizing anti-inflammatory and cyto-protective recombinant Activated Protein C (APC), the researchers uncovered inflammatory processes to be downregulated by APC treatment in addition to recuperation of nervous system processes. Moreover, animal studies demonstrated that administration of recombinant APC significantly attenuated Aβ burden and improved cognitive function of 5xFAD mice. “The downregulation of highly expressed AD biomarkers in 5xFAD could provide insight into the mechanisms by which APC administration benefits AD.”DOI - https://doi.org/10.18632/aging.205624Corresponding authors - Bi Zhao - bizhao@usf.edu, and Ji Li - jli3@umc.eduSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205624Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, APC, Alzheimer’s disease, inflammationAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- March 12, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 4, entitled, “Associations of prenatal one-carbon metabolism nutrients and metals with epigenetic aging biomarkers at birth and in childhood in a US cohort.”Epigenetic gestational age acceleration (EGAA) at birth and epigenetic age acceleration (EAA) in childhood may be biomarkers of the intrauterine environment. In this new study, researchers Anne K. Bozack, Sheryl L. Rifas-Shiman, Andrea A. Baccarelli, Robert O. Wright, Diane R. Gold, Emily Oken, Marie-France Hivert, and Andres Cardenas from Stanford University School of Medicine, Harvard Medical School, Harvard T.H. Chan School of Public Health, Columbia University, and Icahn School of Medicine at Mount Sinai investigated the extent to which first-trimester folate, B12, 5 essential and 7 non-essential metals in maternal circulation are associated with EGAA and EAA in early life. “[...] we hypothesized that OCM [one-carbon metabolism] nutrients and essential metals would be positively associated with EGAA and non-essential metals would be negatively associated with EGAA. We also investigated nonlinear associations and associations with mixtures of micronutrients and metals.”Bohlin EGAA and Horvath pan-tissue and skin and blood EAA were calculated using DNA methylation measured in cord blood (N=351) and mid-childhood blood (N=326; median age = 7.7 years) in the Project Viva pre-birth cohort. A one standard deviation increase in individual essential metals (copper, manganese, and zinc) was associated with 0.94-1.2 weeks lower Horvath EAA at birth, and patterns of exposures identified by exploratory factor analysis suggested that a common source of essential metals was associated with Horvath EAA. The researchers also observed evidence of nonlinear associations of zinc with Bohlin EGAA, magnesium and lead with Horvath EAA, and cesium with skin and blood EAA at birth. Overall, associations at birth did not persist in mid-childhood; however, arsenic was associated with greater EAA at birth and in childhood. “Prenatal metals, including essential metals and arsenic, are associated with epigenetic aging in early life, which might be associated with future health.”DOI - https://doi.org/10.18632/aging.205602Corresponding author - Andres Cardenas - andres.cardenas@stanford.eduSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205602Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, epigenetic age acceleration, metals, folate, B12, prenatal exposuresAbout Aging-USAging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases. Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- March 11, 2024 – Impact Journals #publishes scholarly #journals in the #biomedical sciences with a focus on all areas of cancer and aging research. Aging is one of the most prominent journals published by Impact Journals. Impact Journals will be participating as an exhibitor at the American Association for Cancer Research (AACR) Annual Meeting 2024 from April 5-10 at the San Diego Convention Center in San Diego, California. This year, the AACR meeting theme is “Inspiring Science • Fueling Progress • Revolutionizing Care.”Visit booth number 4159 at the AACR Annual Meeting 2024 to connect with members of the Aging team.Aging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed Central, Web of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
Dr. Jiajian Wang from Sun Yat-Sen University, The Chinese University of Hong Kong, the Chinese Academy of Sciences, and the Shenzhen Key Laboratory of Metabolic Health, describes a #research paper he co-authored and #published in Aging’s Volume 16, Issue 3, entitled, “Generating detailed intercellular communication patterns in psoriasis at the single-cell level using social networking, pattern recognition, and manifold learning methods to optimize treatment strategies.”Here is an audio version of a written Q&A that was submitted by Dr. Jiajian Wang on this research.Full Q&A - https://aging-us.net/2024/03/11/behind-the-study-analyzing-psoriasis-communication-patterns-for-treatment-optimization/Paper DOI - https://doi.org/10.18632/aging.205478Corresponding Authors - Jiajian Wang - jiajianwang2019@gmail.com, and Bo Wu - bowu2004@hotmail.comSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205478Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - communication patterns, single cell transcriptome, cell type-specific regulons (CTSRs), proteomic sequencing, social networkingAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
Missing data in aging studies, especially in the assessment of gait speed (the time it takes individuals to cover a set distance), presents a significant challenge. The elderly are more prone to health and functional issues, which often interfere with data collection efforts. Given that gait speed is a key indicator of functional status and overall health in older individuals, ensuring its availability and accurate measurement is essential for the integrity of aging research.In a new study, researchers Robert Thiesmeier, Ahmad Abbadi, Debora Rizzuto, Amaia Calderón-Larrañaga, Scott M. Hofer, and Nicola Orsini from Karolinska Institutet, Stockholm University, Stockholm Gerontology Research Center, and Oregon Health and Science University address the systematic challenge of missing gait speed data in aging research and explore the application of multiple imputation (MI), a statistical technique that has emerged as a constructive approach to handle such gaps in data. The team critically examined the implementation strategies, methodologies, and the impact that these missing variables could have on the outcomes of aging studies, thereby offering a framework to manage and interpret incomplete datasets in aging research. On February 14, 2024, their research paper was published in Aging’s Volume 16, Issue 4, entitled, “Multiple imputation of systematically missing data on gait speed in the Swedish National Study on Aging and Care.”“[...] this study aims to investigate and assess the performance of different MI strategies specifically targeting the systematically missing discrete variable of gait speed in the SNAC [Swedish National Study on Aging and Care] IPDMA [individual participant data meta-analyses] with only four large cohort studies.”Full blog - https://aging-us.org/2024/03/overcoming-missing-data-in-the-swedish-national-study-on-aging/Paper DOI - https://doi.org/10.18632/aging.205552Corresponding authors - Robert Thiesmeier - robert.thiesmeier@ki.seSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205552Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, simulation, systematically missing values, individual participant data, meta-analysis, gait speedAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- March 6, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 4, entitled, “Exploring the effects of Dasatinib, Quercetin, and Fisetin on DNA methylation clocks: a longitudinal study on senolytic interventions.”Senolytics, small molecules targeting cellular senescence, have emerged as potential therapeutics to enhance health span. However, their impact on epigenetic age remains unstudied. In this new study, researchers Edwin Lee, Natàlia Carreras-Gallo, Leilani Lopez, Logan Turner, Aaron Lin, Tavis L. Mendez, Hannah Went, Alan Tomusiak, Eric Verdin, Michael Corley, Lishomwa Ndhlovu, Ryan Smith, and Varun B. Dwaraka from the Institute For Hormonal Balance, TruDiagnostic, Buck Institute for Research on Aging, and Cornell University aimed to assess the effects of senolytic treatments on DNA methylation (DNAm), epigenetic age, and immune cell subsets. “[...] this study aims to comprehensively assess the impact of senolytic drugs on epigenetic aging through two longitudinal studies to address our research objective. The initial investigation focuses on a combination treatment of Dasatinib and Quercetin, while the subsequent phase incorporates Fisetin into the treatment regimen.”In a Phase I pilot study, 19 participants received Dasatinib and Quercetin (DQ) for 6 months, with DNAm measured at baseline, 3 months, and 6 months. Significant increases in epigenetic age acceleration were observed in first-generation epigenetic clocks and mitotic clocks at 3 and 6 months, along with a notable decrease in telomere length. However, no significant differences were observed in second and third-generation clocks. Building upon these findings, a subsequent investigation evaluated the combination of DQ with Fisetin (DQF), a well-known antioxidant and antiaging senolytic molecule. After one year, 19 participants (including 10 from the initial study) received DQF for 6 months, with DNAm assessed at baseline and 6 months. Remarkably, the addition of Fisetin to the treatment resulted in non-significant increases in epigenetic age acceleration, suggesting a potential mitigating effect of Fisetin on the impact of DQ on epigenetic aging. “Furthermore, our analyses unveiled notable differences in immune cell proportions between the DQ and DQF treatment groups, providing a biological basis for the divergent patterns observed in the evolution of epigenetic clocks. These findings warrant further research to validate and comprehensively understand the implications of these combined interventions.”DOI - https://doi.org/10.18632/aging.205581Corresponding authors - Varun B. Dwaraka - varun@trudiagnostic.comSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- March 5, 2024 – A new #research perspective was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 4, entitled, “On standardization of controls in lifespan studies.”In this new paper, researchers Olga Spiridonova, Dmitrii Kriukov, Nikolai Nemirovich-Danchenko, and Leonid Peshkin from Harvard Medical School's Department of Systems Biology discuss the burgeoning field of the search for interventions to slow down, and even reverse, aging. Currently available literature cites hundreds of supposedly beneficial pharmacological and genetic interventions in model organisms: mice, rats, flies, and worms, where research into physiology is routinely accompanied by lifespan data. However, when experimental animals from one article live as long as controls from another article, comparing the results of interventions across studies can yield misleading outcomes. “Theoretically, all lifespan data are ripe for re-analysis: we could contrast the molecular targets and pathways across studies and help focus the further search for interventions.” Alas, the results of most longevity studies are difficult to compare. This is in part because there are no clear, universally accepted standards for conducting such experiments or even for reporting such data. The situation is worsened by the fact that the authors often do not describe experimental conditions completely. As a result, works on longevity make up a set of precedents, each of which might be interesting in its own right, yet incoherent and incomparable at least for the reason that in a general context, it may indicate, for example, not prolonging the life of an average organism, but compensating for any genetic abnormalities of a particular sample or inappropriate living conditions. “Here we point out specific issues and propose solutions for quality control by checking both inter- and intra-study consistency of lifespan data.”DOI - https://doi.org/10.18632/aging.205604Corresponding author - Leonid Peshkin - pesha@hms.harvard.eduSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205604Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, animal disease models, survival modeling, data standardizationAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- February 29, 2024 – A new #research paper was #published on the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 4, entitled, “Mapping the core senescence phenotype of primary human colon fibroblasts.”Advanced age is the largest risk factor for many diseases and several types of cancer, including colorectal cancer (CRC). Senescent cells are known to accumulate with age in various tissues, where they can modulate the surrounding tissue microenvironment through their senescence associated secretory phenotype (SASP). Recently, researchers showed that there is an increased number of senescent cells in the colons of CRC patients and demonstrated that senescent fibroblasts and their SASP create microniches in the colon that are conducive to CRC onset and progression. However, the composition of the SASP is heterogenous and cell-specific, and the precise senescence profile of colon fibroblasts has not been well-defined. In this new study, to generate a SASP atlas of human colon fibroblasts, researchers Namita Ganesh Hattangady, Kelly Carter, Brett Maroni-Rana, Ting Wang, Jessica Lee Ayers, Ming Yu, and William M. Grady from Fred Hutchinson Cancer Center and the University of Washington School of Medicine induced senescence in primary human colon fibroblasts using various in vitro methods and assessed the resulting transcriptome. “[...] we utilized various relevant stressors to induce senescence in primary cultures of colon fibroblasts and perform RNA sequencing (RNASeq) to define an atlas of stressor-specific senescent profiles and a core senescent profile that is commonly regulated by all senescence inducers.”Using RNA Sequencing and further validation by quantitative RT-PCR and Luminex assays, the team define and validate a ‘core senescent profile’ that might play a significant role in shaping the colon microenvironment. They also performed KEGG analysis and GO analyses to identify key pathways and biological processes that are differentially regulated in colon fibroblast senescence. These studies provide insights into potential driver proteins involved in senescence-associated diseases, like CRC, which may lead to therapies to improve overall health in the elderly and to prevent CRC.“Further studies will be needed to address the limitations of our study and to translate our understanding of the SASP and disease into clinical care.”DOI - https://doi.org/10.18632/aging.205577Corresponding authors - William M. Grady - wgrady@fredhutch.org, and Ming Yu - myu@fredhutch.orgSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205577Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, senescence, senescence associated secretory phenotype, SASP, colorectal cancer, cancerAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- February 28, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 3, entitled, “Prognostic model development and molecular subtypes identification in bladder urothelial cancer by oxidative stress signatures.”Mounting studies indicate that oxidative stress (OS) significantly contributes to tumor progression. In this new study, researchers Ying Dong, Xiaoqing Wu, Chaojie Xu, Yasir Hameed, Mostafa A. Abdel-Maksoud, Taghreed N. Almanaa, Mohamed H. Kotob, Wahidah H. Al-Qahtani, Ayman M. Mahmoud, William C. Cho, and Chen Li from Shenzhen Second People’s Hospital, China Academy of Chinese Medical Sciences, Peking University, The Islamia University of Bahawalpur, King Saud University, University of Vienna, Manchester Metropolitan University, Queen Elizabeth Hospital, and Free University of Berlin focused on bladder urothelial cancer (BLCA), an escalating malignancy worldwide that is growing rapidly. “Our objective was to verify the predictive precision of genes associated with overall survival (OS) by constructing a model that forecasts outcomes for bladder cancer and evaluates the prognostic importance of these genetic markers.”Full press release - https://www.aging-us.com/news-room/Prognostic-Model-Development-and-Molecular-Subtypes-Identification-in-Bladder-Urothelial-CancerDOI - https://doi.org/10.18632/aging.205499Corresponding authors - Yasir Hameed - Yasirhameed2011@gmail.com, William C. Cho - chocs@ha.org.hk, and Chen Li - chen.li@fu-berlin.deSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205499Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, oxidative stress, bladder urothelial cancer, tumor microenvironment, immunotherapyAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- February 27, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 3, entitled, “The anti-aging effect of vitamin D and vitamin D receptor in Drosophila midgut.”Adult stem cells are pivotal for maintaining tissue homeostasis, and their functional decline is linked to aging and its associated diseases, influenced by the niche cells’ environment. Age- and cancer-related reduction of vitamin D and its receptor levels are well documented in human clinical studies. However, the mechanisms through which the vitamin D/vitamin D receptor (VitD/VDR) pathway contributes to anti-aging and extends life expectancy are not well understood. In this new study, researchers Joung-Sun Park, Hyun-Jin Na and Yung-Jin Kim from Pusan National University and Korea Food Research Institute aimed to determine the protective role of the vitamin D/vitamin D receptor pathway in differentiated enterocytes (ECs) during intestinal stem cell (ISC) aging. “This study aimed to determine the protective role of VitD/VDR in differentiated ECs during ISC aging using the adult Drosophila intestine model.”By utilizing a well-established Drosophila midgut model for stem cell aging biology, the researchers revealed that vitamin D receptor knockdown in ECs induced ISC proliferation, EC death, ISC aging, and enteroendocrine cell differentiation. Additionally, age- and oxidative stress-induced increases in ISC proliferation and centrosome amplification were reduced by vitamin D treatment. In conclusion, this study provides direct evidence of the anti-aging role of the VitD/VDR pathway, involving protecting ECs during aging, and provides valuable insights for exploring the molecular mechanisms underlying enhanced healthy aging in Drosophila.“Our findings suggest a direct evidence of the anti-aging role of the vitamin D/vitamin D receptor pathway and provides insights into the molecular mechanisms underlying healthy aging in Drosophila.”DOI - https://doi.org/10.18632/aging.205518Corresponding author - Joung-Sun Park - dreamjs78@pusan.ac.krSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205518Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, Drosophila, vitamin D, vitamin D receptor, anti-aging, intestinal stem cellAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- February 21, 2024 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 3, entitled, “Disruption of mitochondrial unfolded protein response results in telomere shortening in mouse oocytes and somatic cells.”Caseinolytic peptidase P (CLPP) plays a central role in mitochondrial unfolded protein response (mtUPR) by promoting the breakdown of misfolded proteins and setting in motion a cascade of reactions to re-establish protein homeostasis. Global germline deletion of Clpp in mice results in female infertility and accelerated follicular depletion. Telomeres are tandem repeats of 5’-TTAGGG-3’ sequences found at the ends of the chromosomes. Telomeres are essential for maintaining chromosome stability during somatic cell division and their shortening is associated with cellular senescence and aging. In this new study, researchers Mauro Cozzolino, Yagmur Ergun, Emma Ristori, Akanksha Garg, Gizem Imamoglu, and Emre Seli from Yale School of Medicine, IVIRMA Global Research Alliance and Imperial College London asked whether the infertility and ovarian aging phenotype caused by global germline deletion of Clpp is associated with somatic aging, and tested telomere length in tissues of young and aging mice. “In this study, we asked whether the infertility and ovarian aging phenotype caused by global germline deletion of Clpp is associated with somatic aging, and tested telomere length in young and aging mice gametes, gonads and somatic tissues.”The team found that impaired mtUPR caused by the lack of CLPP is associated with accelerated telomere shortening in both oocytes and somatic cells of aging mice. In addition, expression of several genes that maintain telomere integrity was decreased, and double-strand DNA breaks were increased in telomeric regions. Their results highlight how impaired mtUPR can affect telomere integrity and demonstrate a link between loss of mitochondrial protein hemostasis, infertility, and somatic aging.“Our findings demonstrate how loss of mitochondrial protein homeostasis may accelerate telomere shortening in oocytes and somatic cells, and provide a link between reproductive and somatic aging.”DOI - https://doi.org/10.18632/aging.205543Corresponding author - Emre Seli - emre.seli@yale.eduSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205543Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, telomere length, Clpp, mitochondrial dysfunction, unfolded protein responseAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- February 20, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 3, entitled, “Defining the progeria phenome.”Progeroid disorders are a heterogenous group of rare and complex hereditary syndromes presenting with pleiotropic phenotypes associated with normal aging. Due to the large variation in clinical presentation the diseases pose a diagnostic challenge for clinicians which consequently restricts medical research. In this new study, researchers Cecilie Worm, Maya Elena Ramirez Schambye, Garik V. Mkrtchyan, Alexander Veviorskiy, Anastasia Shneyderman, Ivan V. Ozerov, Alex Zhavoronkov, Daniela Bakula, and Morten Scheibye-Knudsen from the University of Copenhagen and Insilico Medicine aimed to accommodate this challenge by compiling a list of known progeroid syndromes and calculating the mean prevalence of their associated phenotypes, defining what they term the ‘progeria phenome’. “In this study, we have utilized phenome explorations to define the phenotypes associated with progerias and to develop tools to diagnose patients and identify new progeroid syndromes.”The data were used to train a support vector machine that is available at https://www.mitodb.com and able to classify progerias based on phenotypes. Furthermore, this allowed the researchers to investigate the correlation of progeroid syndromes and syndromes with various pathogenesis using hierarchical clustering algorithms and disease networks. They detected that ataxia-telangiectasia like disorder 2, spastic paraplegia 49 and Meier-Gorlin syndrome display strong association to progeroid syndromes, thereby implying that the syndromes are previously unrecognized progerias. “In conclusion, our study has provided tools to evaluate the likelihood of a syndrome or patient being progeroid. This is a considerable step forward in our understanding of what constitutes a premature aging disorder and how to diagnose them.”DOI - https://doi.org/10.18632/aging.205537Corresponding author - Morten Scheibye-Knudsen - mscheibye@sund.ku.dkSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205537Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, progeria, premature aging, phenome, clinical phenotypeAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
Crossref is a non-profit organization that logs and updates citations for scientific publications. Each month, Crossref identifies a list of the most popular Aging (Aging-US) papers based on the number of times a DOI is successfully resolved. Below are Crossref’s Top 10 Aging DOIs in 2023.10: Old-age-induced obesity reversed by a methionine-deficient diet or oral administration of recombinant methioninase-producing Escherichia coli in C57BL/6 miceDOI: https://doi.org/10.18632/aging.204783Authors: Yutaro Kubota, Qinghong Han, Jose Reynoso, Yusuke Aoki, Noriyuki Masaki, Koya Obara, Kazuyuki Hamada, Michael Bouvet, Takuya Tsunoda, and Robert M. Hoffman9: Metformin use history and genome-wide DNA methylation profile: potential molecular mechanism for aging and longevityDOI: https://doi.org/10.18632/aging.204498 Authors: Pedro S. Marra, Takehiko Yamanashi, Kaitlyn J. Crutchley, Nadia E. Wahba, Zoe-Ella M. Anderson, Manisha Modukuri, Gloria Chang, Tammy Tran, Masaaki Iwata, Hyunkeun Ryan Cho, and Gen Shinozaki8: Age prediction from human blood plasma using proteomic and small RNA data: a comparative analysisDOI: https://doi.org/10.18632/aging.204787 Authors: Jérôme Salignon, Omid R. Faridani, Tasso Miliotis, Georges E. Janssens, Ping Chen, Bader Zarrouki, Rickard Sandberg, Pia Davidsson, and Christian G. Riedel7: Characterization of the HDAC/PI3K inhibitor CUDC-907 as a novel senolyticDOI: https://doi.org/10.18632/aging.204616 Authors: Fares Al-Mansour, Abdullah Alraddadi, Buwei He, Anes Saleh, Marta Poblocka, Wael Alzahrani, Shaun Cowley, and Salvador Macip6: Potential reversal of biological age in women following an 8-week methylation-supportive diet and lifestyle program: a case seriesDOI: https://doi.org/10.18632/aging.204602 Authors: Kara N. Fitzgerald, Tish Campbell, Suzanne Makarem, and Romilly Hodges5: Leukocyte telomere length, T cell composition and DNA methylation ageDOI: https://doi.org/10.18632/aging.101293 Authors: Brian H. Chen, Cara L. Carty, Masayuki Kimura, Jeremy D. Kark, Wei Chen, Shengxu Li, Tao Zhang, Charles Kooperberg, Daniel Levy, Themistocles Assimes, Devin Absher, Steve Horvath, Alexander P. Reiner, and Abraham Aviv4: DNA methylation GrimAge strongly predicts lifespan and healthspanDOI: https://doi.org/10.18632/aging.101684 Authors: Ake T. Lu, Austin Quach, James G. Wilson, Alex P. Reiner, Abraham Aviv, Kenneth Raj, Lifang Hou, Andrea A. Baccarelli, Yun Li, James D. Stewart, Eric A. Whitsel, Themistocles L. Assimes, Luigi Ferrucci, and Steve Horvath3: Deep biomarkers of aging and longevity: from research to applicationsDOI: https://doi.org/10.18632/aging.102475 Authors: Alex Zhavoronkov, Ricky Li, Candice Ma, and Polina Mamoshina2: An epigenetic biomarker of aging for lifespan and healthspanDOI: https://doi.org/10.18632/aging.101414 Authors: Morgan E. Levine, Ake T. Lu, Austin Quach, Brian H. Chen, Themistocles L. Assimes, Stefania Bandinelli, Lifang Hou, Andrea A. Baccarelli, James D. Stewart, Yun Li, Eric A. Whitsel, James G Wilson, Alex P Reiner, Abraham Aviv, Kurt Lohman, Yongmei Liu, Luigi Ferrucci, and Steve Horvath1: Chemically induced reprogramming to reverse cellular agingDOI: https://doi.org/10.18632/aging.204896Authors: Jae-Hyun Yang, Christopher A. Petty, Thomas Dixon-McDougall, Maria Vina Lopez, Alexander Tyshkovskiy, Sun Maybury-Lewis, Xiao Tian, Nabilah Ibrahim, Zhili Chen, Patrick T. Griffin, Matthew Arnold, Jien Li, Oswaldo A. Martinez, Alexander Behn, Ryan Rogers-Hammond, Suzanne Angeli, Vadim N. Gladyshev, and David A. SinclairAging is an open-access, traditional, peer-reviewed journal that has published high-impact papers in all fields of aging research since 2009. All papers are available to readers (at no cost and free of subscription barriers) in bi-monthly issues at Aging-US.com.For media inquiries, please contact media@impactjournals.com.
BUFFALO, NY- February 15, 2024 – A new #research paper was #published on the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 3, entitled, “GV1001 reduces neurodegeneration and prolongs lifespan in 3xTg-AD mouse model through anti-aging effects.”GV1001, which mimics the activity of human telomerase reverse transcriptase, protects neural cells from amyloid beta (Aβ) toxicity and other stressors through extra-telomeric function, as noted in our prior in vitro studies. As per a recent phase II clinical trial, it improves cognitive function in patients with moderate to severe dementia. However, the underlying protective mechanisms remain unclear. In this new study, researchers Hyun-Hee Park, Hyuk Sung Kwon, Kyu-Yong Lee, Ye Eun Kim, Jeong-Woo Son, Na-Young Choi, Myung-Hoon Han, Dong Woo Park, Sangjae Kim, and Seong-Ho Koh from Hanyang University Guri Hospital, Hanyang University Graduate School of Biomedical Science and Engineering and Teloid Inc. aimed to investigate the effects of GV1001 on neurodegeneration, senescence, and survival in triple transgenic Alzheimer’s disease (AD) (3xTg-AD) mice. “ [...] we hypothesised that GV1001 might have anti-aging effects and improve neurodegeneration and senescence in vivo as a possible mechanism for its beneficial effects on AD.”GV1001 (1 mg/kg) was subcutaneously injected into old 3xTg-AD mice thrice a week until the endpoint for sacrifice, and survival was analysed. Magnetic resonance imaging (MRI) and Prussian blue staining (PBS) were performed to evaluate entry of GV1001 entrance into the brain. Diverse molecular studies were performed to investigate the effect of GV1001 on neurodegeneration and cellular senescence in AD model mice, with a particular focus on BACE, amyloid beta1-42 (Aβ1-42), phosphorylated tau, volume of dentate gyrus, β-galactosidase positive cells, telomere length, telomerase activity, and ageing-associated proteins. GV1001 crossed the blood-brain barrier, as confirmed by assessing the status of ferrocenecarboxylic acid-conjugated GV1001 using magnetic resonance imaging and PBS. GV1001 increased the survival of 3xTg-AD mice. It decreased BACE and Aβ1-42 levels, neurodegeneration (i.e., reduced CA1, CA3 and dentate gyrus volume, decreased levels of senescence-associated β-galactosidase positive cells, and increased telomere length and telomerase activity), and levels of ageing-associated proteins. “We suggest that GV1001 exerts anti-ageing effects in 3xTg-AD mice by reducing neurodegeneration and senescence, which contributes to improved survival.”DOI - https://doi.org/10.18632/aging.205489Corresponding authors - Sangjae Kim - chiron@gemvax.com, and Seong-Ho Koh - ksh213@hanyang.ac.krSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- February 13, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 2, entitled, “IL-17 promotes IL-18 production via the MEK/ERK/miR-4492 axis in osteoarthritis synovial fibroblasts.”The concept of osteoarthritis (OA) as a low-grade inflammatory joint disorder has been widely accepted. Many inflammatory mediators are implicated in the pathogenesis of OA. Interleukin (IL)-18 is a pleiotropic cytokine with versatile cellular functions that are pathogenetically important in immune responses, as well as autoimmune, inflammatory, and infectious diseases. IL-17, a proinflammatory cytokine mainly secreted by Th17 cells, is upregulated in OA patients. However, the role of IL-17 in OA progression is unclear. In this new study, researchers Kun-Tsan Lee, Chih-Yang Lin, Shan-Chi Liu, Xiu-Yuan He, Chun-Hao Tsai, Chih-Yuan Ko, Yuan-Hsin Tsai, Chia-Chia Chao, Po-Chun Chen, and Chih-Hsin Tang from National Chung-Hsing University, Taichung Veterans General Hospital, Shin-Kong Wu Ho-Su Memorial Hospital, Mackay Medical College, China Medical University, Show-Chwan Memorial Hospital, Fu-Jen Catholic University, National Taiwan Normal University, Asia University, and China Medical University Hsinchu Hospital used synovial tissues collected from healthy donors and OA patients to detect the expression level of IL-18 by immunohistochemistry stain. “Elucidation of the molecular mechanisms and main factors involved in OA pathogenesis may help with the development of novel therapeutic targets that relieve OA pain or prevent the disease from progressing.”The OA synovial fibroblasts (OASFs) were incubated with recombinant IL-17 and subjected to Western blot, qPCR, and ELISA to examine IL-18 expression level. The chemical inhibitors and siRNAs which targeted signal pathways were used to investigate signal pathways involved in IL-17-induced IL-18 expression. The microRNAs which participated IL-18 expression were surveyed with online databases miRWalk and miRDB, followed by validation with qPCR. This study revealed significantly higher levels of IL-18 expression in synovial tissue from OA patients compared with healthy controls, as well as increased IL-18 expression in OASFs from rats with severe OA. In vitro findings indicated that IL-17 dose-dependently promoted IL-18 production in OASFs. Molecular investigations revealed that the MEK/ERK/miR-4492 axis stimulated IL-18 production when OASFs were treated with IL-17. “This study provides novel insights into the role of IL-17 in the pathogenesis of OA, which may help to inform OA treatment in the future.”DOI - https://doi.org/10.18632/aging.205462Corresponding authors - Po-Chun Chen - pcchen@ntnu.edu.tw, and Chih-Hsin Tang - chtang@mail.cmu.edu.twSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- February 7, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 2, entitled, “PROX1 interaction with α-SMA-rich cancer-associated fibroblasts facilitates colorectal cancer progression and correlates with poor clinical outcomes and therapeutic resistance.”The tumor microenvironment (TME) plays a vital role in tumor progression through intricate molecular interactions. Cancer-associated fibroblasts (CAFs), notably those expressing alpha-smooth muscle actin (α-SMA) or myofibroblasts, are instrumental in this context and correlate with unfavorable outcomes in colorectal cancer (CRC). While several transcription factors influence TME, the exact regulator causing CAF dysregulation in CRC remains elusive. Prospero Homeobox 1 (PROX1) stands out, as its inhibition reduces α-SMA-rich CAF activity. However, the therapeutic role of PROX1 is debated due to inconsistent study findings.In this new study, researchers Shiue-Wei Lai, Yi-Chiao Cheng, Kee-Thai Kiu, Min-Hsuan Yen, Ying-Wei Chen, Vijesh Kumar Yadav, Chi-Tai Yeh, Kuang-Tai Kuo, and Tung-Cheng Chang from Taipei’s National Defense Medical Center, Taipei Medical University, Taipei Medical University Shuang-Ho Hospital, and National Taitung University used the ULCAN portal and noted an elevated PROX1 level in advanced colon adenocarcinoma, linking to a poor prognosis. Their assays determined the impact of PROX1 overexpression on CRC cell properties, while co-culture experiments spotlighted the PROX1-CAF relationship. Molecular expressions were validated by qRT-PCR and Western blots, with in vivo studies further solidifying the observations.“Our study emphasized the connection between PROX1 and α-SMA in CAFs.”Elevated PROX1 in CRC samples correlated with increased α-SMA in tumors. PROX1 modulation influenced the behavior of specific CRC cells, with its overexpression fostering invasiveness. Kaplan-Meier evaluations demonstrated a link between PROX1 or α-SMA and survival outcomes. Consequently, PROX1, alone or with α-SMA, emerges as a CRC prognostic marker. Co-culture and animal experiments further highlighted this relationship.PROX1 appears crucial in modulating CRC behavior and therapeutic resistance within the TME by influencing CAFs, signifying the combined PROX1/α-SMA gene as a potential CRC prognostic marker. The concept of developing inhibitors targeting this gene set emerges as a prospective therapeutic strategy. However, this study is bound by limitations, including potential challenges in clinical translation, a focused exploration on PROX1/α-SMA potentially overlooking other significant molecular contributors, and the preliminary nature of the inhibitor development proposition.“As we advance in this field, the development and clinical validation of small-molecule inhibitors targeting PROX1/α-SMA become imperative, paving the way to refine and optimize CRC therapeutic interventions.”DOI - https://doi.org/10.18632/aging.205447Corresponding author - Tung-Cheng Chang - 09432@s.tmu.edu.twAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Visit our website at https://www.Aging-US.com.MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- February 6, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 2, entitled, “Epigenetic drift underlies epigenetic clock signals, but displays distinct responses to lifespan interventions, development, and cellular dedifferentiation.”Changes in DNA methylation with age are observed across the tree of life. The stereotypical nature of these changes can be modeled to produce epigenetic clocks capable of predicting chronological age with unprecedented accuracy. Despite the predictive ability of epigenetic clocks and their utility as biomarkers in clinical applications, the underlying processes that produce clock signals are not fully resolved, which limits their interpretability. In this new study, researchers Emily M. Bertucci-Richter, Ethan P. Shealy, and Benjamin B. Parrott from the University of Georgia developed a computational approach to spatially resolve the within read variability or “disorder” in DNA methylation patterns and test if age-associated changes in DNA methylation disorder underlie signals comprising epigenetic clocks. “Herein, we apply novel read-based strategies to resolve age-associated epigenetic disorder across the mouse genome.”The team found that epigenetic clock loci are enriched in regions that both accumulate and lose disorder with age, suggesting a link between DNA methylation disorder and epigenetic clocks. They then developed epigenetic clocks that are based on regional disorder of DNA methylation patterns and compare their performance to other epigenetic clocks by investigating the influences of development, lifespan interventions, and cellular dedifferentiation. The researchers identified common responses as well as critical differences between canonical epigenetic clocks and those based on regional disorder, demonstrating a fundamental decoupling of epigenetic aging processes. “Collectively, we identify key linkages between epigenetic disorder and epigenetic clocks and demonstrate the multifaceted nature of epigenetic aging in which stochastic processes occurring at non-random loci produce predictable outcomes.”DOI - https://doi.org/10.18632/aging.205503Corresponding author - Emily M. Bertucci-Richter - embertucci@gmail.comSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205503Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, epigenetic aging, epigenetic drift, epigenetic rejuvenation, lifespan, DNA methylationAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
Head and neck squamous cell carcinoma (HNSCC) is a prevalent and heterogeneous form of cancer that affects thousands of individuals worldwide. The prognosis for HNSCC patients can vary greatly, depending on factors such as tumor stage and site. The tumor microenvironment (TME) plays a crucial role in tumorigenesis and disease progression, with cellular senescence being a key component. Senescent cells, characterized by cell-cycle arrest, have been shown to have both tumor-suppressive and tumor-promoting effects. However, the prognostic significance of senescence-related TME genes in HNSCC remains poorly understood.In a new study, researchers Young Chan Lee, Yonghyun Nam, Minjeong Kim, Su Il Kim, Jung-Woo Lee, Young-Gyu Eun, and Dokyoon Kim from Kyung Hee University, Kyung Hee University Hospital at Gangdong, and the University of Pennsylvania aimed to investigate the prognostic significance of senescence-related TME genes in HNSCC and their potential implications for immunotherapy response. They utilized data from The Cancer Genome Atlas (TCGA) to identify two distinct subtypes of HNSCC based on the expression of senescence-related TME genes. The team then constructed a risk model consisting of senescence-related TME core genes (STCGs) and validated its prognostic capability in independent cohorts. Their research paper was chosen as an Aging cover paper and published in Volume 16, Issue 2, entitled, “Prognostic significance of senescence-related tumor microenvironment genes in head and neck squamous cell carcinoma.”Full blog - https://aging-us.org/2024/02/senescence-related-tme-genes-as-key-prognostic-predictors-in-hnscc/Paper DOI - https://doi.org/10.18632/aging.205346Corresponding authors - Young-Gyu Eun - ygeun@khu.ac.kr, and Dokyoon Kim - dokyoon.kim@pennmedicine.upenn.eduSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205346Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, cellular senescence, head and neck cancer, immunotherapy, microenvironment, single cellAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- January 31, 2024 – A new #research paper was #published on the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 2, entitled, “Prognostic significance of senescence-related tumor microenvironment genes in head and neck squamous cell carcinoma.”The impact of the senescence related microenvironment on cancer prognosis and therapeutic response remains poorly understood. In this new study, researchers Young Chan Lee, Yonghyun Nam, Minjeong Kim, Su Il Kim, Jung-Woo Lee, Young-Gyu Eun, and Dokyoon Kim from Kyung Hee University, Kyung Hee University Hospital at Gangdong, and the University of Pennsylvania investigated the prognostic significance of senescence related tumor microenvironment genes (PSTGs) and their potential implications for immunotherapy response. Using the Cancer Genome Atlas- head and neck squamous cell carcinoma (HNSC) data, the researchers identified two subtypes based on the expression of PSTGs, acquired from tumor-associated senescence genes, tumor microenvironment (TME)-related genes, and immune-related genes, using consensus clustering. Using the LASSO, they constructed a risk model consisting of senescence related TME core genes (STCGs). The two subtypes exhibited significant differences in prognosis, genetic alterations, methylation patterns, and enriched pathways, and immune infiltration. “Our risk model stratified patients into high-risk and low-risk groups and validated in independent cohorts.”The high-risk group showed poorer prognosis and immune inactivation, suggesting reduced responsiveness to immunotherapy. Additionally, the team observed a significant enrichment of STCGs in stromal cells using single-cell RNA transcriptome data. Their findings highlight the importance of the senescence related TME in HNSC prognosis and response to immunotherapy. “This study contributes to a deeper understanding of the complex interplay between senescence and the TME, with potential implications for precision medicine and personalized treatment approaches in HNSC.”DOI - https://doi.org/10.18632/aging.205346Corresponding authors - Young-Gyu Eun - ygeun@khu.ac.kr, and Dokyoon Kim - dokyoon.kim@pennmedicine.upenn.eduSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205346Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, cellular senescence, head and neck cancer, immunotherapy, microenvironment, single cellAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMedia Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- January 30, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 1, entitled, “XRCC1: a potential prognostic and immunological biomarker in LGG based on systematic pan-cancer analysis.”X-ray repair cross-complementation group 1 (XRCC1) is a pivotal contributor to base excision repair, and its dysregulation has been implicated in the oncogenicity of various human malignancies. However, a comprehensive pan-cancer analysis investigating the prognostic value, immunological functions, and epigenetic associations of XRCC1 remains lacking.In this new study, researchers Guobing Wang, Yunyue Li, Rui Pan, Xisheng Yin, Congchao Jia, Yuchen She, Luling Huang, Guanhu Yang, Hao Chi, and Gang Tian from Southwest Medical University, The Affiliated Hospital of Southwest Medical University, Yibin Hospital of T.C.M, Medical School of Nanchang University, Fourth Military Medical University, and Ohio University aimed to address this knowledge gap by conducting a systematic investigation employing bioinformatics techniques across 33 cancer types.“Our analysis encompassed XRCC1 expression levels, prognostic and diagnostic implications, epigenetic profiles, immune and molecular subtypes, Tumor Mutation Burden (TMB), Microsatellite Instability (MSI), immune checkpoints, and immune infiltration, leveraging data from TCGA, GTEx, CELL, Human Protein Atlas, Ualcan, and cBioPortal databases.”Notably, XRCC1 displayed both positive and negative correlations with prognosis across different tumors. Epigenetic analysis revealed associations between XRCC1 expression and DNA methylation patterns in 10 cancer types, as well as enhanced phosphorylation. Furthermore, XRCC1 expression demonstrated associations with TMB and MSI in the majority of tumors. Interestingly, XRCC1 gene expression exhibited a negative correlation with immune cell infiltration levels, except for a positive correlation with M1 and M2 macrophages and monocytes in most cancers. Additionally, the researchers observed significant correlations between XRCC1 and immune checkpoint gene expression levels. Lastly, their findings implicated XRCC1 in DNA replication and repair processes, shedding light on the precise mechanisms underlying its oncogenic effects. “Overall, our study highlights the potential of XRCC1 as a prognostic and immunological pan-cancer biomarker, thereby offering a novel target for tumor immunotherapy."DOI - https://doi.org/10.18632/aging.205426Corresponding authors - Guanhu Yang - guanhuyang@gmail.com, Hao Chi - Chihao7511@163.com, and Gang Tian - tiangang@swmu.edu.cnSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, X-ray repair cross-complementation group 1, pan-cancer, prognosis, immune infiltration, tumor microenvironmentAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- January 24, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 1, entitled, “Targeting of FSP1 regulates iron homeostasis in drug-tolerant persister head and neck cancer cells via lipid-metabolism-driven ferroptosis.”Research has demonstrated that some tumor cells can transform into drug-tolerant persisters (DTPs), which serve as a reservoir for the recurrence of the disease. In this new study, researchers Yang-Che Wu, Chin-Sheng Huang, Ming-Shou Hsieh, Chih-Ming Huang, Syahru Agung Setiawan, Chi-Tai Yeh, Kuang-Tai Kuo, and Shao-Cheng Liu from Taipei Medical University-Shuang Ho Hospital, Taipei Medical University, Taitung Mackay Memorial Hospital, Tajen University, National Taitung University, and Taipei City’s National Defense Medical Center investigated lipid-metabolism-driven ferroptosis and its role in drug resistance and DTP generation in head and neck squamous cell carcinoma (HNSCC).“The regulatory roles of ferroptosis suppressor protein 1 (FSP1) in HNSCC metabolic regulation were investigated.”High levels of FSP1 were discovered in the tissues of patients who experienced relapse after cisplatin treatment. RNA sequencing indicated that a series of genes related to lipid metabolism were also highly expressed in tissues from these patients. Consistent results were obtained in primary DTP cells isolated from patients who experienced relapse. The Cancer Genome Atlas database confirmed this finding. This revealed that the activation of drug resistance in cancer cells is influenced by FSP1, intracellular iron homeostasis, and lipid metabolism. Next, the team generated human oral squamous cell carcinoma DTP cells (HNSCC cell line) to cisplatin and observed higher expression of FSP1 and lipid-metabolism-related targets in vitro. The shFSP1 blockade attenuated HNSCC-DTP cell stemness and downregulated tumor invasion and the metastatic rate. They found that cisplatin induced FSP1/ACSL4 axis expression in HNSC-DTPC cells. Finally, the researchers evaluated the HNSCC CSC-inhibitory functions of iFSP1 (a metabolic drug and ferroptosis inducer) used for neo-adjuvant chemotherapy; this was achieved by inducing ferroptosis in a patient-derived xenograft mouse model.“The present findings elucidate the link between iron homeostasis, ferroptosis, and cancer metabolism in HNSCC-DTP generation and acquisition of chemoresistance. The findings may serve as a suitable model for cancer treatment testing and prediction of precision treatment outcomes. In conclusion, this study provides clinically oriented platforms for evaluating metabolism-modulating drugs (FSP1 inhibitors) and new drug candidates of drug resistance and ferroptotic biomarkers.”Corresponding authors - Ming-Shou Hsieh - 22057@s.tmu.edu.tw, and Shao-Cheng Liu - m871435@mail.ndmctsgh.edu.twAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- January 23, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 1, entitled, “Systematic analysis of the prognostic value and immunological function of LTBR in human cancer.”Lymphotoxin beta receptor (LTBR) is a positive T cell proliferation regulator gene. It is closely associated with the tumor immune microenvironment. However, its role in cancer and immunotherapy is unclear. In this new study, researchers Yinteng Wu, Shijian Zhao, Wenliang Guo, Ying Liu, Marìa Del Mar Requena Mullor, Raquel Alarcòn Rodrìguez, and Ruqiong Wei from The First Affiliated Hospital of Guangxi Medical University, The Eighth Affiliated Hospital of Guangxi Medical University and University of Almerìa analyzed the expression level and prognostic value of LTBR in clinical stages, immune subtypes, and molecular subtypes. The correlation between LTBR and immune regulatory genes, immune checkpoint genes, and RNA modification genes was then analyzed. Correlations between LTBR and immune cells, scores, cancer-related functional status, tumor stemness index, mismatch repair (MMR) genes, and DNA methyltransferase were also analyzed. In addition, the team analyzed the role of LTBR in DNA methylation, mutational status, tumor mutation burden (TMB), and microsatellite instability (MSI). Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA) were used to explore the role of LTBR in pan-cancer. Finally, the drugs associated with LTBR were analyzed. “In this work, we looked into the expression of LTBR at multiple levels.”The expression of LTBR was confirmed using quantitative real-time PCR and Western blot. LTBR is significantly overexpressed in most cancers and is associated with low patient survival. In addition, LTBR expression was strongly correlated with immune cells, score, cancer-related functional status, tumor stemness index, MMR genes, DNA methyltransferase, DNA methylation, mutational status, TMB, and MSI. Enrichment analysis revealed that LTBR was associated with apoptosis, necroptosis, and immune-related pathways. Finally, multiple drugs targeting LTBR were identified. LTBR is overexpressed in several tumors and is associated with a poor prognosis. It is related to immune-related genes and immune cell infiltration.“Notably, we identified LTBR as a potential target for cancer immunotherapy and a marker of immune infiltration and poor prognosis. This study offers new possibilities for the diagnosis and treatment of cancer patients, instilling hope for improved outcomes.”DOI - https://doi.org/10.18632/aging.205356Corresponding author - Ruqiong Wei - ruqiongwei@sr.gxmu.edu.cnSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6McMEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- January 22, 2024 – On January 3, 2024, Mikhail V. Blagosklonny M.D., Ph.D., from Roswell Park Comprehensive Cancer Center #published a new brief #report in Oncoscience (Volume 11), entitled, “My battle with cancer. Part 1.”“In January 2023, diagnosed with numerous metastases of lung cancer in my brain, I felt that I must accomplish a mission. If everything happens for a reason, my cancer, in particular, I must find out how metastatic cancer can be treated with curative intent. This is my mission now, and the reason I was ever born. In January 2023, I understood the meaning of life, of my life. I was born to write this article. In this article, I argue that monotherapy with targeted drugs, even when used in sequence, cannot cure metastatic cancer. However, preemptive combinations of targeted drugs may, in theory, cure incurable cancer. Also, I share insights on various topics, including rapamycin, an anti-aging drug that can delay but not prevent cancer, through my personal journey.”DOI - https://doi.org/10.18632/oncoscience.593Corresponding author - Mikhail V. Blagosklonny - Blagosklonny@oncotarget.com, Blagosklonny@rapalogs.comSign up for free Altmetric alerts about this article -https://oncoscience.altmetric.com/details/email_updates?id=10.18632%2Foncoscience.593Subscribe for free publication alerts from Oncoscience - https://www.oncoscience.us/subscribe/Keywords - cancer, lung cancer, brain metastases, capmatinib, resistance, METAbout OncoscienceOncoscience is a traditional, peer-reviewed, bio-medical oncology research journal with FREE publication for authors and open-access for readers.To learn more about Oncoscience, please visit https://www.oncoscience.us/ and connect with us:Facebook - https://www.facebook.com/OncoscienceX - https://twitter.com/OncoscienceJrnlInstagram - https://www.instagram.com/oncosciencejrnl/YouTube - https://www.youtube.com/@OncoscienceJournalLinkedIn - https://www.linkedin.com/company/oncoscience/Media ContactMEDIA@IMPACTJOURNALS.COM18009220957
Lung cancer is a significant global health issue, being the second most commonly diagnosed cancer and the leading cause of cancer-related death worldwide. Non-small-cell lung cancer (NSCLC) represents the majority of lung cancer cases and is often diagnosed at an advanced stage. Epidermal growth factor receptor (EGFR) mutations are more common in Asian NSCLC populations than in Western populations. Activating EGFR mutations, such as exon 19 deletions and L858R, are predictive of response to tyrosine kinase inhibitors (TKIs) and have revolutionized the treatment landscape for patients with EGFR-mutated NSCLC. However, most clinical trials tend to lack data for the elderly population, even though a significant proportion of lung cancer patients are aged 65 years and older. This underrepresentation of elderly patients in clinical trials limits our understanding of the effectiveness and safety of EGFR-TKIs in this specific population.In this new study, researchers Ling-Jen Hung, Ping-Chih Hsu, Cheng-Ta Yang, Chih-Hsi Scott Kuo, John Wen-Cheng Chang, Chen-Yang Huang, Ching-Fu Chang, and Chiao-En Wu from Chang Gung University and Taoyuan General Hospital conducted a multi-institute retrospective study to investigate the effectiveness and safety of afatinib, gefitinib, and erlotinib for treatment-naïve elderly patients with EGFR-mutated advanced NSCLC. On January 8, 2024, their research paper was published in Aging’s Volume 16, Issue 1, entitled, “Effectiveness and safety of afatinib, gefitinib, and erlotinib for treatment-naïve elderly patients with epidermal growth factor receptor-mutated advanced non-small-cell lung cancer: a multi-institute retrospective study.”Full blog - https://aging-us.org/2024/01/efficacy-and-safety-of-egfr-tkis-for-elderly-patients-with-nsclc/Paper DOI - https://doi.org/10.18632/aging.205395Corresponding author - Chiao-En Wu - 8805017@cgmh.org.twSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205395Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, elderly patients, epidermal growth factor receptor, tyrosine kinase inhibitor, non-small-cell lung cancer, real-world evidenceAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- January 17, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 1, entitled, “Aberrant RBMX expression is relevant for cancer prognosis and immunotherapy response.”Cancer accounts for the highest rates of morbidity and mortality worldwide. RNA binding motif protein X-linked (RBMX) is a nuclear RNA-binding protein, associated with certain types of cancer by participating in the integration of sister chromatids and a combination of ribonucleoprotein complexes. However, the specific role of RBMX in cancer immunity remains unknown.In this new study, researchers Yilei Sheng, Kunjian Lei, Chengpeng Sun, Jia Liu, Zewei Tu, Xingen Zhu, and Kai Huang from Nanchang University, The Second Affiliated Hospital of Nanchang University, Jiangxi Key Laboratory of Neurological Tumors and Cerebrovascular Diseases, JXHC Key Laboratory of Neurological Medicine, and Yale School of Medicine present the aberrant expression levels, single-cell distributions, effective prognostic roles, immune cell infiltration associations, and immunotherapy responses of RBMX as a biomarker in various types of cancer. Moreover, they validate the aberrant expression of RBMX in clinical cancer samples. “[...] a pan-cancer analysis is necessary for the identification of novel biological targets and biomarkers involved in carcinogenesis, cancer progression, and immunotherapy response. Such knowledge would improve the precision of cancer therapy.”The researchers also evaluated the relationships between RBMX expression and myeloid-derived suppressor cells in clinical samples by immunofluorescent staining. Results showed that knockdown of RBMX can impair the proliferation, migration, and invasion of liver cancer cells. Finally, the team indicated that RBMX may play an immunoregulatory role in cancer progression, affecting the therapeutic effects of immune checkpoint inhibitors in patients with cancer.“In conclusion, we performed an integrated analysis of RBMX, revealing its effective role in predicting cancer prognosis and response to immunotherapy. Abnormal expression of RBMX is associated with immune regulation, prognosis, the tumor microenvironment, immune cell infiltration, MSI, and TMB. The results of this study indicated that RBMX may play an independent role in clinical diagnosis and prediction.”DOI - https://doi.org/10.18632/aging.205363Corresponding authors - Zewei Tu - 401441619022@email.ncu.edu.cn, Xingen Zhu - ndefy89006@ncu.edu.cn, Kai Huang - kaihuang@ncu.edu.cnSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205363Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, RBMX, cancer prognosis, immunotherapy response, proliferation, invasionAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- January 15, 2024 – A new #research paper was #published on the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 1, entitled, “Effects of resveratrol on in vitro circadian clock gene expression in young and older human adipose-derived progenitor cells.”Observational studies in preclinical models demonstrate age-related declines in circadian functions. In this new study, researchers Sophie G.C. Kapar, Maria F. Pino, Fanchao Yi, Miguel A. Gutierrez-Monreal, Karyn A. Esser, Lauren M. Sparks, and Melissa L. Erickson from AdventHealth and the University of Florida hypothesized that age would be associated with declines in function of cell-autonomous circadian clocks in human tissue. “Accordingly, we cultured adipose progenitor cells (APCs) from previously collected white-adipose tissue biopsies from abdominal subcutaneous depots of young (Age: 23.4 ± 2.1 yrs) vs. older female participants (Age: 70.6 ± 5.9 yrs).” Using an in vitro model, the researchers compared rhythmic gene expression profiles of core clock components, as an indicator of circadian oscillatory function. They observed consistent circadian rhythmicity of core clock components in young and older-APCs. Expression analysis showed increased levels of some components in older-APCs (CLOCK, CRY1, NR1D1) vs. young. The team also investigated resveratrol (RSV), a well-known longevity-enhancing effector, for its effects on rhythmic clock gene expression profiles. They found that RSV resulted in gained rhythmicity of some components (CLOCK and CRY), loss of rhythmicity in others (PER2, CRY2), and altered some rhythmic parameters (NR1D1 and NR1D2), consistent in young and older-APCs. The observation of detectable circadian rhythmicity retained in vitro suggests that the oscillatory function of the cell-autonomous core clock in APCs is preserved at this stage of the aging process. “RSV impacts core clock gene expression in APCs, implicating its potential as a therapeutic agent for longevity by targeting the core clock.”DOI - https://doi.org/10.18632/aging.205292Corresponding authors - Lauren M. Sparks - Lauren.Sparks@AdventHealth.com, and Melissa L. Erickson - Melissa.L.Erickson@AdventHealth.comSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205292Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, circadian clock, circadian rhythm, adipose-derived progenitor cells, resveratrolAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
Traditional Chinese medicine has long been explored for its potential in treating various diseases, including cancer. Lithospermum erythrorhizon, or purple gromwell, is a mysterious plant native to East Asia, and its dried root is often referred to as Zicao. Acetylshikonin, a compound derived from Zicao, has shown promise in exhibiting a variety of anti-cancer properties. While the effects of acetylshikonin on lung cancer are not yet fully understood, recent research has shed light on its potential as a therapeutic agent. In a new study, researchers Shih-Sen Lin, Tsung-Ming Chang, Augusta I-Chin Wei, Chiang-Wen Lee, Zih-Chan Lin, Yao-Chang Chiang, Miao-Ching Chi, and Ju-Fang Liu from Shin Kong Wu Ho-Su Memorial Hospital, Chang Gung Memorial Hospital, Chang Gung University of Science and Technology, Ming Chi University of Technology, Taipei Medical University, and China Medical University aimed to explore the mechanisms underlying acetylshikonin-induced cell death in non-small cell lung cancer (NSCLC). On December 19, 2023, their research paper was published in Aging’s Volume 15, Issue 24, entitled, “Acetylshikonin induces necroptosis via the RIPK1/RIPK3-dependent pathway in lung cancer.”Full blog - https://aging-us.org/2024/01/rooted-in-chinese-medicine-zicaos-anti-cancer-effects-on-lung-cancer/Paper DOI - https://doi.org/10.18632/aging.205316Corresponding authors - Ju-Fang Liu - jufangliu@tmu.edu.twSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205316Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, human lung cancer, acetylshikonin, ROS, necroptosisAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- January 10, 2024 – A new #editorial paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 24, entitled, “Exploring clonal hematopoiesis and its impact on aging, cancer, and patient care.”In this new editorial, researchers Julieta Elena Rodriguez, Jean Baptiste Micol and Capucine Baldini from Gustave Roussy discuss clonal hematopoiesis. Clonal hematopoiesis (CH) is a term that refers to the presence in blood cells of hematologic malignancy-associated somatic mutations without fulfilling the diagnostic criteria of hematologic disease. Emerging evidence suggests that CH is a consequence of an expansion of cells harboring initiating driver mutations, potentially linked to the aging hematopoietic system. While these detectable somatic mutations are rare in individuals under 40 years old, they become increasingly prevalent in the elderly population, a term called age-related clonal hematopoiesis (ARCH), reaching up to 18.4% in those aged 90 years or older. Aging itself is a significant stressor associated with CH, particularly in individuals over 70 years old. DNMT3A, TET2, and ASXL1 mutations are more common with advancing age. “Recent evidence also indicates that CH may play a role in solid tumors, such as an increased risk of incident lung cancer [4]. While initial studies associated CH mutations with worse survival outcomes [5], newer findings suggest that solid tumor patients with CH may experience longer survival [6]. However, the underlying mechanisms behind this relationship remain to be elucidated.”DOI - https://doi.org/10.18632/aging.205404Corresponding author - Capucine Baldini - capucine.baldini@gustaveroussy.frSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205404Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, clonal hematopoiesis, solid tumorsAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- January 9, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 24, entitled, “Systemic changes induced by autologous stem cell ovarian transplant in plasma proteome of women with impaired ovarian reserves.”Patients with poor ovarian response (POR) and premature ovarian insufficiency (POI) are challenging to treat, with oocyte donation remaining as the only feasible option to achieve pregnancy in some cases. The Autologous stem cell ovarian transplantation (ASCOT) technique allows follicle development, enabling pregnancies and births of healthy babies in these patients. Previous research suggests that growth factors and cytokines secreted by stem cells are partially responsible for their regenerative properties. Indeed, ASCOT beneficial effects are associated with the presence of different bone marrow derived stem cell- secreted factors in plasma. In this new study, researchers Anna Buigues, Noelia Ramírez-Martin, Jessica Martínez, Nuria Pellicer, Marcos Meseguer, Antonio Pellicer, and Sonia Herraiz from IVIRMA Global Research Alliance aimed to assess whether ASCOT induces any modifications in the plasma proteomic profile of patients with impaired ovarian reserves.“In this study, we aimed to assess if the ASCOT technique modifies the signature of the human plasma proteome, reveal the mechanisms underlying its beneficial effects on the ovary, and identify key regulators of ovarian aging.”Discriminant analysis highlighted clear distinctions between the plasma proteome before (PRE), during stem cell mobilization and collection (APHERESIS) and three months after ASCOT (POST) in patients with POR and POI. Both the stem cell mobilization and ASCOT technique induced statistically significant modifications in the plasma composition, reversing some age-related protein expression changes. In the POR group, functional analysis revealed an enrichment in processes related to the complement cascade, immune system, and platelet degranulation, while in the POI group, enriched processes were also associated with responses to oxygen-containing compounds and growth hormones, and blood vessel maturation. “In conclusion, our findings highlight the potential proteins and biological processes that may promote the follicle activation and growth observed after ASCOT.”DOI - https://doi.org/10.18632/aging.205400Corresponding author - Sonia Herraiz - sonia_herraiz@iislafe.esSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205400Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, plasma proteomic profile, autologous stem cell ovarian transplantation, poor ovarian response, premature ovarian insufficiencyAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- January 3, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 24, entitled, “Mapping of the gene network that regulates glycan clock of ageing.”Glycans are an essential structural component of immunoglobulin G (IgG) that modulate its structure and function. However, regulatory mechanisms behind this complex posttranslational modification are not well known. Previous genome-wide association studies (GWAS) identified 29 genomic regions involved in regulation of IgG glycosylation, but only a few were functionally validated. One of the key functional features of IgG glycosylation is the addition of galactose (galactosylation), a trait which was shown to be associated with ageing.In this new study, researchers Azra Frkatović-Hodžić, Anika Mijakovac, Karlo Miškec, Arina Nostaeva, Sodbo Z. Sharapov, Arianna Landini, Toomas Haller, Erik van den Akker, Sapna Sharma, Rafael R. C. Cuadrat, Massimo Mangino, Yong Li, Toma Keser, Najda Rudman, Tamara Štambuk, Maja Pučić-Baković, Irena Trbojević-Akmačić, Ivan Gudelj, Jerko Štambuk, Tea Pribić, Barbara Radovani, Petra Tominac, Krista Fischer, Marian Beekman, Manfred Wuhrer, Christian Gieger, Matthias B. Schulze, Clemens Wittenbecher, Ozren Polasek, Caroline Hayward, James F. Wilson, Tim D. Spector, Anna Köttgen, Frano Vučković, Yurii S. Aulchenko, Aleksandar Vojta, Jasminka Krištić, Lucija Klarić, Vlatka Zoldoš, and Gordan Lauc from Genos Glycoscience Research Laboratory, University of Zagreb, Novosibirsk State University, Lomonosov Moscow State University, University of Edinburgh, University of Tartu, Leiden University Medical Center, Delft University of Technology, Helmholtz Zentrum Muenchen, German Center for Diabetes Research (DZD), King’s College London, Guy’s and St Thomas’ Foundation Trust, University of Freiburg, University of Rijeka, German Institute of Human Nutrition Potsdam-Rehbruecke, University of Potsdam, Harvard T.H. Chan School of Public Health, Chalmers University of Technology, University of Split School of Medicine, Algebra University College, Johns Hopkins Bloomberg School of Public Health, and Institute of Cytology and Genetics SB RAS performed GWAS of IgG galactosylation (N=13,705) and identified 16 significantly associated loci, indicating that IgG galactosylation is regulated by a complex network of genes that extends beyond the galactosyltransferase enzyme that adds galactose to IgG glycans. “Here, we conducted a GWAS of IgG galactosylation phenotypes in a study that almost doubles the sample size (N=13,705) compared to previous GWAS of IgG N-glycome [33] and focused on the genes with in silico evidence for involvement in the IgG galactosylation process.”Gene prioritization identified 37 candidate genes. Using a recently developed CRISPR/dCas9 system, the researchers manipulated gene expression of candidate genes in the in vitro IgG expression system. Upregulation of three genes, EEF1A1, MANBA and TNFRSF13B, changed the IgG glycome composition, which confirmed that these three genes are involved in IgG galactosylation in this in vitro expression system.“Further research is needed to fully elucidate [the] functional mechanism behind their role in ageing and to reveal the complete network of gene interactions regulating the complex process of IgG glycosylation.”DOI - https://doi.org/10.18632/aging.205106Corresponding authors - Azra Frkatović-Hodžić - afrkatovic@genos.hr, and Gordan Lauc - glauc@genos.hrVisit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- January 2, 2024 – A new #research paper was #published on the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 24, entitled, “Age-related alterations in the oscillatory dynamics serving verbal working memory processing.”Working memory (WM) is a foundational cognitive function involving the temporary storage of information. Unfortunately, WM is also one of the most sensitive cognitive functions to the detrimental effects of aging. Expanding the field’s understanding of age-related WM changes is critical to advancing the development of strategies to mitigate age-related WM declines. In this new study, researchers Seth D. Springer, Hannah J. Okelberry, Madelyn P. Willett, Hallie J. Johnson, Chloe E. Meehan, Mikki Schantell, Christine M. Embury, Maggie P. Rempe, and Tony W. Wilson from Boys Town National Research Hospital, University of Nebraska Medical Center, Washington University School of Medicine, and Creighton University investigated the neural mechanisms serving WM function in seventy-eight healthy aging adults (range: 20.2–65.2 years) using magnetoencephalography (MEG) and a Sternberg WM task with letter stimuli. “We hypothesized that older adults would require stronger engagement of key left hemispheric frontal and parieto-occipital WM hubs. Additionally, we expected that prefrontal activity lateralization (i.e., stronger left hemispheric activity) during WM performance would diminish as a function of age, with older individuals tending to utilize a more bilaterally distributed WM network.”Neural activity during the different phases of the WM task (i.e., encoding, maintenance, and retrieval) were imaged using a time-frequency resolved beamformer and whole-brain statistics were performed. The researchers found stronger increases in theta activity and stronger decreases in alpha and beta activity (i.e., more negative relative to baseline) as a function of healthy aging. Specifically, age-related increases in theta activity were detected during the encoding period in the primary visual and left prefrontal cortices. Additionally, alpha and beta oscillations were stronger (i.e., more negative) during both encoding and maintenance in the left prefrontal cortex in older individuals. Finally, alpha and beta oscillations during the retrieval phase were stronger (i.e., more negative) in older participants within the prefrontal, parietal, and temporal cortices. “Together, these results indicate that healthy aging strongly modulates the neural oscillatory dynamics serving WM function.”DOI - https://doi.org/10.18632/aging.205403Corresponding author - Tony W. Wilson - tony.wilson@boystown.orgSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, oscillation, magnetoencephalography, MEG, theta, alphaAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- December 27, 2023 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 23, entitled, “Angelica gigas extract inhibits acetylation of eNOS via IRE1α sulfonation/RIDD-SIRT1-mediated posttranslational modification in vascular dysfunction.”Angelica gigas NAKAI (AG) is a popular traditional medicinal herb widely used to treat dyslipidemia owing to its antioxidant activity. Vascular disease is intimately linked to obesity-induced metabolic syndrome, and AG extract (AGE) shows beneficial effects on obesity-associated vascular dysfunction. However, the effectiveness of AGE against obesity and its underlying mechanisms have not yet been extensively investigated. In this new study, researchers Geum-Hwa Lee, Hwa-Young Lee, Young-Je Lim, Ji-Hyun Kim, Su-Jin Jung, Eun-Soo Jung, Soo-Wan Chae, Juwon Lee, Junghyun Lim, Mohammad Mamun Ur Rashid, Kyung Hyun Min, and Han-Jung Chae from Jeonbuk National University and Jeonbuk National University Hospital supplemented 40 high fat diet (HFD) rats with 100–300 mg/kg/day of AGE to determine its efficacy in regulating vascular dysfunction. “[...] the primary aim of this study is to examine the inhibitory effects of AGE on dyslipidemia-associated vascular dysfunction, with a focus on its potential mechanisms of action.”The vascular relaxation responses to acetylcholine were impaired in HFD rats, while the administration of AGE restored the diminished relaxation pattern. Endothelial dysfunction, including increased plaque area, accumulated reactive oxygen species, and decreased nitric oxide (NO) and endothelial nitric oxide synthase (eNOS) Ser1177 phosphorylation, were observed in HFD rats, whereas AGE reversed endothelial dysfunction and its associated biochemical signaling. Furthermore, AGE regulated endoplasmic reticulum (ER) stress and IRE1α sulfonation and its subsequent sirt1 RNA decay through controlling regulated IRE1α-dependent decay (RIDD) signaling, ultimately promoting NO bioavailability via the SIRT1-eNOS axis in aorta and endothelial cells.Independently, AGE enhanced AMPK phosphorylation, additionally stimulating SIRT1 and eNOS deacetylation and its associated NO bioavailability. Decursin, a prominent constituent of AGE, exhibited a similar effect in alleviating endothelial dysfunctions. These data suggest that AGE regulates dyslipidemia-associated vascular dysfunction by controlling ROS-associated ER stress responses, especially IRE1α-RIDD/sirt1 decay and the AMPK-SIRT1 axis.“Ultimately, this study presents clearly evidence that AGE is a promising natural product-based functional food/herbal medicine candidate for preventing or regulating hyperlipidemic cardiovascular complications.”DOI - https://doi.org/10.18632/aging.205343Corresponding authors - Kyung Hyun Min - khmin1492@jbnu.ac.kr, and Han-Jung Chae - hjchae@jbnu.ac.krAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Visit https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/MEDIA@IMPACTJOURNALS.COM
Neurons, the building blocks of the nervous system, play a vital role in our body’s function and longevity. Unlike other cells, neurons do not undergo replicative aging. However, they are still susceptible to various sources of damage throughout life, leading to neuronal death. Understanding the mechanisms behind aging and neuronal death is crucial for uncovering the secrets of brain longevity and developing potential interventions to promote healthy aging.In a new editorial, researchers Fang Fang, Robert Usselman and Renee Reijo Pera from the University of Science and Technology of China, Florida Institute of Technology and McLaughlin Research Institute discussed new interconnected mechanisms of neuronal functionality and available tools to investigate neuronal aging and longevity. On December 13, 2023, their editorial was published in Aging’s Volume 15, Issue 23, entitled, “Aging and neuronal death.”Full blog - https://aging-us.org/2023/12/understanding-the-mechanisms-of-brain-aging-and-longevity-in-neurons/Paper DOI - https://doi.org/10.18632/aging.205433Corresponding author - Renee Reijo Pera - reneer@mclaughlinresearch.orgSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205433Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, neurodegeneration, reactive oxygen species, histone h3k79 methyltransferase, dopaminergic neuronsAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- December 20, 2023 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 23, entitled, “Benidipine calcium channel blocker promotes the death of cigarette smoke-induced senescent cells and improves lung emphysema.”Smoking is the main risk factor for many lung diseases including chronic obstructive pulmonary disease. Cigarette smoke (CS) contains carcinogenic and reactive oxygen species that favor DNA mutations and perturb the homeostasis and environment of cells. CS induces lung cell senescence resulting in a stable proliferation arrest and a senescence-associated secretory phenotype. It was recently reported that senescent cell accumulation promotes several lung diseases. In this new study, researchers Alberta Palazzo, Gabriela Makulyte, Delphine Goerhig, Jean-Jacques Médard, Vincent Gros, François Trottein, Serge Adnot, David Vindrieux, Jean-Michel Flaman, and David Bernard from Université de Lyon, Equipe Labellisée la Ligue Contre le Cancer, Université Paris Est Créteil, Hôpital Henri Mondor, and Université Lille performed a chemical screen, using an FDA-approved drug library, to identify compounds selectively promoting the death of CS-induced senescent lung cells. “Here, our aim was to identify senolytic compounds in the context of CS-induced senescence and to assess whether they improved lung emphysema.”Aside from the well-known senolytic, ABT-263, the researchers identified other potentially new senescence-eliminating compounds, including a new class of molecules, the dihydropyridine family of calcium voltage-gated channel (CaV) blockers. Among these blockers, Benidipine decreased senescent lung cells and ameliorates lung emphysema in a mouse model. The dihydropyridine family of CaV blockers thus constitutes a new class of senolytics that could improve lung diseases. “Hence, our work paves the way for further studies on the senolytic activity of CaV blockers in different senescence contexts and age-related diseases.”DOI - https://doi.org/10.18632/aging.205259Corresponding author - David Bernard - david.bernard@lyon.unicancer.frSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205259Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, senolytic, cigarette smoke, lung disease, cellular senescence, calcium channelAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- December 19, 2023 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 23, entitled, “Sirtuin 6 activation rescues the age-related decline in DNA damage repair in primary human chondrocytes.”While advanced age is widely recognized as the greatest risk factor for osteoarthritis (OA), the biological mechanisms behind this connection remain unclear. Previous work has demonstrated that chondrocytes from older cadaveric donors have elevated levels of DNA damage as compared to chondrocytes from younger donors. In this new study, researchers Michaela E. Copp, Jacqueline Shine, Hannon L. Brown, Kirti R. Nimmala, Oliver B. Hansen, Susan Chubinskaya, John A. Collins, Richard F. Loeser, and Brian O. Diekman from University of North Carolina at Chapel Hill, North Carolina State University, Rush University Medical Center, and Thomas Jefferson University aimed to determine whether a decline in DNA repair efficiency is one explanation for the accumulation of DNA damage with age, and to quantify the improvement in repair with activation of Sirtuin 6 (SIRT6). “In this study, we use irradiation as an acute model of DNA damage to bring the level of damage to equivalent levels across chondrocytes from donors of various ages.”After acute damage with irradiation, DNA repair was shown to be more efficient in chondrocytes from young (≤45 years old) as compared to middle-aged (50–65 years old) or older (>70 years old) cadaveric donors. Activation of SIRT6 with MDL-800 improved the repair efficiency, while inhibition with EX-527 reduced the rate of repair and increased the percentage of cells that retain high levels of damage. In addition to affecting repair after acute damage, treating chondrocytes from older donors with MDL-800 for 48 hours significantly reduced the amount of baseline DNA damage. Chondrocytes isolated from the knees of mice between 4 months and 22 months of age revealed both an increase in DNA damage with aging, and a decrease in DNA damage following MDL-800 treatment. Lastly, treating murine cartilage explants with MDL-800 lowered the percentage of chondrocytes with high p16 promoter activity, which supports the concept that using SIRT6 activation to maintain low levels of DNA damage may prevent the initiation of senescence.“In conclusion, the findings presented here support the hypothesis that the efficiency of DNA damage repair declines with age in chondrocytes and that SIRT6 activation improves repair both in response to an acute irradiation challenge and in the context of age-related damage accumulation. These results emphasize the critical role of SIRT6 in DNA repair and support further studies investigating the use of MDL-800 (or alternative SIRT6 activators) in mitigating senescence induction and ameliorating OA development.”DOI - https://doi.org/10.18632/aging.205394Corresponding author - Brian O. Diekman - bdiekman@email.unc.eduAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- December 15, 2023 – A new #researchpaper was #published on the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 23, entitled, “Uncovering a unique pathogenic mechanism of SARS-CoV-2 omicron variant: selective induction of cellular senescence.”SARS-CoV-2 variants are constantly emerging with a variety of changes in the conformation of the spike protein, resulting in alterations of virus entry mechanisms. Solely omicron variants use the endosomal clathrin-mediated entry. In this new study, researchers Franziska Hornung, Nilay Köse-Vogel, Claude Jourdan Le Saux, Antje Häder, Lea Herrmann, Luise Schulz, Lukáš Radosa, Thurid Lauf, Tim Sandhaus, Patrick Samson, Torsten Doenst, Daniel Wittschieber, Gita Mall, Bettina Löffler, and Stefanie Deinhardt-Emmer from Jena University, Leibniz Centre for Photonics in Infection Research (LPI), University of California San Francisco, Klinik für Herz- und Thoraxchirurgie, and University Hospital Bonn investigated the influence of defined altered spike formations to study their impact on premature cellular senescence.“In our study, in vitro infections of SARS-CoV-2 variants delta (B.1.617.2) and omicron (B.1.1.529) were analyzed by using human primary small alveolar epithelial cells and human ex vivo lung slices. We confirmed cellular senescence in human lungs of COVID-19 patients. Hence, global gene expression patterns of infected human primary alveolar epithelial cells were identified via mRNA sequencing.”Solely omicron variants of SARS-CoV-2 influenced the expression of cell cycle genes, highlighted by an increased p21 expression in human primary lung cells and human ex vivo lungs. Additionally, an upregulated senescence-associated secretory phenotype (SASP) was detected. Transcriptomic data indicate an increased gene expression of p16, and p38 in omicron-infected lung cells. Significant changes due to different SARS-CoV-2 infections in human primary alveolar epithelial cells with an overall impact on premature aging could be identified. A substantially different cellular response with an upregulation of cell cycle, inflammation- and integrin-associated pathways in omicron infected cells indicates premature cellular senescence.“This difference may be attributed to the distinct endocytic cell entry and intracellular pathways of the omicron variant when compared to the delta variant. The induction of cellular senescence in lung tissue following acute SARS-CoV-2 infection could potentially contribute to the reported cytokine storm and the development of long-COVID.”DOI - https://doi.org/10.18632/aging.205297Corresponding author - Stefanie Deinhardt-Emmer - stefanie.deinhardt-emmer@med.uni-jena.deSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, SARS-CoV-2, variant of concern, cellular senescence, lung airway cellsAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- December 13, 2023 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 22, entitled, “Nectandrin B significantly increases the lifespan of Drosophila - Nectandrin B for longevity.”Phytochemicals are increasingly recognized in the field of healthy aging as potential therapeutics against various aging-related diseases. Nutmeg, derived from the Myristica fragrans tree, is an example. Nutmeg has been extensively studied and proven to possess antioxidant properties that protect against aging and alleviate serious diseases such as cancer, heart disease, and liver disease. However, the specific active ingredient in nutmeg responsible for these health benefits has not been identified thus far. In this new study, researchers Ji-Seon Ahn, Nasir Uddin Mahbub, Sura Kim, Han-Byeol Kim, Jong-Soon Choi, Hea-Jong Chung, and Seong-Tshool Hong from Korea Basic Science Institute, Jeonbuk National University Medical School and Chung-Ang University present evidence that Nectandrin B (NecB), a bioactive lignan compound isolated from nutmeg, significantly extended the lifespan of the fruit fly Drosophila melanogaster by as much as 42.6% compared to the control group. “[...] we hypothesized that NecB might possess anti-aging efficacy.”The dramatic reduction of intracellular ROS levels by NecB captured the researchers’ attention. NecB also improved age-related symptoms including locomotive deterioration, body weight gain, eye degeneration, and neurodegeneration in aging D. melanogaster. The researchers wrote that this result represents the most substantial improvement in lifespan observed in animal experiments to date, suggesting that NecB may hold promise as a potential therapeutic agent for promoting longevity and addressing age-related degeneration.“We strongly believe that NecB urgently needs further attention and research, as we believe it has made a potential contribution to our understanding of the aging process as well as its application as a potential therapeutic agent for longevity and age-related.”DOI - https://doi.org/10.18632/aging.205234Corresponding authors - Jong-Soon Choi - jschoi@kbsi.re.kr, Hea-Jong Chung - hjchung84@kbsi.re.kr, and Seong-Tshool Hong - seonghong@jbnu.ac.krSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205234Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, Myristica fragrans, nutmeg, Nectandrin B, lifespan, longevityAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- December 12, 2023 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 22, entitled, “Tat-heat shock protein 10 ameliorates age-related phenotypes by facilitating neuronal plasticity and reducing age-related genes in the hippocampus.”In this new study, researchers Hyo Young Jung, Hyun Jung Kwon, Kyu Ri Hahn, Woosuk Kim, Dae Young Yoo, Yeo Sung Yoon, Dae Won Kim, and In Koo Hwang from Seoul National University, Chungnam National University, Gangneung-Wonju National University, Hallym University, and Konkuk University investigated the effects of heat shock protein 10 (HSP10) protein on memory function, hippocampal neurogenesis, and other related genes/proteins in adult and aged mice. “In the present study, we investigated the effects of HSP10 on hippocampal function in both adult and aged mice.”To translocate the HSP10 protein into the hippocampus, the Tat-HSP10 fusion protein was synthesized, and Tat-HSP10, not HSP10, was successfully delivered into the hippocampus based on immunohistochemistry and western blotting. Tat-HSP10 (0.5 or 2.0 mg/kg) or HSP10 (control protein, 2.0 mg/kg) was administered daily to 3- and 21-month-old mice for 3 months, and observed the senescence maker P16 was significantly increased in aged mice and the treatment with Tat-HSP10 significantly decreased P16 expression in the hippocampus of aged mice. In novel object recognition and Morris water maze tests, aged mice demonstrated decreases in exploratory preferences, exploration time, distance moved, number of object contacts, and escape latency compared to adult mice. Treatment with Tat-HSP10 significantly improved exploratory preferences, the number of object contacts, and the time spent swimming in the target quadrant in aged mice but not adults. Administration of Tat-HSP10 increased the number of proliferating cells and differentiated neuroblasts in the dentate gyrus of adult and aged mice compared to controls, as determined by immunohistochemical staining for Ki67 and doublecortin, respectively. Additionally, Tat-HSP10 treatment significantly mitigated the reduction in sirtuin 1 mRNA level, N-methyl-D-aspartate receptor 1, and postsynaptic density 95 protein levels in the hippocampus of aged mice. In contrast, Tat-HSP10 treatment significantly increased sirtuin 3 protein levels in both adult and aged mouse hippocampus. These suggest that Tat-HSP10 can potentially reduce hippocampus-related aging phenotypes.“Our results suggest that Tat-HSP10 treatment facilitates mitochondrial function, and Tat-HSP10 supplementation ameliorates the aging phenotypes in the mouse hippocampus.”DOI - https://doi.org/10.18632/aging.205182Corresponding authors - Dae Won Kim - kimdw@gwnu.ac.kr, and In Koo Hwang - vetmed2@snu.ac.krKeywords - aging, heat shock protein 10, hippocampus, memory, neurogenesis, synaptic plasticityAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by deficits in communication and social interaction, as well as repetitive behaviors. It has been observed that children born to older fathers have an increased risk of developing ASD and other neurodevelopmental disorders. This phenomenon suggests that paternal age may have an impact on the risk of ASD in offspring.Recent research has focused on understanding the potential mechanisms underlying the association between paternal age and ASD. One area of interest is the epigenome, specifically DNA methylation, which refers to the addition or removal of methyl groups to DNA molecules. DNA methylation can affect gene expression and play a role in various biological processes.In a new study, researchers Ramya Potabattula, Andreas Prell, Marcus Dittrich, Caroline Nava, Christel Depienne, Yosra Bejaoui, Nady El Hajj, Thomas Hahn, Martin Schorsch, and Thomas Haaf from Julius Maximilians University, Groupe Hospitalier Pitié-Salpêtrière, University Hospital Essen, Hamad Bin Khalifa University, and Fertility Center in Wiesbaden, Germany, explored the relationship between paternal age, DNA methylation of the BEGAIN gene, and the risk of ASD. The BEGAIN gene encodes a protein involved in protein-protein interactions at synapses, which are crucial for proper brain function. On November 28, 2023, their research paper was published in Aging’s Volume 15, Issue 22, entitled, "Effects of paternal and chronological age on BEGAIN methylation and its possible role in autism."Full blog - https://aging-us.org/2023/12/what-makes-children-of-older-fathers-at-increased-risk-of-autism/Paper DOI - https://doi.org/10.18632/aging.205275Corresponding author - Thomas Haaf - thomas.haaf@uni-wuerzburg.deSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205275Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, age and sex effect, autism spectrum disorder, BEGAIN, chronological aging, paternal age effect, sperm methylationAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- December 6, 2023 – A new #editorial paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 22, entitled, “Artificial intelligence for aging research in cancer drug development.”Aging is a multifactorial and complex process associated with various diseases, including cancer. In light of the growing aging population, the need for effective cancer treatments is more significant than ever. Artificial intelligence (AI) is playing an increasingly crucial role in aging research and cancer drug development in revealing the critical drivers of outcomes among a wide range of intrinsic and extrinsic factors. In recent years, the use of AI in aging research has been rapidly increasing, suggesting that AI-based analysis of healthcare data may enhance clinical care. In this new editorial, researchers Dorsa Shirini, Lawrence H. Schwartz and Laurent Dercle from Columbia University Medical Center provide an overview of the potential benefits as well as the technical caveats of adopting AI to help researchers identify new targets, develop more effective therapies, and accelerate the discovery process of drug development in the context of aging research. “In this review, we discuss how we could leverage AI technologies to consider a patient’s unique aging profile and tailor cancer treatment more precisely to the individual. This approach would help optimize treatment outcomes, minimize treatment-related risks, and improve the overall quality of care for patients, considering the complex interplay between aging and cancer treatment response.”DOI - https://doi.org/10.18632/aging.204914Corresponding authors - Laurent Dercle - ld2752@cumc.columbia.eduSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204914Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, artificial intelligence, cancer researchAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- December 5, 2023 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 22, entitled, “Contribution of membrane raft redox signalling to visfatin-induced inflammasome activation and podocyte injury.”The number of obese patients with end stage renal disease has increased significantly worldwide in the last few decades. Obesity results in an increased risk for chronic kidney diseases like diabetes and hypertension which consequently result in chronic kidney disease or even end-stage renal disease. However, the exact mechanism of how obesity increases the advancement of chronic kidney disease is still uncertain.Recently, researchers Saisudha Koka, Sreenidhi Surineni, Gurinder Bir Singh, and Krishna M. Boini from the University of Houston, Texas A&M University and the University of California Riverside have shown that adipokine visfatin-induced NLRP3 inflammasome activation contributes to podocyte injury. However, the molecular mechanisms of how visfatin induces the Nlrp3 inflammasome activation and podocyte damage is still unknown. The present study tested whether the membrane raft (MR) redox signaling pathway plays a central role in visfatin-induced NLRP3 inflammasomes formation and activation in podocytes. “In this study, it is proposed that visfatin induces the NLRP3 inflammasome activation in podocytes, leading to glomerular inflammatory injury in the kidney and the development of CKD, may be primarily driven by NADPH oxidase-mediated membrane raft redox signalling.”Upon visfatin stimulation, an aggregation of NADPH oxidase subunits, gp91phox and p47phox, was observed in the MR clusters, forming an MR redox signaling platform in podocytes. The formation of this signaling platform was blocked by prior treatment with MR disruptor MCD or NADPH oxidase inhibitor DPI. In addition, visfatin stimulation significantly increased the colocalization of Nlrp3 with Asc or Nlrp3 with caspase-1, IL-β production, cell permeability in podocytes compared to control cells. Pretreatment with MCD, DPI, WEHD significantly abolished the visfatin-induced colocalization of NLRP3 with Asc or NLRP3 with caspase-1, IL-1β production and cell permeability in podocytes. Furthermore, Immunofluorescence analysis demonstrated that visfatin treatment significantly decreased the podocin and nephrin expression (podocyte damage) and prior treatments with DPI, WEHD, MCD attenuated this visfatin-induced podocin and nephrin reduction. In conclusion, their results suggest that visfatin stimulates membrane raft clustering in the membrane of podocytes to form redox signaling platforms by aggregation and activation of NADPH oxidase subunits enhancing O2·− production, leading to NLRP3 inflammasome activation in podocytes and ultimate podocyte injury.“Through experiments conducted on cultured podocytes, we have demonstrated, for the first time that membrane raft-associated redox signalling is essential for the NLRP3 inflammasomes assembly and activation in response to visfatin, subsequently resulting in podocyte dysfunction and injury. These findings shed light on a novel mechanism underlying inflammasome activation and injury of podocytes triggered by visfatin.”DOI - https://doi.org/10.18632/aging.205243Corresponding author - Krishna M. Boini - kmboini@uh.eduVideo short - https://www.youtube.com/watch?v=cIzaHj31GBoVisit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- November 30, 2023 – A new #researchpaper was #published on the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 22, entitled, “Chronological aging impacts abundance, function and microRNA content of extracellular vesicles produced by human epidermal keratinocytes.”The disturbance of intercellular communication is one of the hallmarks of aging. In their new study, researchers Taku Nedachi, Christelle Bonod, Julie Rorteau, Wafae Chinoune, Yuri Ishiuchi, Sandrine Hughes, Benjamin Gillet, Nicolas Bechetoille, Dominique Sigaudo-Roussel, and Jérôme Lamartine from the University of Lyon, Toyo University and Gattefossé SAS aimed to clarify the impact of chronological aging on extracellular vesicles (EVs), a key mode of communication in mammalian tissues. “The present study was therefore conducted to elucidate whether the characteristics of EVs released from cultured human keratinocytes can be modulated during aging process.”The researchers focused on epidermal keratinocytes, the main cells of the outer protective layer of the skin which is strongly impaired in the skin of elderly. EVs were purified from conditioned medium of primary keratinocytes isolated from infant or aged adult skin. A significant increase of the relative number of EVs released from aged keratinocytes was observed whereas their size distribution was not modified.By small RNA sequencing, the researchers described a specific microRNA (miRNA) signature of aged EVs with an increase abundance of miR-30a, a key regulator of barrier function in human epidermis. EVs from aged keratinocytes were found to be able to reduce the proliferation of young keratinocytes, to impact their organogenesis properties in a reconstructed epidermis model and to slow down the early steps of skin wound healing in mice, three features observed in aged epidermis. This work reveals that intercellular communication mediated by EVs is modulated during aging process in keratinocytes and might be involved in the functional defects observed in aged skin.“To conclude, we have shown here that aging modulates EVs abundance, function and microRNA content in human keratinocytes.”DOI - https://doi.org/10.18632/aging.205245Corresponding author - Jérôme Lamartine - jerome.lamartine@univ-lyon1.frSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205245Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, keratinocytes, microRNA, senescence, exosomesAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- November 28, 2023 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 21, entitled, “1,5-anhydro-D-fructose induces anti-aging effects on aging-associated brain diseases by increasing 5’-adenosine monophosphate-activated protein kinase activity via the peroxisome proliferator-activated receptor-γ co-activator-1α/brain-derived neurotrophic factor pathway.”5’-Adenosine monophosphate-activated protein kinase (AMPK) is a metabolic sensor that serves as a cellular housekeeper; it also controls energy homeostasis and stress resistance. Thus, correct regulation of this factor can enhance health and survival. AMPK signaling may have a critical role in aging-associated brain diseases. Some in vitro studies have shown that 1,5-anhydro-D-fructose (1,5-AF) induces AMPK activation. In this new study, researchers Kiyoshi Kikuchi, Shotaro Otsuka, Seiya Takada, Kazuki Nakanishi, Kentaro Setoyama, Harutoshi Sakakima, Eiichiro Tanaka, and Ikuro Maruyama from Kagoshima University investigated the effects of 1,5-AF on the AMPK/PGC-1α/BDNF pathway in multiple animal models of human aging-associated brain diseases.“In the present study, we experimentally evaluated the effects of 1,5-AF on aging-associated brain diseases in vivo using an animal model of acute ischemic stroke (AIS), stroke-prone spontaneously hypertensive rats (SHRSPs), and the spontaneous senescence-accelerated mouse-prone 8 (SAMP8) model.”In the AIS model, intraperitoneal injection of 1,5-AF reduced cerebral infarct volume, neurological deficits, and mortality. In SHRSPs, oral administration of 1,5-AF reduced blood pressure and prolonged survival. In the SAMP8 model, oral administration of 1,5-AF alleviated aging-related decline in motor cognitive function. Although aging reduced the expression levels of peroxisome proliferator-activated receptor-γ co-activator-1α (PGC-1α) and brain-derived neurotrophic factor (BDNF), the researchers found that 1,5-AF activated AMPK, which led to upregulation of the PGC-1α/BDNF pathway. “Our results suggest that 1,5-AF can induce endogenous neurovascular protection, potentially preventing aging-associated brain diseases. Clinical studies are needed to determine whether 1,5-AF can prevent aging-associated brain diseases.”DOI - https://doi.org/10.18632/aging.205228Corresponding authors - Kiyoshi Kikuchi - kikuchi_kiyoshi@kurume-u.ac.jp, and Ikuro Maruyama - maruyama-i@eva.hi-ho.ne.jpSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205228Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, AMP-activated protein kinases, brain-derived neurotrophic factor, peroxisome proliferator-activated receptors, blood pressureAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- November 22, 2023 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 21, entitled, “Antibiotics that target mitochondria extend lifespan in C. elegans.”Aging is a continuous degenerative process caused by a progressive decline of cell and tissue functions in an organism. It is induced by the accumulation of damage that affects normal cellular processes, ultimately leading to cell death. It has been speculated for many years that mitochondria play a key role in the aging process. In this new study, researchers Gloria Bonuccelli, Darren R. Brooks, Sally Shepherd, Federica Sotgia, and Michael P. Lisanti from the University of Salford aimed to characterize the implications of mitochondria in aging using Caenorhabditis elegans (C. elegans) as an organismal model. The C. elegans were treated with a panel of mitochondrial inhibitors and assessed for survival. “In our study, we assessed survival by evaluating worm lifespan, and we assessed aging markers by evaluating the pharyngeal muscle contraction, the accumulation of lipofuscin pigment and ATP levels.” Their results show that treatment of worms with either doxycycline, azithromycin (inhibitors of the small and the large mitochondrial ribosomes, respectively), or a combination of both, significantly extended median lifespan of C. elegans, enhanced their pharyngeal pumping rate, reduced their lipofuscin content and their energy consumption (ATP levels), as compared to control untreated worms, suggesting an aging-abrogating effect for these drugs. Similarly, DPI, an inhibitor of mitochondrial complex I and II, was capable of prolonging the median lifespan of treated worms. On the other hand, subjecting worms to vitamin C, a pro-oxidant, failed to extend C. elegans lifespan and upregulated its energy consumption, revealing an increase in ATP level. “Therefore, our longevity study reveals that mitochondrial inhibitors (i.e., mitochondria-targeting antibiotics) could abrogate aging and extend lifespan in C. elegans.”DOI - https://doi.org/10.18632/aging.205229Corresponding authors - Michael P. Lisanti - m.p.lisanti@salford.ac.uk, and Federica Sotgia - f.sotgia@salford.ac.ukSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205229Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, C. elegans, lifespan, lipofuscin, antibiotics, mitochondria, metabolism, DPIAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- November 16, 2023 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 21, entitled, “Parental age effect on the longevity and healthspan in Drosophila melanogaster and Caenorhabditis elegans.”Several studies have investigated the effect of parental age on biological parameters such as reproduction, lifespan, and health; however, the results have been inconclusive, largely due to inter-species variation and/or modest effect sizes.In their new study, researchers Camille Lenzi, Alexis Piat, Pascal Schlich, Judith Ducau, Jean-Claude Bregliano, Hugo Aguilaniu, and Anne Laurençon from the IM Projet, Caduceum, INRAE, IBDM, Instituto Serrapilheira, and Universite Claude Bernard-Lyon 1 examined the effect of parental age on the lifespan, reproductive capacity, and locomotor activity of genetic isogenic lines of the nematode Caenorhabditis elegans and the fruit fly Drosophila melanogaster. “We decided to investigate parental age impact on the lifespan of their progeny on selected genomes of flies and worms to gain insights on the molecular mechanisms at work.”The researchers found that the progeny of successive generations of old parents had significantly shorter lifespans than the progeny of young parents in both species. Moreover, they investigated the fertility, fecundity, and locomotor activity of C. elegans. Interestingly, both the shorter lifespan and deteriorated healthspan of the progeny were significantly improved by switching to only one generation of younger parents. “Collectively, these data demonstrate that the detrimental effect of older parental age on the longevity of the progeny can be reversed, suggesting the existence of a beneficial non–genetic mechanism.”DOI - https://doi.org/10.18632/aging.205098Corresponding author - Anne Laurençon - anne.laurencon@ens-lyon.frSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205098Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, life span, intergenerational plasticity, maternal effect, nematode, drosophilaAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- November 15, 2023 – A new #researchpaper was #published on the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 21, entitled, “Longitudinal characterization of behavioral, morphological and transcriptomic changes in a tauopathy mouse model.”Neurodegenerative disorders, such as Alzheimer’s disease (AD), have the gradual onset of neurobiological changes preceding clinical diagnosis by decades. In their new study, researchers Qing Cao, Manasa Kumar, Allea Frazier, Jamal B. Williams, Shengkai Zhao, and Zhen Yan from the State University of New York at Buffalo’s Jacobs School of Medicine and Biomedical Sciences aimed to elucidate how brain dysfunction proceeds in neurodegenerative disorders.“[...] we performed longitudinal characterization of behavioral, morphological, and transcriptomic changes in a tauopathy mouse model, P301S transgenic mice.” P301S mice exhibited cognitive deficits as early as 3 months old, and deficits in social preference and social cognition at 5–6 months. They had a significant decrease of arborization in basal dendrites of hippocampal pyramidal neurons from 3 months and apical dendrites of PFC pyramidal neurons at 9 months. Transcriptomic analysis of genome-wide changes revealed the enrichment of synaptic gene upregulation at 3 months of age, while most of these synaptic genes were downregulated in PFC and hippocampus of P301S mice at 9 months. These time-dependent changes in gene expression may lead to progressive alterations of neuronal structure and function, resulting in the manifestation of behavioral symptoms in tauopathies.“In conclusion, our longitudinal characterization of behavioral, morphological and transcriptomic changes in a tauopathy mouse model is to elucidate potential mechanisms that drive the progression of AD and related neurodegenerative disorders. Manipulation of key molecular players coupled with electrophysiological measurements of neuronal functions in future studies will help identify early intervention strategies for these diseases.”DOI - https://doi.org/10.18632/aging.205057Corresponding author - Zhen Yan - zhenyan@buffalo.eduSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205057Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, Alzheimer’s disease, tau, cognitive behaviors, transcriptomic, neuronal morphologyAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- November 14, 2023 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 20, entitled, “Alcohol consumption and epigenetic age acceleration across human adulthood.”The alcohol-associated biological aging remains to be studied across adulthood. In their new study, researchers Mengyao Wang, Yi Li, Meng Lai, Drew R. Nannini, Lifang Hou, Roby Joehanes, Tianxiao Huan, Daniel Levy, Jiantao Ma, and Chunyu Liu from Boston University School of Public Health, Northwestern University Feinberg School of Medicine, National Institutes of Health, Framingham Heart Study, and Tufts University conducted linear regression analyses to investigate the associations between alcohol consumption and two DNA methylation-based biological age acceleration metrics in 3823 Framingham Heart Study participants (24–92 years and 53.8% women) adjusting for covariates. “We also investigated whether the two epigenetic aging metrics mediated the association of alcohol consumption with hypertension.”They found that higher long-term average alcohol consumption was significantly associated with biological age acceleration assessed by GrimAge acceleration (GAA) and PhenoAge acceleration (PAA) in middle-aged (45–64 years, n = 1866) and older (65–92 years, n = 1267) participants while not in young participants (24–44 years, n = 690). For example, one additional standard drink of alcohol (~14 grams of ethanol per day) was associated with a 0.71 ± 0.15-year (p = 2.1e-6) and 0.60 ± 0.18-year (p = 7.5e-4) increase in PAA in middle-aged and older participants, respectively, but the association was not significant in young participants (p = 0.23). One additional standard serving of liquor (~14 grams of ethanol) was associated with a greater increase in GAA (0.82-year, p = 4.8e-4) and PAA (1.45-year, p = 7.4e-5) than beer (GAA: 0.45-year, p = 5.2e-4; PAA: 0.48-year, p = 0.02) and wine (GAA: 0.51-year, p = 0.02; PAA: 0.91-year, p = 0.008) in middle-aged participant group. “We observed that up to 28% of the association between alcohol consumption and hypertension was mediated by GAA or PAA in the pooled sample. Our findings suggest that alcohol consumption is associated with greater biological aging quantified by epigenetic aging metrics, which may mediate the association of alcohol consumption with quantitative traits, such as hypertension.”DOI - https://doi.org/10.18632/aging.205153Corresponding authors - Jiantao Ma - jiantao.ma@tufts.edu, and Chunyu Liu - liuc@bu.eduSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205153Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, alcohol consumption, epigenetic aging, DNA methylation, hypertensionAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
Pancreatic cancer is one of the deadliest forms of cancer, with a very low survival rate and limited treatment options. Understanding the molecular mechanisms that drive the development and progression of this disease is crucial for finding new ways to prevent and treat it. One of the key players in pancreatic cancer is the WNT signaling pathway, which regulates many aspects of cell growth, differentiation and survival. WNT signaling is often dysregulated in pancreatic cancer, leading to uncontrolled cell proliferation, invasion and resistance to therapy.“The canonical WNT pathway is reportedly an essential protagonist in organ development as well as oncogenesis in multiple cancers.”How does WNT signaling become so powerful in pancreatic cancer cells? In a new study, researchers Jing Wang, Dominik T. Koch, Felix O. Hofmann, Daniel Härtwig, Iris Beirith, Klaus Peter Janssen, Alexandr V. Bazhin, Hanno Niess, Jens Werner, Bernhard W. Renz, and Matthias Ilmer from Ludwig-Maximilians-University, University of Science and Technology of China, Technical University of Munich, and German Cancer Consortium revealed a novel role for a receptor called LGR6 in enhancing WNT signals in this disease. Their research paper was published on September 27, 2023, in Aging’s Volume 15, Issue 20, entitled, “WNT enhancing signals in pancreatic cancer are transmitted by LGR6.”Full blog - https://aging-us.org/2023/11/how-a-receptor-boosts-wnt-signals-in-pancreatic-cancer/Paper DOI - https://doi.org/10.18632/aging.205101Corresponding author - Matthias Ilmer - mailmer@med.lmu.deSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205101Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, pancreatic ductal adenocarcinoma, WNT signaling, epithelial-mesenchymal transition, LGR6, cancer stem cellsAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- November 8, 2023 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 20, entitled, “Tissue immunoexpression of IL-6 and IL-18 in aging men with BPH and MetS and their relationship with lipid parameters and gut microbiota-derived short chain fatty acids.”Recent studies indicate that inflammation is one of the causes of the development of benign prostatic hyperplasia (BPH). Inflammation may result from past infections, metabolic disorders, but also from the state of functioning of the intestinal microbiota. In this new study, researchers Weronika Ratajczak, Maria Laszczyńska, Aleksandra Rył, Barbara Dołęgowska, Olimpia Sipak, Ewa Stachowska, Marcin Słojewski, and Anna Lubkowska from Poland’s Pomeranian Medical University and State University of Applied Sciences aimed to assess whether the diagnostic lipid parameters for metabolic syndrome and short-chain fatty acids (SCFAs) are related to the immunoexpression of interleukins in prostate tissue with benign hyperplasia. The study involved 103 men with BPH, who were divided into two groups depending on the presence of MetS. “We analysed tissue immunoexpression of two proinflammatory interleukins: IL-6, which is known to be involved in the development of BPH, and IL-18, which has not been analysed so far.”The results of their study indicated that men with BPH + MetS in the stroma of the prostate have a significantly higher overall percentage of IL-6+ cells compared to men without MetS (p = 0.034). The analysis of IL-18 immunoexpression in prostate tissue indicated that in men with BPH + MetS, the glandular part of the prostate had a significantly higher percentage of cells with strong IL-18 expression (p = 0.040). They also noticed a relationship between tissue expression of IL-6 and IL-18 and lipid parameters (TG and HDL). “We conclude that lipid disorders occurring in men with BPH increase inflammation in the prostate gland. Moreover, it has also been demonstrated for the first time that, indirectly, through SCFAs, the gut microbiota can act to prevent or create an inflammatory microenvironment in the prostate gland.”DOI - https://doi.org/10.18632/aging.205091Corresponding author - Anna Lubkowska - anna.lubkowska@pum.edu.plSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205091Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, benign prostatic hyperplasia (BPH), metabolic syndrome (MetS), lipids, interleukin 6 (IL-6), interleukin 18 (IL-18), short-chain fatty acidsAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- November 7, 2023 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 20, entitled, “Deciphering reproductive aging in women using a NOD/SCID mouse model for distinct physiological ovarian phenotypes.”Female fertility is negatively correlated with age, with noticeable declines in oocyte quantity and quality until menopause. To understand this physiological process and evaluate human approaches for treating age-related infertility, preclinical studies in appropriate animal models are needed. In this new study, researchers María Marchante, Noelia Ramirez-Martin, Anna Buigues, Jessica Martinez, Nuria Pellicer, Antonio Pellicer, and Sonia Herraiz from IVIRMA, University of Valencia and Instituto Investigación Sanitaria La Fe aimed to characterize an immunodeficient physiological aging mouse model displaying ovarian characteristics of different stages during women's reproductive life. “The main purpose of our study was to establish a physiological ovarian aging mouse model that could be employed to evaluate potential therapeutic interventions derived from human origin.”NOD/SCID mice of different ages (8-, 28-, and 36–40-week-old) were employed to mimic ovarian phenotypes of young, Advanced Maternal Age (AMA), and old women (~18–20-, ~36–38-, and >45-years-old, respectively). Mice were stimulated, mated, and sacrificed to recover oocytes and embryos. Then, ovarian reserve, follicular growth, ovarian stroma, mitochondrial dysfunction, and proteomic profiles were assessed. Age-matched C57BL/6 mice were employed to cross-validate the reproductive outcomes.The quantity and quality of oocytes were decreased in AMA and Old mice. These age-related effects associated spindle and chromosome abnormalities, along with decreased developmental competence to blastocyst stage. Old mice had less follicles, impaired follicle activation and growth, an ovarian stroma inconducive to growth, and increased mitochondrial dysfunctions. Proteomic analysis corroborated these histological findings. Based on that, NOD/SCID mice can be used to model different ovarian aging phenotypes and potentially test human anti-aging treatments.“In summary, in this study we characterized the quality of the ovarian microenvironment and reproductive outcomes of an immunodeficient murine model of physiological ovarian aging by evaluating fertility outcomes, ovarian reserve and stroma, mitochondrial dysfunctions, and the ovarian proteome at different stages. This model adequately mimicked the characteristics of the reproductive stages in women, without external agents compromising folliculogenesis, or disrupting molecular mechanisms and ovarian function, which could mask the processes of physiological aging.”DOI - https://doi.org/10.18632/aging.205086Corresponding author - Sonia Herraiz - sonia_herraiz@iislafe.esAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- November 1, 2023 – A new research perspective was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 20, entitled, “Cholinergic centro-cingulate network in Parkinson disease and normal aging.”In their new perspective, researchers Nicolaas I. Bohnen, Sygrid van der Zee and Roger Albin from University of Michigan, Veterans Administration Ann Arbor Healthcare System, University of Groningen, and the University Medical Center Groningen discussed Parkinson disease (PD). Decreased cholinergic binding within the recently identified centro-cingulate brain network has been shown to robustly correlate with the severity of cognitive impairment in PD. This network with key hubs within the cingulum, operculum and peri-central cortical regions also correlates with elements of parkinsonian motor impairments, including postural instability and gait difficulties, such as falls or freezing. “We recently reported novel data-driving findings suggesting that cholinergic innervation deficits in centro-cingulate brain regions may be an important contributor to cognitive impairments in PD [1].”MRI neuroimaging studies have shown that the anterior midcingulate cortex is a key node for cognitive aspects of movement generation, i.e., intentional motor control. Recent evidence also suggests a novel aspect of organization of primary motor cortex, describing “effector” regions for fine movement control intercalated with interlinked “inter-effector” regions devoted to whole-body control. A distinguishing feature of inter-effector regions is tight linkage to the cingular and opercular regions. Such inter-effector regions have been proposed to be part of a greater somato-cognitive action network necessary for integration of goals and movement. Recent evidence also points to vulnerabilities of cholinergic nerve terminals in the centro-cingulate network in older non-PD adults. These features of normal aging underscore that cortical cholinergic terminal losses in age-associated neurodegenerative disorders are likely not exclusively the result of disease-specific etiologies but also related to otherwise normal aging. “Practical implications of this overlap are that addressing disease-specific and general aging etiologies involved in neurodegeneration, may be of benefit in age-associated neurodegenerative disorders where significant cholinergic systems degeneration is present.”DOI - https://doi.org/10.18632/aging.205209Corresponding author - Nicolaas I. Bohnen - nbohnen@umich.eduSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205209Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, centro-cingulate network, cholinergic, cognition, motor, Parkinson diseaseAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- October 31, 2023 – A new priority research paper was published on the cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 20, entitled, “Proteomic quantification of native and ECM-enriched mouse ovaries reveals an age-dependent fibro-inflammatory signature.”The ovarian microenvironment becomes fibrotic and stiff with age, in part due to increased collagen and decreased hyaluronan. However, the extracellular matrix (ECM) is a complex network of hundreds of proteins, glycoproteins, and glycans which are highly tissue specific and undergo pronounced changes with age. In this new study, researchers Shweta S. Dipali, Christina D. King, Jacob P. Rose, Joanna E. Burdette, Judith Campisi, Birgit Schilling, and Francesca E. Duncan from Northwestern University’s Feinberg School of Medicine, the Buck Institute for Research on Aging and the University of Illinois at Chicago used label-free quantitative proteomic methods to define comprehensive, age-dependent changes in the murine ovarian proteome and ECM in an unbiased manner. “To obtain an unbiased and comprehensive profile of age-associated alterations to the murine ovarian proteome and ECM, we used a label-free quantitative proteomic methodology.”The researchers validated conditions to enrich for the ECM prior to proteomic analysis. Following analysis by data-independent acquisition (DIA) and quantitative data processing, they observed that both native and ECM-enriched ovaries clustered separately based on age, indicating distinct age-dependent proteomic signatures. The team identified a total of 4,721 proteins from both native and ECM-enriched ovaries, of which 383 proteins were significantly altered with advanced age, including 58 ECM proteins. Several ECM proteins upregulated with age have been associated with fibrosis in other organs, but to date their roles in ovarian fibrosis are unknown. Pathways regulating DNA metabolism and translation were downregulated with age, whereas pathways involved in ECM remodeling and immune response were upregulated. Interestingly, immune-related pathways were upregulated with age even in ECM-enriched ovaries, suggesting a novel interplay between the ECM and the immune system. Moreover, the researchers identified putative markers of unique immune cell populations present in the ovary with age. These findings provide evidence from a proteomic perspective that the aging ovary provides a fibroinflammatory milieu, and their study suggests target proteins which may drive these age-associated phenotypes for future investigation.”“To our knowledge, this is the first study to utilize unbiased proteomic approaches to investigate the effect of reproductive aging on the murine ovarian proteome and matrisome.DOI - https://doi.org/10.18632/aging.205190Corresponding authors - Francesca E. Duncan - f-duncan@northwestern.edu, and Birgit Schilling - bschilling@buckinstitute.orgAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/MEDIA@IMPACTJOURNALS.COM
Between 1904 and 2008, researchers found that approximately 75% of patients with Werner syndrome (WS) worldwide were of Japanese descent. WS is a rare genetic disorder that causes premature aging and increases the risk of various age-related diseases, such as diabetes, cardiovascular disease and cancer. One of the hallmarks of WS is the loss of subcutaneous fat, which is the layer of fat under the skin that helps regulate body temperature and store energy. Subcutaneous fat loss leads to severe insulin resistance, which means that the body cannot use glucose effectively and has high blood sugar levels. But what causes subcutaneous fat loss in WS? And how does it affect the metabolism and health of WS patients? In a new study, researchers Daisuke Sawada, Hisaya Kato, Hiyori Kaneko, Daisuke Kinoshita, Shinichiro Funayama, Takuya Minamizuka, Atsushi Takasaki, Katsushi Igarashi, Masaya Koshizaka, Aki Takada-Watanabe, Rito Nakamura, Kazuto Aono, Ayano Yamaguchi, Naoya Teramoto, Yukari Maeda, Tomohiro Ohno, Aiko Hayashi, Kana Ide, Shintaro Ide, Mayumi Shoji, Takumi Kitamoto, Yusuke Endo, Hideyuki Ogata, Yoshitaka Kubota, Nobuyuki Mitsukawa, Atsushi Iwama, Yasuo Ouchi, Naoya Takayama, Koji Eto, Katsunori Fujii, Tomozumi Takatani, Tadashi Shiohama, Hiromichi Hamada, Yoshiro Maezawa, and Koutaro Yokote from Chiba University Graduate School of Medicine, Chiba University Hospital, Kazusa DNA Research Institute, The University of Tokyo, Kyoto University, and International University of Welfare and Health School of Medicine aimed to shed light on these questions by investigating the molecular mechanisms of subcutaneous fat dysfunction in WS. On October 3, 2023, their research paper was published in Aging’s Volume 15, Issue 19, entitled, “Senescence-associated inflammation and inhibition of adipogenesis in subcutaneous fat in Werner syndrome.”“[...] research on WS is important as it can provide insights into the pathogenesis and development of treatments not only for WS but also for general age-related diseases."Full blog - https://aging-us.org/2023/10/rapamycins-therapeutic-potential-in-treating-werner-syndrome/Paper DOI - https://doi.org/10.18632/aging.205078Corresponding authors - Hisaya Kato - hisayakato@chiba-u.jp, Yoshiro Maezawa - yoshiromaezawa@chiba-u.jp, and Koutaro Yokote - kyokote@faculty.chiba-u.jpSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205078Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, Werner syndrome, premature aging, lipodystrophy, stromal vascular fraction, SASPAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
Dr. Dechao Feng from the Department of Urology, Institute of Urology, West China Hospital, Sichuan University, discusses a research paper he co-authored that was published by Aging (Aging-US) in Volume 15, Issue 18, entitled, “Identification of senescence-related lncRNA prognostic index correlating with prognosis and radiosensitivity in prostate cancer patients.”DOI - https://doi.org/10.18632/aging.204888Corresponding authors - Dechao Feng - fdcfenix@stu.scu.edu.cn, and Ping Han - hanping@scu.edu.cnVideo interview - https://www.youtube.com/watch?v=zHiWwd5RlJwTranscription - https://aging-us.net/2023/10/26/behind-the-study-senescence-related-lncrna-prognostic-index-in-prostate-cancer/Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204888Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, prostate cancer, senescence-related lncRNA prognostic index, biochemical recurrence, radiosensitivity, androgen responseAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
Dr. Frank Pun, Diana Zagirova, Dr. Anatoly Urban, and Geoffrey Leung from Insilico Medicine Hong Kong Ltd., discuss a research paper they co-authored that was published by Aging (Aging-US) in Volume 15, Issue 18, entitled, “Biomedical generative pre-trained based transformer language model for age-related disease target discovery.”DOI - https://doi.org/10.18632/aging.205055Corresponding author - Alex Zhavoronkov - alex@insilico.comVideo interview - https://www.youtube.com/watch?v=kIJvrY7n3n0Interview transcription - https://aging-us.net/2023/10/25/behind-the-study-biomedical-transformer-language-model-for-age-related-disease-discovery/Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205055Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, transformers, deep learning, therapeutic target discovery, aging biomarkers, human agingAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- October 25, 2023 – A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 19, entitled, “Live while the DNA lasts. The role of autophagy in DNA loss and survival of diploid yeast cells during chronological aging.”Aging is inevitable and affects all cell types. Thus, yeast cells are often used as a model in aging studies. There are two approaches to studying aging in yeast: replicative aging, which describes the proliferative potential of cells, and chronological aging, which is used for studying post-mitotic cells. In this new study, while analyzing the chronological lifespan (CLS) of diploid Saccharomyces cerevisiae cells, researchers Tuguldur Enkhbaatar, Marek Skoneczny, Karolina Stępień, Mateusz Mołoń, and Adrianna Skoneczna from the Polish Academy of Sciences and Rzeszów University discovered a remarkable phenomenon: ploidy reduction during aging progression. “To uncover the mechanism behind this unusual process we used yeast strains undergoing a CLS assay, looking for various aging parameters.”Cell mortality, regrowth ability, autophagy induction and cellular DNA content measurements indicated that during the CLS assay, dying cells lost their DNA, and only diploids survived. The researchers demonstrated that autophagy was responsible for the gradual loss of DNA. The nucleophagy marker activation at the start of the CLS experiment correlated with the significant drop in cell viability. The activation of piecemeal microautophagy of nucleus (PMN) markers appeared to accompany the chronological aging process until the end. “Our findings emphasize the significance of maintaining at least one intact copy of the genome for the survival of post-mitotic diploid cells.”During chronological aging, cellular components, including DNA, are exposed to increasing stress, leading to DNA damage and fragmentation in aging cells. The researchers propose that PMN-dependent clearance of damaged DNA from the nucleus helps prevent genome rearrangements. However, as long as one copy of the genome can be rebuilt, cells can still survive.“The observations we made in aging research using yeast as the eukaryotic cell model may help to understand the mechanisms that prevent aneuploidy during aging or cancerogenesis in cells where chromothripsis has occurred.”DOI - https://doi.org/10.18632/aging.205102Corresponding author - Adrianna Skoneczna - ada@ibb.waw.plSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205102Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, genome instability, lifespan, autophagy, double-strand breaksAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- October 24, 2023 – A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 19, entitled, “Metabolic switch in the aging astrocyte supported via integrative approach comprising network and transcriptome analyses.”Dysregulated central-energy metabolism is a hallmark of brain aging. Supplying enough energy for neurotransmission relies on the neuron-astrocyte metabolic network. In their new study, researchers Alejandro Acevedo, Felipe Torres, Miguel Kiwi, Felipe Baeza-Lehnert, L. Felipe Barros, Dasfne Lee-Liu, and Christian González-Billault from Universidad de Chile, Cedenna, University of California, San Diego, Centro de Estudios Científicos (CECs), Geroscience Center for Brain Health and Metabolism (GERO), Universidad San Sebastián, and the Buck Institute for Research on Aging aimed to identify genes contributing to age-associated brain functional decline.“[...] we formulated an approach to analyze the metabolic network by integrating flux, network structure and transcriptomic databases of neurotransmission and aging.” Their findings support that during brain aging: (1) The astrocyte undergoes a metabolic switch from aerobic glycolysis to oxidative phosphorylation, decreasing lactate supply to the neuron, while the neuron suffers intrinsic energetic deficit by downregulation of Krebs cycle genes, including mdh1 and mdh2 (Malate-Aspartate Shuttle); (2) Branched-chain amino acid degradation genes were downregulated, identifying dld as a central regulator; (3) Ketone body synthesis increases in the neuron, while the astrocyte increases their utilization, in line with neuronal energy deficit in favor of astrocytes. “The genes identified here are valuable candidates for future studies to understand the molecular mechanisms of healthy brain aging and prevent brain age-associated failure using energy metabolism as a target.”DOI - https://doi.org/10.18632/aging.204663Corresponding authors - Christian González-Billault - chrgonza@uchile.cl, and Dasfne Lee-Liu - dasfne.lee@uss.clSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204663Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, astrocyte, neuron, brain aging, flux balance analysis, network centralityAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
Dr. Wenbo Yu, Stanley from the Centre for Cancer Biology, SA Pathology and University of South Australia details a #research perspective he co-authored that was #published by Aging (Aging-US) in Volume 15, Issue 17, entitled, “A Poisson distribution-based general model of cancer rates and a cancer risk-dependent theory of aging.”#author #authorinterview #interview #aging #cancer #entropy #poisson #perspective #openaccess #openscience #peerreview #journal #publication #meded #agingshort #videoDOI - https://doi.org/10.18632/aging.205016Corresponding author - Wenbo Yu - stanley.yu@sa.gov.auVideo interview - https://www.youtube.com/watch?v=1n7puuJridoTranscription - https://aging-us.net/2023/10/23/behind-the-study-poisson-distribution-based-model-of-cancer-rates-cancer-risk-dependent-theory-of-aging/Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205016Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, cancer incidence model, poisson distribution, entropyAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- October 18, 2023 – A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 19, entitled, “Reduction of double-strand DNA break repair exacerbates vascular aging.”Advanced age is the greatest risk factor for cardiovascular disease (CVD), the leading cause of death. Arterial function is impaired in advanced age which contributes to the development of CVD. One underexplored hypothesis is that DNA damage within arteries leads to this dysfunction, yet evidence demonstrating the incidence and physiological consequences of DNA damage in arteries, and in particular, in the microvasculature, in advanced age is limited.In their new study, researchers Samuel I. Bloom, Jordan R. Tucker, Daniel R. Machin, Hossein Abdeahad, AdeLola O. Adeyemo, Tyler G. Thomas, R. Colton Bramwell, Lisa A. Lesniewski, and Anthony J. Donato from The University of Utah, Florida State University and the Veterans Affairs Medical Center-Salt Lake City began by assessing the abundance of DNA damage in human and mouse lung microvascular endothelial cells and found that aging increases the percentage of cells with DNA damage. “To explore the physiological consequences of increases in arterial DNA damage, we evaluated measures of endothelial function, microvascular and glycocalyx properties, and arterial stiffness in mice that were lacking or heterozygous for the double-strand DNA break repair protein ATM kinase.”Surprisingly, in young mice, vascular function remained unchanged which led the researchers to rationalize that perhaps aging is required to accumulate DNA damage. Indeed, in comparison to wild type littermate controls, mice heterozygous for ATM that were aged to ~18 mo (Old ATM +/−) displayed an accelerated vascular aging phenotype characterized by increases in arterial DNA damage, senescence signaling, and impairments in endothelium-dependent dilation due to elevated oxidative stress. Furthermore, old ATM +/− mice had reduced microvascular density and glycocalyx thickness as well as increased arterial stiffness. “Collectively, these data demonstrate that DNA damage that accumulates in arteries in advanced age contributes to arterial dysfunction that is known to drive CVD.”DOI - https://doi.org/10.18632/aging.205066Corresponding author - Anthony J. Donato - tony.donato@utah.eduSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.20506Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, DNA damage, vascular function, endothelial cell, senescence, oxidative stress, arterial stiffnessAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- October 16, 2023 – A new research paper was published on the cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 19, entitled, “BMAL1 modulates senescence programming via AP-1.”Cellular senescence and circadian dysregulation are biological hallmarks of aging. Whether they are coordinately regulated has not been thoroughly studied. In this new study, researchers Sarah K. Jachim, Jian Zhong, Tamas Ordog, Jeong-Heon Lee, Aditya V. Bhagwate, Nagaswaroop Kengunte Nagaraj, Jennifer J. Westendorf, João F. Passos, Aleksey V. Matveyenko, and Nathan K. LeBrasseur from the Mayo Clinic in Rochester, Minnesota, hypothesized that BMAL1, a pioneer transcription factor and master regulator of the molecular circadian clock, plays a role in the senescence program. “Here, we demonstrate BMAL1 is significantly upregulated in senescent cells and has altered rhythmicity compared to non-senescent cells.”Through BMAL1-ChIP-seq, they showed that BMAL1 is uniquely localized to genomic motifs associated with AP-1 in senescent cells. Integration of BMAL1-ChIP-seq data with RNA-seq data revealed that BMAL1 presence at AP-1 motifs is associated with active transcription. Finally, the researchers showed that BMAL1 contributes to AP-1 transcriptional control of key features of the senescence program, including altered regulation of cell survival pathways, and confers resistance to drug-induced apoptosis. “Overall, these results highlight a previously unappreciated role of the core circadian clock component BMAL1 on the molecular phenotype of senescent cells.”DOI - https://doi.org/10.18632/aging.205112Corresponding authors - Nathan K. LeBrasseur - lebrasseur.nathan@mayo.eduSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205112Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, AP-1, circadian clock, cellular senescence, senolytic, transcription regulationAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
Sleep is vital for our health and well-being, but as we age, we tend to experience less and less of it. In particular, we lose some of the deep sleep stages, known as slow wave sleep (SWS), that are crucial for memory consolidation and brain maintenance. This can affect cognitive performance and increase our risk of developing dementia.Not everyone is equally vulnerable to the negative effects of poor sleep quality. Some people seem to be more resilient and able to cope with less SWS without compromising their mental abilities. What makes them different? One possible factor is cognitive reserve (CR).CR is a concept that refers to the brain’s ability to adapt and compensate for age-related changes or brain damage. It is influenced by various aspects of our life experiences, such as education, occupation, leisure activities, social interactions, and mental stimulation. People with higher CR are thought to have more efficient brain networks, more cognitive strategies, and more brain reserve (i.e., more neurons and connections) that can buffer the impact of aging or pathology on cognition.In a new study, researchers Valentin Ourry, Stéphane Rehel, Claire André, Alison Mary, Léo Paly, Marion Delarue, Florence Requier, Anne Hendy, Fabienne Collette, Natalie L. Marchant, Francesca Felisatti, Cassandre Palix, Denis Vivien, Vincent de la Sayette, Gaël Chételat, Julie Gonneaud, and Géraldine Rauchs from Normandie University, UNI – ULB Neuroscience Institute, University of Liege, University College London, and CHU de Caen aimed to identify individuals in whom sleep disturbances might have greater behavioral consequences. On September 28, 2023, their research paper was published in Aging’s Volume 15, Issue 18, entitled, “Effect of cognitive reserve on the association between slow wave sleep and cognition in community-dwelling older adults.”Full blog -Paper DOI -https://doi.org/10.18632/aging.204943Corresponding author - Géraldine Rauchs - geraldine.rauchs@inserm.frSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204943Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, sleep, cognitive reserve, cognitionAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- October 11, 2023 – A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 18, entitled, “Pathways explaining racial/ethnic and socio-economic disparities in dementia incidence: the UK Biobank study.”Pathways explaining racial/ethnic disparities in dementia risk are under-evaluated. In their new study, researchers May A. Beydoun, Hind A. Beydoun, Marie T. Fanelli-Kuczmarski, Jordan Weiss, Michael F. Georgescu, Osorio Meirelles, Donald M. Lyall, Michele K. Evans, and Alan B. Zonderman from the National Institute on Aging, Fort Belvoir Community Hospital, Stanford University, and the University of Glasgow examined those disparities and their related pathways among UK Biobank study respondents (50–74 y, N = 323,483; 3.6% non-White minorities) using a series of Cox proportional hazards and generalized structural equations models (GSEM).“The present study examines pathways that might explain racial, ethnic, and socio-economic disparities in AD or all-cause dementia in a large cohort study, the UK Biobank. Our study used several methodologies, including structural equation modeling coupled with survival analysis techniques to examine complex mediating effects between race, ethnicity, socioeconomic status, and dementia or AD [Alzheimer’s disease] risk in a sex-specific manner focusing on lifestyle, biological and cognitive pathways. It is also an attempt at replicating a previous study conducted among US older adults [24].”Results: After ≤15 years, 5,491 all-cause dementia cases were diagnosed. Racial minority status (RACE_ETHN, Non-White vs. White) increased dementia risk by 24% (HR = 1.24, 95% CI: 1.07–1.45, P = 0.005), an association attenuated by socio-economic status (SES), (HR = 1.12, 95% CI: 0.96–1.31). Total race-dementia effect was mediated through both SES and Life’s Essential 8 lifestyle sub-score (LE8LIFESTYLE), combining diet, smoking, physical activity, and sleep factors. SES was inversely related to dementia risk (HR = 0.69, 95% CI: 0.67, 0.72, P < 0.001). Pathways explaining excess dementia risk among racial minorities included ‘RACE_ETHN(−) → SES(−) → DEMENTIA’, ‘RACE_ETHN(−) → SES(−) → Poor cognitive performance, COGN(+) → DEMENTIA’ and ‘RACE_ETHN(−) → SES(+) → LE8LIFESTYLE(−) → DEMENTIA’.“Pending future interventions, lifestyle factors including diet, smoking, physical activity, and sleep are crucial for reducing racial and socio-economic disparities in dementia.”DOI - https://doi.org/10.18632/aging.205058Corresponding author - May A. Beydoun - baydounm@mail.nih.govSubscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, dementia, Alzheimer’s disease, health disparities, socio-economic status, structural equations modelingAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- October 10, 2023 – A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 18, entitled, “High-throughput single-cell profiling of B cell responses following inactivated influenza vaccination in young and older adults.”Seasonal influenza contributes to a substantial disease burden, resulting in approximately 10 million hospital visits and 50 thousand deaths in a typical year in the United States. 70 - 85% of the mortality occurs in people over the age of 65. Influenza vaccination is the best protection against the virus, but it is less effective for the elderly, which may be in part due to differences in the quantity or type of B cells induced by vaccination. In their new study, researchers Meng Wang, Ruoyi Jiang, Subhasis Mohanty, Hailong Meng, Albert C. Shaw, and Steven H. Kleinstein from Yale University / Yale School of Medicine investigated this possibility.“[...] we sorted pre- and post-vaccination peripheral blood B cells from three young and three older adults with strong antibody responses to the inactivated influenza vaccine and employed single-cell technology to simultaneously profile the gene expression and the B cell receptor (BCR) of the B cells.”Prior to vaccination, the researchers observed a higher somatic hypermutation frequency and a higher abundance of activated B cells in older adults than in young adults. Following vaccination, young adults mounted a more clonal response than older adults. The expanded clones included a mix of plasmablasts, activated B cells, and resting memory B cells in both age groups, with a decreased proportion of plasmablasts in older adults. Differential abundance analysis identified additional vaccine-responsive cells that were not part of expanded clones, especially in older adults. “To summarize, we showed a quantitative difference in B cell response following vaccination between age groups, with expansion dominated by plasmablasts in the young, and activated B cells in older adults. [...] Overall, this study provides insights into the B cell vaccine response differences between young and older adults and may be beneficial to design more effective vaccines in the older age groups.”DOI - https://doi.org/10.18632/aging.204778Corresponding authors - Albert C. Shaw - albert.shaw@yale.edu, and Steven H. Kleinstein - steven.kleinstein@yale.eduSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204778Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, B cell receptor, repertoire, clonal expansion, single-cell RNA-seqAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- October 4, 2023 – A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 18, entitled, “Biomedical generative pre-trained based transformer language model for age-related disease target discovery.”Target discovery is crucial for the development of innovative therapeutics and diagnostics. However, current approaches often face limitations in efficiency, specificity, and scalability, necessitating the exploration of novel strategies for identifying and validating disease-relevant targets. Advances in natural language processing have provided new avenues for predicting potential therapeutic targets for various diseases. In their new study, researchers Diana Zagirova, Stefan Pushkov, Geoffrey Ho Duen Leung, Bonnie Hei Man Liu, Anatoly Urban, Denis Sidorenko, Aleksandr Kalashnikov, Ekaterina Kozlova, Vladimir Naumov, Frank W. Pun, Ivan V. Ozerov, Alex Aliper, and Alex Zhavoronkov from Insilico Medicine present a novel approach for predicting therapeutic targets using a large language model (LLM). “We trained a domain-specific BioGPT model on a large corpus of biomedical literature consisting of grant text and developed a pipeline for generating target prediction.”This study demonstrates that pre-training of the LLM model with task-specific texts improves its performance. Applying the developed pipeline, the researchers retrieved prospective aging and age-related disease targets and showed that these proteins are in correspondence with the database data. Moreover, they propose CCR5 and PTH as potential novel dual-purpose anti-aging and disease targets which were not previously identified as age-related but were highly ranked in their approach. “Overall, our work highlights the high potential of transformer models in novel target prediction and provides a roadmap for future integration of AI approaches for addressing the intricate challenges presented in the biomedical field.”DOI - https://doi.org/10.18632/aging.205055Corresponding author - Alex Zhavoronkov - alex@insilico.comSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205055Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, transformers, deep learning, therapeutic target discovery, aging biomarkers, human agingAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- October 2, 2023 – A new priority research paper was published on the cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 18, entitled, “Gene expression signatures of human senescent corneal and conjunctival epithelial cells.”In this new study, researchers Koji Kitazawa, Akifumi Matsumoto, Kohsaku Numa, Yasufumi Tomioka, Zhixin A. Zhang, Yohei Yamashita, Chie Sotozono, Pierre-Yves Desprez, and Judith Campisi from the Buck Institute for Research on Aging, Kyoto Prefectural University of Medicine and Lawrence Berkeley National Laboratory aimed to investigate the senescent phenotypes of human corneal and conjunctival epithelial cells.“Here, we induced cellular senescence in human corneal and conjunctival epithelium using X-irradiation, and analyzed gene expression profiles of each cell type to determine the characteristics of senescent ocular surface cells.”The team examined cell morphology, senescence-associated β-galactosidase (SA-β-gal) activity, cell proliferation, and expression of senescence markers (p16 and p21). RNA sequencing analysis was conducted to compare gene expression profiles between senescent and non-senescent cells. Finally, the potential involvement of senescent cells in the pathogenesis of ocular surface diseases was investigated.X-irradiated corneal and conjunctival epithelial cells exhibited typical senescence phenotypes, i.e., flattened morphologies, increased SA-β-gal activity, decreased cell proliferation, and increased expression of senescence markers, p16 and p21. RNA-seq analysis revealed substantial differences in gene expression profiles between senescent corneal (SCo) and conjunctival epithelial cells (SCj). Moreover, SCj were detected in pathological conjunctival tissues associated with limbal stem cell deficiency (LSCD) due to Stevens-Johnson syndrome or chemical burns, potentially being involved in abnormal differentiation.“This study highlights the cellular and molecular characteristics of senescent ocular surface cells, particularly in SCj that show abnormal keratin expression, and their potential roles in severe ocular surface diseases and pathology.”DOI - https://doi.org/10.18632/aging.205113Corresponding authors - Koji Kitazawa - kkitazaw@koto.kpu-m.ac.jp, and Judith Campisi - jcampisi@buckinstitute.orgSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205113Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, cellular senescence, cornea, conjunctiva, Stevens-Johnson syndrome, limbal stem cell deficiencyAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
R-loops are structures that form when the nascent RNA hybridizes with the template DNA strand, displacing the non-template strand. Nascent RNA refers to the newly synthesized RNA molecule that is produced during the process of transcription. Transcription is the first step in gene expression where the information in a DNA sequence is used to create an RNA molecule. In addition to transcription, R-loops are involved in various biological processes, such as splicing, DNA repair and chromatin remodeling. However, when R-loop homeostasis is disrupted, they can also cause transcriptional impairment, genome instability and cellular dysfunction."R-loops have been shown and studied in a wide range of organisms and while they have important regulatory roles, persistent R-loops can be detrimental to cell function and survival, having been closely linked to both gene expression dysregulation and increased genome instability."In a new editorial paper, researcher Hana Hall from the Purdue Institute for Integrative Neuroscience at Purdue University, discusses the role of R-loops in neuronal aging and neurodegeneration. On September 13, 2023, her editorial was published in Aging’s Volume 15, Issue 17, and entitled, “R-loops in neuronal aging.” Hall summarizes her recent study and the current knowledge on how R-loop levels change during aging, how they affect gene expression and neuronal function, and how they are regulated by different factors.Full blog - https://aging-us.org/2023/09/the-role-of-r-loops-in-neuronal-aging/Paper DOI - https://doi.org/10.18632/aging.205070Corresponding author - Hana Hall - hallh@purdue.eduSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205070Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, R-loops, neuron, transcription, genome instability, neurodegenerationAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- September 27, 2023 – A new editorial paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 17, entitled, “Promising trends in lung cancer care, but are we overlooking the majority?”In their new editorial, researchers Bhavina Sharma and Apar Kishor Ganti from the University of Nebraska Medical Center discuss challenges and opportunities for better lung cancer care for the elderly. Lung cancer is the third most common cancer in the United States, after female breast cancer and prostate cancer. It accounts for more cancer-related deaths in both men and women than any other types of cancer. The incidence of new lung cancer has decreased between 1999-2019, mirroring the fall in tobacco use in the past few decades. Lung cancer-related mortality has also decreased with the recent advances in screening techniques and treatment strategies. However, the incidence of lung cancer and lung cancer mortality is still disproportionately higher among older patients (65 years and older). Multiple studies have shown that older patients are more likely to be undertreated because of their chronological age, even after accounting for their comorbidities and socioeconomic status. Common reasons for this disparity are insufficient study evidence, lack of appropriate resources and support, patient factors such as socioeconomic status, as well as variations in individual physician practices and preferences. Even though the median age of lung cancer diagnosis is 71 years, and more than two-thirds of patients are older than 65 years, older patients are less likely to be enrolled in clinical trials. “Although there is now increasing effort and guidance by major cancer societies and regulatory groups to increase inclusion of older patients, better conscious collaboration between the stakeholders is necessary for effective implementation of the strategies discussed and to enhance enrollment and retention of older cancer patients.”DOI - https://doi.org/10.18632/aging.204662Corresponding author - Apar Kishor Ganti - aganti@unmc.eduSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204662Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, lung cancer, clinical trialsAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- September 26, 2023 – A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 17, entitled, “Availability of living donor optimizes timing of liver transplant in high-risk waitlisted cirrhosis patients.”Liver transplant (LT) candidates have become older and frailer. Growing non-alcoholic steatohepatitis (NASH) and comorbid disease burden in recent years is also predisposing them for poor waitlist outcomes. In this new study, researchers Fakhar Ali Qazi Arisar, Shiyi Chen, Catherine Chen, Noorulsaba Shaikh, Ravikiran Sindhuvalada Karnam, Wei Xu, Sumeet K. Asrani, Zita Galvin, Gideon Hirschfield, Keyur Patel, Cynthia Tsien, Nazia Selzner, Mark Cattral, Leslie Lilly, and Mamatha Bhat from the University Health Network, University of Toronto, Baylor University Medical Center, and Dow University of Health Sciences aimed to evaluate the impact of access to living donor liver transplantation (LDLT) in waitlisted patients at highest risk of dropout. “We reviewed all adult patients with decompensated cirrhosis listed for LT from November 2012 to December 2018.”Patients with a potential living donor (pLD) available were identified. Survival analyses with Cox Proportional Hazards models and time to LT with Competing risk models were performed followed by prediction model development. Out of 860 patients who met inclusion criteria, 360 (41.8%) had a pLD identified and 496 (57.6%) underwent LT, out of which 170 (34.2%) were LDLT. The benefit of pLD was evident for all, but patients with moderate to severe frailty at listing (interaction p = 0.03), height <160 cm (interaction p = 0.03), and Model for end-stage liver disease (MELD)-Na score <20 (interaction p < 0.0001) especially benefited. “Our study identifies that certain patient subgroups (short stature, MELD <20, and moderate to severe frailty) are at the highest risk for waitlist mortality with prolonged waiting time for a deceased donor organ offer. These patient subgroups, which represent a growing share of the waitlist population in recent years, would be especially protected against death or delisting if they had access to living donation at the time of listing. Certainly, LDLT is beneficial to all, with improved waitlist mortality and post-transplant outcomes.”DOI - https://doi.org/10.18632/aging.204982Corresponding author - Mamatha Bhat - mamatha.bhat@uhn.caSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204982Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, living donor liver transplant, frailty, old age, short-statured, MELD score, prediction modelAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY- September 20, 2023 – A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 17, entitled, “Development of a DNA damage-induced senescence model in osteoarthritic chondrocytes.”Senescent cells (SnCs) have been described to accumulate in osteoarthritis (OA) joint tissues in response to injury, thereby participating in OA development and progression. However, clinical therapeutic approaches targeting SnCs using senolysis, although promising in preclinical OA models, have not yet proven their efficacy in patients with knee OA. This pitfall may be due to the lack of understanding of the mechanisms underlying chondrocyte senescence. In their new study, researchers Mélina Georget, Anaïs Defois, Romain Guiho, Nina Bon, Sophie Allain, Cécile Boyer, Boris Halgand, Denis Waast, Gaël Grimandi, Alban Fouasson-Chailloux, Jérôme Guicheux, and Claire Vinatier from Nantes Université aimed to generate models of chondrocyte senescence.“In this context, our study aims to develop in vitro models of chondrocyte senescence by investigating the ability of etoposide and IL-1β treatments to produce a reliable chondrocyte senescent model.”This study used etoposide, to induce DNA damage-related senescence or chronic exposure to IL-1β to entail inflammation-related senescence in human OA chondrocytes. Several hallmarks of cellular senescence, such as cell cycle arrest, expression of cyclin-dependent kinase inhibitors, DNA damages, and senescence-associated secretory profile were evaluated. Chronic exposure to IL-1β induces only partial expression of senescence markers and does not allow us to conclude on its ability to induce senescence in chondrocytes. On the other hand, etoposide treatment reliably induces DNA damage-related senescence in human articular chondrocytes evidenced by loss of proliferative capacity, DNA damage accumulation, and expression of some SASP components.“Etoposide-induced senescence model may help investigate the initiation of cellular senescence in chondrocytes, and provide a useful model to develop therapeutic approaches to target senescence in OA.”DOI - https://doi.org/10.18632/aging.204881Corresponding author - Claire Vinatier - claire.vinatier@univ-nantes.frSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204881Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, senescence, osteoarthritis, etoposide, chondrocytesAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
A new priority research paper was published on the cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 17, entitled, “Fail-tests of DNA methylation clocks, and development of a noise barometer for measuring epigenetic pressure of aging and disease.”In this new study, researchers Xiaoyue Mei, Joshua Blanchard, Connor Luellen, Michael J. Conboy, and Irina M. Conboy from the University of California, Berkeley, show that Elastic Net (EN) DNA methylation (DNAme) clocks have low accuracy of predictions for individuals of the same age and a low resolution between healthy and disease cohorts; caveats inherent in applying linear model to non-linear processes. “We found that change in methylation of cytosines with age is, interestingly, not the determinant for their selection into the clocks.” Moreover, an EN clock’s selected cytosines change when non-clock cytosines are removed from the training data; as expected from optimization in a machine learning (ML) context, but inconsistently with the identification of health markers in a biological context. To address these limitations, the researchers moved from predictions to measurement of biological age, focusing on the cytosines that on average remain invariable in their methylation through lifespan, postulated to be homeostatically vital. They established that dysregulation of such cytosines, measured as the sums of standard deviations of their methylation values, quantifies biological noise, which in their hypothesis is a biomarker of aging and disease. “We term this approach a ‘noise barometer’ - the pressure of aging and disease on an organism.” These noise-detecting cytosines are particularly important as sums of SD on the entire 450K DNAme array data yield a random pattern through chronology. Testing how many cytosines of the 450K arrays become noisier with age, the team found that the paradigm of DNAme noise as a biomarker of aging and disease remarkably manifests in ~1/4 of the total. In that large set even the cytosines that have on average constant methylation through age show increased SDs and can be used as noise detectors of the barometer.DOI - https://doi.org/10.18632/aging.205046Corresponding author - Irina M. Conboy - iconboy@berkeley.eduSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205046Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, DNA methylation, epigenetics, clocks’ fail-test, biological noiseAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
In the realm of cancer research, one persistent trend has emerged — the incidence of invasive melanoma rises steadily with advancing age. While this insidious disease remains rare in children and adolescents, it progressively asserts its presence as individuals grow older. The connection between age and melanoma incidence persists around the world, albeit with varying rates in different countries. Australia has the highest melanoma rates in the world. According to the Melanoma Institute Australia, every 30 minutes an Australian is diagnosed with melanoma and every 6 hours an Australian dies from it. Thankfully, research is making a difference. In the last decade, the 5-year overall survival rate for advanced melanoma has increased from less than 10% to more than 50%. In 2011, melanoma was Australia’s 7th most deadly cancer. In 2021, melanoma was Australia’s 11th most deadly cancer.In a new editorial paper, researchers John F. Thompson and Gabrielle J. Williams from the Melanoma Institute Australia at The University of Sydney discuss the intricacies of how age influences different varieties of melanoma incidence, prognosis and treatment. On August 17, 2023, their editorial was published in Aging’s Volume 15, Issue 16, entitled, “The effect of age on melanoma incidence and prognosis.”Full blog - https://aging-us.org/2023/09/the-impact-of-age-on-melanoma-insights-from-recent-research/Paper DOI - https://doi.org/10.18632/aging.204653Corresponding author - John F. Thompson - john.thompson@melanoma.org.auVideo short - https://www.youtube.com/watch?v=V0wwfLEJGW0Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204653Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, melanoma, incidence, age, prognosisAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/X - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
A new editorial paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 16, entitled, “Microvascular contributions to white matter injury in Alzheimer’s disease.”
In their new editorial, researchers Zsolt Bagi, Larry S. Sherman and Stephen A. Back from Augusta University discuss mechanisms of cognitive impairment and dementia. Impairments in cognitive and executive function of presumed cerebral microvascular origin are important and recently recognized neuropathological manifestations of vascular contributions to cognitive impairment and dementia (VCID). It has been long known that hypertensive cerebrovascular disease also involves a spectrum of subcortical small vessel diseases, such as arteriolosclerosis and lipohyalinosis of small penetrating arterioles, which contribute to progressive injury of periventricular, frontal and parietal white matter (WM).
“However, until recently, recognition of the role of WM injury during aging and the progression of Alzheimer disease and related dementias (AD/ADRD) was very limited.”
Despite growing interest in VCID and AD/ADRD, there have been few studies of mechanistic links between subcortical small vessel disease, WM injury and cognitive decline. Even though WM constitutes >80% of the human cerebral hemispheres, a PubMed search of AD and WM injury yielded only 381 articles (including reviews) vs. 193,303 articles for AD alone. Notably, 50% of diagnosed AD patients have mixed vascular and AD pathology. Hence, there is a critical need to explore connections between AD, WM injury and cerebral small vessel disease to define mechanisms and diagnostic features of mixed vascular and AD neuropathological change (ADNC).
“To provide rigorous access to human WM lesions, we recently developed a unique rapid autopsy brain procurement protocol using specimens donated by participants in the Adult Changes in Thought (ACT) study, a prospective, population-based study of aging and incident dementia among men and women in Seattle, Washington [5].”
DOI - https://doi.org/10.18632/aging.204997
Corresponding author - Zsolt Bagi - zbagi@augusta.edu
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Keywords - aging, cerebrovascular, neuropathology, vasodilation, parenchymal, arteriole
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at https://www.Aging-US.com and connect with us:
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A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 16, entitled, “Copy number variation as a tool for implementing pregnancy as an aging model.”Copy number variations (CNV) are a major contributor to genome variability. CNVs have been linked to aging and other degradable phenotypes such as pregnancy physiology. In this new study, researchers Mariana Andrawus, Lital Sharvit, Noga Touitou, Batia Lerrer, Haim Y. Cohen, and Gil Atzmon from University of Haifa and Bar-Ilan University used CNVs from pregnant mice to demonstrate how pregnancy can be used as a model of aging. “We hypothesize that pregnancy can serve as a model for aging by demonstrating similar biomarkers, pathologies, and genetic and epigenetic effects [3]. To test this hypothesis, we designed a study that assesses CNVs associated with human longevity (unpublished results) in pregnancy.”Candidate CNVs were selected by applying case-control analysis in human centenarians compared with control groups. These CNVs were aligned with the mouse genome and their copy variation was assessed using qRT-PCR in liver and blood tissue samples from pregnant mice throughout pregnancy (baseline; first, second, and third trimester; post-partum). Eight of the ten selected CNVs demonstrated a significant decline/increase trend throughout the pregnancy followed by opposite direction soon after delivery in the liver and blood of the mouse tissues. Furthermore, significant differential expression was detected among the candidate CNVs’ close vicinity genes (APA2A, LSS, RBDHF1, PLAAT1, and SCL17A2), but not in the WSCD2 gene. Establishing a genetic link between longevity and pregnancy is a significant step toward implementing the pregnancy process as a model for aging. These results in pregnant mice highlight the mechanism and similarities between pregnancy and aging. “Investigating the mechanisms that cause such rejuvenation after labor could change our aging treatment paradigm.”DOI - https://doi.org/10.18632/aging.204936Corresponding author - Gil Atzmon - gatzmon@univ.haifa.ac.ilVideo short - https://www.youtube.com/watch?v=82466m-S-tUSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204936Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, pregnancy, copy number variation, gene expressionAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 16, entitled, “Reorganization of pancreas circadian transcriptome with aging.”
The evolutionarily conserved circadian system allows organisms to synchronize internal processes with 24-h cycling environmental timing cues, ensuring optimal adaptation. Like other organs, the pancreas function is under circadian control. Recent evidence suggests that aging by itself is associated with altered circadian homeostasis in different tissues which could affect the organ’s resiliency to aging-related pathologies.
Pancreas pathologies of either endocrine or exocrine components are age-related. Whether pancreas circadian transcriptome output is affected by age is still unknown. In their new study, researchers Deepak Sharma, Caitlin R. Wessel, Mahboobeh Mahdavinia, Fabian Preuss, and Faraz Bishehsari from Rush University and University of Wisconsin-Parkside profiled the impact of age on the pancreatic transcriptome over a full circadian cycle and elucidated a circadian transcriptome reorganization of pancreas by aging.
“Here we carried out a 24-h circadian transcriptomic analysis of pancreas from male mice at young and old ages.”
The researchers defined a comprehensive circadian transcriptome landscape and identified biological pathways that are reflective of aging pancreas. Additionally, analysis of the pancreatic microenvironment revealed novel mechanistic insights into the fibroblast-mediated regulation of rhythmicity in aged pancreas. The team suggests that the circadian transcriptome in aging pancreas re-organizes in response to age-specific signals from the cellular microenvironment, primarily modulated by fibroblasts.
“Our study highlights gain of rhythms in the extrinsic cellular pathways in the aged pancreas and extends a potential role to fibroblast-associated mechanisms.”
DOI - https://doi.org/10.18632/aging.204929
Corresponding author - Faraz Bishehsari - Faraz_Bishehsari@rush.edu
Video short - https://www.youtube.com/watch?v=dhHK8udB1eg
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Keywords - aging, circadian rhythms, RNA transcriptomics, pancreas
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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A new research paper was published on the cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 16, entitled, “Dectin-1 stimulation promotes a distinct inflammatory signature in the setting of HIV-infection and aging.”Dectin-1 is an innate immune receptor that recognizes and binds β-1, 3/1, 6 glucans on fungi. In this new study, researchers Archit Kumar, Jiawei Wang, Allen Esterly, Chris Radcliffe, Haowen Zhou, Brent Vander Wyk, Heather G. Allore, Sui Tsang, Lydia Barakat, Subhasis Mohanty, Hongyu Zhao, Albert C. Shaw, and Heidi J. Zapata evaluated Dectin-1 function in myeloid cells in a cohort of HIV-positive and HIV-negative young and older adults. “The HIV-positive and HIV-negative groups were comparable in age and gender distribution, incidence of comorbidities such as diabetes, metabolic syndrome, cardiovascular disease and pulmonary disease.”Stimulation of monocytes with β-D-glucans induced a pro-inflammatory phenotype in monocytes of HIV-infected individuals that was characterized by increased levels of IL-12, TNF-α, and IL-6, with some age-associated cytokine increases also noted. Dendritic cells showed a striking HIV-associated increase in IFN-α production. These increases in cytokine production paralleled increases in Dectin-1 surface expression in both monocytes and dendritic cells that were noted with both HIV and aging. Differential gene expression analysis showed that HIV-positive older adults had a distinct gene signature compared to other cohorts characterized by a robust TNF-α and coagulation response (increased at baseline), a persistent IFN-α and IFN-γ response, and an activated dendritic cell signature/M1 macrophage signature upon Dectin-1 stimulation. Dectin-1 stimulation induced a strong upregulation of MTORC1 signaling in all cohorts, although increased in the HIV-Older cohort (stimulation and baseline). In sum, this study demonstrates that the HIV Aging population has a distinct immune signature in response to Dectin-1 stimulation. This signature may contribute to the pro-inflammatory environment that is associated with HIV and aging.“Overall, this study demonstrates that age, HIV-infection and co-morbidities can alter the individual immune response. In particular our study showed a unique immune signature in the setting of both HIV and aging in response to Dectin-1 stimulation.”DOI - https://doi.org/10.18632/aging.204927Corresponding author - Heidi J. Zapata - heidi.zapata@yale.eduVideo short - https://www.youtube.com/watch?v=MpMBDvv0dDISign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204927Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, immune response, innate immune cells, HIV-infection, dectin-1About Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
A new editorial paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 15, entitled, “Epigenetic aging in oocytes.”
Aging-related phenotypes span many different tissues and cell types, and start to occur at different ages - a different typical age for every cell type. In their new editorial, researchers Peera Wasserzug-Pash and Michael Klutstein from The Hebrew University of Jerusalem discuss one of the earliest occurring aging events in the human body, which is the beginning of female reproductive aging and deterioration. The clinical cut-off for advanced maternal age (AMA), a condition associated with poor reproductive outcomes, is 35 years old.
“The early onset of reproductive aging poses a significant challenge to clinicians since a global consistent increase in maternal age at first birth has occurred in recent decades, effectively shortening the available time window for reproduction [1].”
As the rate of patients with advanced maternal age rises, and with it, the number of patients in fertility clinics, so does the necessity for a fundamental understanding of the reproductive aging process. In recent years, it has been established that there is a substantial dominating influence of oocyte quality loss on age-related fertility decline. This is best demonstrated by the rise in IVF success rates in reproductively aged women when they receive an egg donation from a younger woman. Oocyte quality loss is characterized by diminished cellular function and an increased occurrence of chromosomal nondisjunctions.
“Our recent publication [4] addresses the question of additional, epigenetic mechanisms that lead to the occurrence of age-related oocyte quality loss.”
DOI - https://doi.org/10.18632/aging.204976
Corresponding author - Michael Klutstein - michaelk@ekmd.huji.ac.il
Video short - https://www.youtube.com/watch?v=KHOVKKaJykY&t=45s
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Keywords - aging, oocytes, heterochromatin, epigenetics, maturation
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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The lacrimal gland, found in the upper outer part of the eye’s hollow area, is an important gland that makes tears to protect the eye from infections. It’s split into two parts: one near the inside of the eyelid that can be seen when the eyelid is flipped, and another part with ducts lower in the eye that connects to its counterpart. In their fully functioning status, these ducts release fluid onto the surface of the eye. As humans age (especially women), the lacrimal gland gradually becomes infiltrated by aberrant immune cells and can ultimately lead to an uncomfortable condition known as dry eye disease.
“Burning and redness in the eyes, grittiness and blurry vision make life miserable and currently, eye drops with a variety of lubricant components and in the most severe cases, immunosuppressors, are the only therapies approved for this disease.”
In a well-written new editorial paper, researchers Claudia M. Trujillo-Vargas and Cintia S. de Paiva from the Department of Ophthalmology at Baylor College of Medicine artfully discuss their recent studies which shed light on the immune system’s role in dry eye disease. On August 11, 2023, their editorial was published in Aging’s Volume 15, Issue 15, entitled, “Our search of immune invaders in the aged lacrimal gland.”
Full blog - https://aging-us.org/2023/08/dry-eyes-it-may-be-immune-infiltration-in-aging-lacrimal-glands/
Paper DOI - https://doi.org/10.18632/aging.204651
Corresponding author - Cintia S. de Paiva - cintiadp@bcm.edu
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Keywords - aging, lacrimal gland, ectopic lymphoid structures, immune invasion
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Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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A new research paper was published in Aging (Aging-US) Volume 15, Issue 15, entitled, “Cardiovascular events and death after catheter ablation in very old patients with nonvalvular atrial fibrillation.”
Catheter ablation of atrial fibrillation (AF) is recommended for selected older patients. However, the preventive effects of AF ablation on cardiovascular events and death remain unclear, especially in older patients. In this new study, researchers Keisuke Okawa, Satoshi Taya, Takeshi Morimoto, Ryu Tsushima, Yuya Sudo, Ai Sakamoto, Eisuke Saito, Masahiro Sogo, Masatomo Ozaki, and Masahiko Takahashi from Kagawa Prefectural Central Hospital and Hyogo Medical University aimed to investigate the impact of AF ablation on the incidence of cardiovascular events and death in very old nonvalvular AF (NVAF) patients.
“We conducted a prospective cohort study of consecutive patients with NVAF aged ≥80 years and using direct oral anticoagulants (DOACs).”
The researchers defined cardiovascular events as acute heart failure (AHF), strokes and systemic embolisms (SSEs), acute coronary syndrome (ACS), and sudden cardiac death (SCD) and cardiovascular death as AHF/SSE/ACS-related death and SCD. They compared the 3-year incidence of cardiovascular events and death between the patients who underwent AF ablation (Ablation group) and those who received medical therapy only (Medication group).
Among the 782 NVAF patients using DOACs, propensity score matching provided 208 patients in each group. The Ablation group had a significantly lower 3-year incidence of cardiovascular events and death than the Medication group: cardiovascular events, 24 (13.2%) vs. 43 (23.3%), log-rank P = 0.009 and hazard ratio (HR) 0.52 (95% confidence interval (CI) 0.32–0.86) and cardiovascular deaths, 5 (3.0%) vs. 15 (7.8%), log-rank P = 0.019 and HR 0.32 (95% CI 0.16–0.88).
“In very old NVAF patients using DOACs, those who underwent AF ablation had a lower incidence of both cardiovascular events and death than those who received medical therapy only.”
DOI - https://doi.org/10.18632/aging.204952
Corresponding author - Keisuke Okawa - k-ookawa@chp-kagawa.jp
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Keywords - aging, atrial fibrillation, catheter ablation, cardiovascular event, cardiovascular death, very old patient
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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A new research paper was published by Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) in Volume 15, Issue 15, entitled, “Associations between klotho and telomere biology in high stress caregivers.”
Aging biomarkers may be related to each other through direct co-regulation and/or through being regulated by common processes associated with chronological aging or stress. Klotho is an aging regulator that acts as a circulating hormone with critical involvement in regulating insulin signaling, phosphate homeostasis, oxidative stress, and age-related inflammatory functioning.
In this new study, researchers Ryan L. Brown, Elissa E. Epel, Jue Lin, Dena B. Dubal, and Aric A. Prather from the Department of Psychiatry and Behavioral Sciences, University of California, San Francisco, Department of Biochemistry and Biophysics, University of California, San Francisco, and the Department of Neurology and Weill Institute of Neurosciences, University of California, San Francisco discuss the association between klotho levels and telomere length of specific sorted immune cells among a healthy sample of mothers caregiving for a child with autism spectrum disorder (ASD) or a child without ASD - covarying age and body mass index - in order to understand if high stress associated with caregiving for a child with an ASD may be involved in any association between these aging biomarkers.
“Here we examine the relationship between two important biomarkers of aging, klotho and telomere length, in a healthy sample stratified into groups based on a combination of (a) stressor exposure and (b) level of perceived stress (i.e., high-stress mothers of children with ASD compared to low-stress mothers of neurotypical children).”
In 178 caregiving women, the researchers found that klotho levels were positively associated with telomere length in PBMCs (an effect driven by CD4+ and CD8+CD28− T cells) among high-stress mothers of children with an ASD, but not among low-stress mothers of neurotypical children. There were no significant associations between klotho and telomerase activity in either group, across cell types assessed here.
“Our results suggest that klotho levels and telomere length may be associated through a coordinated downregulation of longevity factors occurring under higher stress caregiving conditions.”
DOI - https://doi.org/10.18632/aging.204961
Corresponding author - Ryan L. Brown - ryan.brown@ucsf.edu
Video short - https://www.youtube.com/watch?v=y0P4vsf1IIk
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Keywords - aging, aging biology, stress, klotho, telomeres, telomerase
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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A new research paper was published on the cover of Aging (Aging-US) Volume 15, Issue 15, entitled, “Natural aging and ovariectomy induces parallel phosphoproteomic alterations in skeletal muscle of female mice.”
The loss of skeletal muscle strength mid-life in females is associated with the decline of estrogen. In this new study, researchers Mina P. Peyton, Tzu-Yi Yang, LeeAnn Higgins, Todd W. Markowski, Kevin Murray, Cha Vue, Laurie L. Parker, and Dawn A. Lowe from the University of Minnesota questioned how estrogen deficiency might impact the overall skeletal muscle phosphoproteome after contraction, as force production induces phosphorylation of several muscle proteins.
“Importantly, identification of these altered phosphosites and candidate kinases and phosphatases sensitive to the presence of estrogen will help advance our understanding of the contributions of estrogen deficiency to muscle strength loss in aging females.”
Phosphoproteomic analyses of the tibialis anterior muscle after contraction in two mouse models of estrogen deficiency, ovariectomy (Ovariectomized (Ovx) vs. Sham) and natural aging-induced ovarian senescence (Older Adult (OA) vs. Young Adult (YA)), identified a total of 2,593 and 3,507 phosphopeptides in Ovx/Sham and OA/YA datasets, respectively. Further analysis of estrogen deficiency-associated proteins and phosphosites identified 66 proteins and 21 phosphosites from both datasets. Of these, 4 estrogen deficiency-associated proteins and 4 estrogen deficiency-associated phosphosites were significant and differentially phosphorylated or regulated, respectively.
Comparative analyses between Ovx/Sham and OA/YA using Ingenuity Pathway Analysis (IPA) found parallel patterns of inhibition and activation across IPA-defined canonical signaling pathways and physiological functional analysis, which were similarly observed in downstream GO, KEGG, and Reactome pathway overrepresentation analysis pertaining to muscle structural integrity and contraction, including AMPK and calcium signaling. IPA Upstream regulator analysis identified MAPK1 and PRKACA as candidate kinases and calcineurin as a candidate phosphatase sensitive to estrogen.
“In summary, our results from contracted skeletal muscle highlight CAST Ser-82 as a candidate phosphosite, and MAPK1/ERK2, PRKACA, and calcineurin as candidate upstream regulators sensitive to estrogen deficiency that may contribute to changes in the force-generating capacity of skeletal muscle.”
DOI - https://doi.org/10.18632/aging.204959
Corresponding author - Dawn A. Lowe - lowex017@umn.edu
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Keywords - aging, estrogen deficiency, CAST, MAPK, PKA, calcineurin
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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A new editorial paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 14, entitled, “A novel theory of ageing independent of damage accumulation.”
The underlying cause or causes of aging are an enduring mystery, but in 1977 Kirkwood postulated that organisms might gain a fitness advantage by reducing investment in somatic maintenance if this allowed them to invest more resources in more crucial processes such as reproduction. The accumulation of somatic damage was therefore inevitable, and his disposable soma theory has dominated gerontology ever since.
However, as our understanding of aging increases, it is becoming increasingly difficult to align all the aspects of aging with accumulating damage. For example, mutations that increase damage accumulation can also increase longevity, while rejuvenation revelations such as parabiosis and Yamanaka factors indicate that youthfulness can be regained without high energetic cost and despite high levels of damage.
In their new editorial, researchers James Wordsworth and Daryl Shanley from Newcastle University discuss their recently published paper on selective destruction theory (SDT). SDT suggests a mechanism of aging which is both independent of accumulating damage and consistent with epigenetic rejuvenation. The authors used agent-based modeling to describe how aging could undergo positive selection independent of energetic costs.
“The mechanism of selective destruction is currently theoretical. In our most developed model, we demonstrated that if slow cells induced epigenetic changes in faster cells causing their metabolism to slow (rather than killing them) it not only reduced unnecessary cell death, but also further reduced the likelihood of overactivity disorders by preventing the spread of fast cells.”
DOI - https://doi.org/10.18632/aging.204956
Corresponding author - James Wordsworth - James.Wordsworth2@newcastle.ac.uk
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Keywords - aging, ageing, evolution, damage, cell competition, metabolic slowdown
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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A new research paper was published in Aging (Aging-US) Volume 15, Issue 14, entitled, “Inhibiting NLRP3 signaling in aging podocytes improves their life- and health-span.”
The decrease in the podocyte’s lifespan and health-span that typify healthy kidney aging cause a decrease in their normal structure, physiology and function. The ability to halt and even reverse these changes becomes clinically relevant when disease is superimposed on an aged kidney. NLRP3 [nod-like receptor protein 3] expression is increased in podocytes of mice with advanced age and contributes to their damage.
“However, the functional consequence of increased levels of NLRP3 in aged podocytes is unknown.”
In this new study, researchers Natalya Kaverina, R. Allen Schweickart, Gek Cher Chan, Joseph C. Maggiore, Diana G. Eng, Yuting Zeng, Sierra R. McKinzie, Hannah S. Perry, Adilijiang Ali, Christopher O’Connor, Beatriz Maria Veloso Pereira, Ashleigh B. Theberge, Joshua C. Vaughan, Carol J. Loretz, Anthony Chang, Neil A. Hukriede, Markus Bitzer, Jeffrey W. Pippin, Oliver Wessely, and Stuart J. Shankland from the University of Washington, Cleveland Clinic Foundation, National University Hospital Singapore, University of Pittsburgh, University of Michigan, and the University of Chicago hypothesized that reducing NLRP3 signaling earlier at middle-age improves overall podocyte health and slows down healthy podocyte aging in mice.
“To this end, we performed a comprehensive analysis of inflammasome signaling including pharmacological and genetic NLRP3 loss-of-function approaches.”
RNA-sequencing of podocytes from middle-aged mice showed an inflammatory phenotype with increases in the NLRP3 inflammasome, signaling for IL2/Stat5, IL6 and TNF, interferon gamma response, allograft rejection and complement, consistent with inflammaging. Furthermore, injury-induced NLRP3 signaling in podocytes was further augmented in aged mice compared to young ones. The NLRP3 inflammasome (NLRP3, Caspase-1, IL1β IL-18) was also increased in podocytes of middle-aged humans.
Higher transcript expression for NLRP3 in human glomeruli was accompanied by reduced podocyte density and increased global glomerulosclerosis and glomerular volume. Pharmacological inhibition of NLRP3 with MCC950, or gene deletion, reduced podocyte senescence and the genes typifying aging in middle-aged mice, which was accompanied by an improved podocyte lifespan and health-span. Moreover, modeling the injury-dependent increase in NLRP3 signaling in human kidney organoids confirmed the anti-senescence effect of MC9950. Finally, NLRP3 also impacted liver aging.
“In summary, our results demonstrate for the first time that aging podocytes acquire an inflammatory phenotype, which include the NLRP3 inflammasome and which is consistent with inflammaging.”
DOI - https://doi.org/10.18632/aging.204897
Corresponding authors - Oliver Wessely - wesselo@ccf.org, and Stuart J. Shankland - stuartjs@uw.edu
Keywords - aging, kidney, podocyte, NLRP3 inflammasome, reporter
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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A new research perspective was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 14, entitled, “Towards disease-oriented dosing of rapamycin for longevity: does aging exist or only age-related diseases?”
In his new research perspective, Dr. Mikhail V. Blagosklonny from Roswell Park Comprehensive Cancer Center discusses aging and rapamycin (Sirolimus) — the only drug that consistently extends life span in countless animal studies in all species tested. He writes that individuals taking rapamycin and those not taking it will ultimately succumb to age-related diseases. However, if administered in disease-oriented dosages for an extended period of time, individuals taking rapamycin may experience a delayed onset of such diseases, and live longer.
“The goal is to delay a particular disease that is expected to be life-limiting in a particular person.”
Age-related diseases, quasi-programmed during development, progress at varying rates in different individuals. Rapamycin is a prophylactic anti-aging drug that decelerates early development of age-related diseases. Dr. Blagosklonny further discusses the hyperfunction theory of quasi-programmed diseases, which challenges the need for the traditional concept of aging itself.
“I emphasize that aging is not programmed but, in contrast, quasi-programmed. Quasi means pseudo; seemingly; apparently but not really. Some scientists deliberately represent hyperfunction theory as theory of programmed aging. It’s the opposite. Quasi-program is a continuation of a real program. Quasi-program has no intent, no purpose and it is always harmful.”
DOI - https://doi.org/10.18632/aging.204920
Corresponding author - Mikhail V. Blagosklonny - Blagosklonny@oncotarget.com
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Keywords - aging, mTOR, hyperfunction, lifespan, health span, cancer, Alzheimer’s disease
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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A new research paper was published on the cover of Aging (Aging-US) Volume 15, Issue 14, entitled, “Human senescent fibroblasts trigger progressive lung fibrosis in mice.”
Cell senescence has recently emerged as a potentially relevant pathogenic mechanism in fibrosing interstitial lung diseases (f-ILDs), particularly in idiopathic pulmonary fibrosis. In a new study, researchers Fernanda Hernandez-Gonzalez, Neus Prats, Valentina Ramponi, José Alberto López-Domínguez, Kathleen Meyer, Mònica Aguilera, María Isabel Muñoz Martín, Daniel Martínez, Alvar Agusti, Rosa Faner, Jacobo Sellarés, Federico Pietrocola, and Manuel Serrano from Hospital Clinic Barcelona, The Barcelona Institute of Science and Technology (BIST), Instituto de Investigaciones Biomédicas August Pi i Sunyer (IDIBAPS), Centro de Investigación Biomédica en Red Enfermedades Respiratorias (CIBERES), University of Barcelona, Karolinska Institute, Catalan Institution for Research and Advanced Studies (ICREA), and Altos Labs hypothesized that senescent human fibroblasts may suffice to trigger a progressive fibrogenic reaction in the lung.
“Here we: (1) explored this hypothesis in vivo; (2) investigated the potential underlying biological mechanisms in vitro; and (3) studied the effects of one experimental senolytic compound (navitoclax) and two anti-fibrotic drugs currently used in the treatment of IPF in humans (nintedanib and pirfenidone), both in vivo and in vitro.”
To address this, senescent human lung fibroblasts, or their secretome (SASP), were instilled into the lungs of immunodeficient mice. The researchers found that human senescent fibroblasts engraft in the lungs of immunodeficient mice and trigger progressive lung fibrosis associated to increasing levels of mouse senescent cells, whereas non-senescent fibroblasts do not trigger fibrosis. They also found that the SASP of human senescent fibroblasts is pro-senescence and pro-fibrotic both in vitro when added to mouse recipient cells and in vivo when delivered into the lungs of mice, whereas the conditioned medium (CM) from non-senescent fibroblasts lacks these activities. Finally, navitoclax, nintedanib and pirfenidone were found to ameliorate lung fibrosis induced by senescent human fibroblasts in mice, while only navitoclax displayed senolytic activity.
“We conclude that human senescent fibroblasts, through their bioactive secretome, trigger a progressive fibrogenic reaction in the lungs of immunodeficient mice that includes the induction of paracrine senescence in the cells of the host, supporting the concept that senescent cells actively contribute to disease progression in patients with f-ILDs.”
DOI - https://doi.org/10.18632/aging.204825
Corresponding authors - Manuel Serrano - mserrano@altoslabs.com, and Federico Pietrocola - federico.pietrocola@ki.se
Keywords - aging, mouse model, cellular senescence, pulmonary fibrosis, antifibrotics, senolytic
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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“We created datasets for predicting whether or not a compound extends the lifespan of C. elegans [...]”
Predicting Lifespan-Extending Chemical Compounds for C. elegans With Machine Learning
BUFFALO, NY- July 26, 2023 – A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 13, entitled, “Predicting lifespan-extending chemical compounds for C. elegans with machine learning and biologically interpretable features.”
Recently, there has been a growing interest in the development of pharmacological interventions targeting aging, as well as in the use of machine learning for analyzing aging-related data. In this new study, researchers Caio Ribeiro, Christopher K. Farmer, João Pedro de Magalhães, and Alex A. Freitas from the University of Kent and University of Birmingham use machine learning methods to analyze data from DrugAge, a database of chemical compounds (including drugs) modulating lifespan in model organisms.
“To this end, we created four types of datasets for predicting whether or not a compound extends the lifespan of C. elegans (the most frequent model organism in DrugAge), using four different types of predictive biological features, based on: compound-protein interactions, interactions between compounds and proteins encoded by aging-related genes, and two types of terms annotated for proteins targeted by the compounds, namely Gene Ontology (GO) terms and physiology terms from the WormBase’s Phenotype Ontology.”
To analyze these datasets, the researchers used a combination of feature selection methods in a data pre-processing phase and the well-established random forest algorithm for learning predictive models from the selected features. In addition, they interpreted the most important features in the two best models in light of the biology of aging. One noteworthy feature was the GO term “Glutathione metabolic process”, which plays an important role in cellular redox homeostasis and detoxification. The team also predicted the most promising novel compounds for extending lifespan from a list of previously unlabelled compounds. These include nitroprusside, which is used as an antihypertensive medication.
“Overall, our work opens avenues for future work in employing machine learning to predict novel life-extending compounds.”
Read the full paper: DOI: https://doi.org/10.18632/aging.204866
Corresponding Authors: Caio Ribeiro, Alex A. Freitas
Corresponding Emails: C.E.Ribeiro@kent.ac.uk, A.A.Freitas@kent.ac.uk
Keywords: lifespan-extension compounds, longevity drugs, machine learning, feature selection
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BUFFALO, NY- July 25, 2023 – A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 13, entitled, “MSK1 is required for the beneficial synaptic and cognitive effects of enriched experience across the lifespan.”
Positive experiences, such as social interaction, cognitive training and physical exercise, have been shown to ameliorate some of the harms to cognition associated with aging. Animal models of positive interventions, commonly known as environmental enrichment, strongly influence neuronal morphology and synaptic function and enhance cognitive performance. While the profound structural and functional benefits of enrichment have been appreciated for decades, little is known as to how the environment influences neurons to respond and adapt to these positive sensory experiences.
In this new study, researchers Lorenzo Morè, Lucia Privitera, Daniel D. Cooper, Marianthi Tsogka, J. Simon C. Arthur, and Bruno G. Frenguelli from the University of Warwick, University of Central Lancashire and University of Dundee show that adult and aged male wild-type mice that underwent a 10-week environmental enrichment protocol demonstrated improved performance in a variety of behavioral tasks, including those testing spatial working and spatial reference memory, and an enhancement in hippocampal long-term potentiation.
“Recently, a neuronal protein kinase, mitogen- and stress-activated protein kinase 1 (MSK1) has been identified as being a prime effector within the mammalian brain of the beneficial effects of enrichment in the early phase of the lifespan (birth to 4 months) [34–38].”
Aged animals in particular benefitted from enrichment, performing spatial memory tasks at levels similar to healthy adult mice. Many of these benefits, including in gene expression, were absent in mice with a mutation in an enzyme, MSK1, which is activated by BDNF, a growth factor implicated in rodent and human cognition. The researchers conclude that enrichment is beneficial across the lifespan and that MSK1 is required for the full extent of these experience-induced improvements of cognitive abilities, synaptic plasticity and gene expression.
“We show that MSK1 retains its importance in converting positive experience into tangible synaptic and cognitive benefits well into old age, reinforcing the aged brain’s capacity to benefit from positive experience, MSK1’s prominence as a key player in the response to enrichment, and its potential as a target for enviromimetics.”
Read the full paper: DOI: https://doi.org/10.18632/aging.204833
Corresponding Author: Bruno G. Frenguelli
Corresponding Email: b.g.frenguelli@warwick.ac.uk
Keywords: cognitive reserve, synaptic plasticity, anxiety, spatial memory, LTP
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About Aging-US: Launched in 2009, Aging publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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Why do some individuals maintain cognitive abilities throughout their lifespan and others do not? The better question may be: How can certain individuals preserve their cognitive abilities and delay the onset of dementia despite the presence of significant neuropathologies that would otherwise suggest cognitive decline? This question remains unanswered.
“What contributes to this ‘resilience’ [3], that is why some successfully cope with progressive neuropathology while others cannot tolerate the same level of neurodegeneration, is not fully understood.”
This unanswered question has driven researchers to consider the idea of “cognitive reserve.” The rather new concept of cognitive reserve suggests that certain factors, such as engaging in education, mental stimulation and challenging activities, can create a buffer against cognitive decline and delay the onset of cognitive impairment or dementia. Researchers continue to study cognitive reserve to better understand its mechanisms and potential implications for maintaining brain health and designing effective interventions.
In a new editorial paper, researchers Monica E. Nelson, Ross Andel and Jakub Hort from the University of South Florida’s School of Aging Studies discussed the outcomes, lessons and future implications of their previous 2022 study. The team examined the influence of cognitive reserve proxies on the relationship between brain integrity and cognition. On July 14, 2023, their editorial was published in Aging’s Volume 15, Issue 13, entitled, “Cognitive reserve, neuropathology, and progression towards Alzheimer’s disease.”
Full blog - https://aging-us.org/2023/07/exploring-the-impact-of-cognitive-reserve-on-cognitive-resilience/
Paper DOI - https://doi.org/10.18632/aging.204909
Corresponding author - Monica E. Nelson - mnelson10@usf.edu
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Keywords - aging, dementia, neuropathology, Alzheimer’s disease, MRI, volumetry
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 13, entitled, “Cognitive rescue in aging through prior training in rats.”
Cognitive decline in spatial memory is seen in aging. Understanding affected processes in aging is vital for developing methods to improve wellbeing. Daily memory persistence can be influenced by events around the time of learning or by prior experiences in early life.
Fading memories in young can last longer if a novel event is introduced around encoding, a process called behavioral tagging. In this new study based on this principle, researchers Alexandra Gros and Szu-Han Wang from The University of Edinburgh asked what processes are affected in aging and if prior training can rescue them.
“Here we asked if cognitive training in young and mid-life would improve cognitive aging and which elements of the cognitive processes at old age are preferentially protected through such training.”
Two groups of aged rats received training in an appetitive delayed matching-to-place task. One of the groups additionally received prior training of the same task in young and in mid-life, constituting a longitudinal study. The results showed long-term memory decline in late aging without prior training. This would reflect affected encoding and consolidation.
On the other hand, short-term memory was preserved and novelty at memory reactivation and reconsolidation enabled memory maintenance in aging. Prior training improved cognition by facilitating task performance, strengthening short-term and intermediate memory, and enabling encoding-boosted long-term memory. Learning ability, short-term memories, motor and motivation functions remained intact in older age, suggesting a phase when memory-associated processes are compromised before apparent navigation or learning deficits in advanced aging. Overall, the study's findings suggest a selective impairment in encoding for long-term memory formation in early aging and an additional impairment in consolidation in later aging.
“Prior training shows profound benefits in cognitive aging and it can provide a translatable model to simulate human cognition which is built upon lifelong experiences.”
DOI - https://doi.org/10.18632/aging.204808
Corresponding author - Szu-Han Wang - s.wang@ed.ac.uk Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204808
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Keywords - aging, memory consolidation, reconsolidation, memory modulation, lifelong training, cognitive stimulation
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 13, entitled, “Budding uninhibited by benzimidazoles-1 (BUB1) regulates EGFR signaling by reducing EGFR internalization.”
EGFR signaling initiates upon ligand binding which leads to activation and internalization of the receptor-ligand complex. In this new study, researchers Shyam Nyati, Grant Young, Corey Speers, Mukesh K. Nyati, and Alnawaz Rehemtulla from the University of Michigan, Henry Ford Health System and Case Western Reserve University evaluated if BUB1 impacted EGFR signaling by regulating EGFR receptor internalization and activation.
“We postulate that BUB1 helps in the formation and stabilization of EGFR dimers at the membrane and may regulate endocytosis of activated EGFR into either clathrin dependent (EEA1 coated) or independent (caveolin coated) vesicles thus impacting receptor recycling or degradation and subsequently signaling amplitude and duration [38, 39].”
BUB1 was ablated genomically (siRNA) or biochemically (2OH-BNPP1) in cells. EGF ligand was used to initiate EGFR signaling while disuccinimidyl suberate (DSS) was used for cross linking cellular proteins. EGFR signaling was measured by western immunoblotting and receptor internalization was evaluated by fluorescent microscopy (pEGFR (pY1068) colocalization with early endosome marker EEA1).
siRNA mediated BUB1 depletion led to an overall increase in total EGFR levels and more phospho-EGFR (Y845, Y1092, and Y1173) dimers while the amount of total EGFR (non-phospho) dimers remained unchanged. BUB1 inhibitor (BUB1i) decreased EGF mediated EGFR signaling including pEGFR Y845, pAKT S473 and pERK1/2 in a time dependent manner. Additionally, BUB1i also reduced EGF mediated pEGFR (Y845) dimers (asymmetric dimers) without affecting total EGFR dimers (symmetric dimers) indicating that dimerization of inactive EGFR is not affected by BUB1. Furthermore, BUB1i blocked EGF mediated EGFR degradation (increase in EGFR half-life) without impacting half-lives of HER2 or c-MET. BUB1i also reduced co-localization of pEGFR with EEA1 positive endosomes suggesting that BUB1 might modulate EGFR endocytosis.
“Our data provide evidence that BUB1 protein and its kinase activity may regulate EGFR activation, endocytosis, degradation, and downstream signaling without affecting other members of the receptor tyrosine kinase family.”
DOI - https://doi.org/10.18632/aging.204820
Corresponding authors - Shyam Nyati - snyati1@hfhs.org, and Alnawaz Rehemtulla - alnawaz@umich.edu
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Keywords - aging, BUB1, EGFR, cancer, signaling, endocytosis
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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A new editorial paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 12, entitled, “Advancing screening for cognitive impairment: the memtrax continuous recognition test.”
Extensive efforts to find a treatment for Alzheimer’s disease (AD) span over 40 years, with the often-repeated request for better means to assess the principal dysfunction of this disease, memory impairment. Tremendous costs and resources have already been consumed in the development of treatments for this prevalent and well recognized condition, e.g., over $40 billion. These pervasive failures support the urgent need for instruments far superior to those used even in recent studies.
The critical impairment in AD is a disorder of neuroplasticity. Thus, cognitive tests which can rapidly, sensitively, frequently, inexpensively, and precisely measure the aspects of memory specifically attacked by AD are principally needed. In this new editorial, researchers J. Wesson Ashford, James O. Clifford and Michael F. Bergeron from Stanford University discuss a continuous recognition test of memory called MemTrax that has been developed to quickly and accurately quantify memory processing, storage and rate of retrieval.
“The precision of MemTrax would best improve the specification of the severity of cognitive impairment in early phases of Alzheimer’s disease, a period of this disease when paper and pencil and historical recollection only provide poor estimates of function [4].”
Further, MemTrax can precisely assess the rate of change over time with repeat testing. By assessing performance metrics and rate of recognition response, MemTrax can screen for many varieties of cognitive impairment and thus would be an ideal tool for use in the elderly U.S. population for the Medicare Annual Wellness Visit. With a test such as MemTrax or other effective online testing, populations can be broadly and inexpensively assessed for AD-related cognitive impairment and then brought into clinical studies to determine what environmental, genetic, or interventional remedies can prevent further development of AD and the pace and/or extent of cognitive decline.
“MemTrax is especially well suited for assessment of very early AD, including early mild cognitive impairment, a time when the focus should be on prevention of AD pathology, not removal of AD pathology.”
DOI - https://doi.org/10.18632/aging.204828
Corresponding author - J. Wesson Ashford - ashford@stanford.edu
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Keywords - aging, Alzheimer’s disease, memory, online testing, response time, continuous recognition test
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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In a groundbreaking study, researchers have unlocked a new frontier in the fight against aging and age-related diseases. The study, conducted by a team of scientists at Harvard Medical School, has published the first chemical approach to reprogram cells to a younger state. Previously, this was only achievable using a powerful gene therapy.
On July 12, 2023, researchers Jae-Hyun Yang, Christopher A. Petty, Thomas Dixon-McDougall, Maria Vina Lopez, Alexander Tyshkovskiy, Sun Maybury-Lewis, Xiao Tian, Nabilah Ibrahim, Zhili Chen, Patrick T. Griffin, Matthew Arnold, Jien Li, Oswaldo A. Martinez, Alexander Behn, Ryan Rogers-Hammond, Suzanne Angeli, Vadim N. Gladyshev, and David A. Sinclair from Harvard Medical School, University of Maine and Massachusetts Institute of Technology (MIT) published a new research paper in Aging, titled, “Chemically induced reprogramming to reverse cellular aging.”
The team's findings build upon the discovery that the expression of specific genes, called Yamanaka factors, could convert adult cells into induced pluripotent stem cells (iPSCs). This Nobel Prize-winning discovery raised the question of whether it might be possible to reverse cellular aging without causing cells to become too young and turn cancerous.
In this new study, the researchers screened for molecules that could, in combination, reverse cellular aging and rejuvenate human cells. They developed high-throughput cell-based assays to distinguish young cells from old and senescent cells, including transcription-based aging clocks and a real-time nucleocytoplasmic protein compartmentalization (NCC) assay. In an exciting discovery, the team has identified six chemical cocktails that restore NCC and genome-wide transcript profiles to youthful states and reverse transcriptomic age in less than a week.
The Harvard researchers previously demonstrated that it is indeed possible to reverse cellular aging without uncontrolled cell growth by virally-introducing specific Yamanaka genes into cells. Studies on the optic nerve, brain tissue, kidney, and muscle have shown promising results, with improved vision and extended lifespan observed in mice and, recently, a report of improved vision in monkeys.
The implications of this new discovery are far-reaching, opening avenues for regenerative medicine and, potentially, whole-body rejuvenation. By developing a chemical alternative to age reversal via gene therapy, this research could revolutionize the treatment of aging, injuries and age-related diseases and offers the potential for lower costs and shorter timelines in development. On the heels of positive results in reversing blindness in monkeys in April 2023, preparations for human clinical trials of the lab’s age reversal gene therapy are in progress.
“Until recently, the best we could do was slow aging. New discoveries suggest we can now reverse it,” said David A. Sinclair, A.O., Ph.D., Professor in the Department of Genetics and co-Director of the Paul F. Glenn Center for Biology of Aging Research at Harvard Medical School and lead scientist on the project. “This process has previously required gene therapy, limiting its widespread use.”
The team at Harvard envisions a future where age-related diseases can be effectively treated, injuries can be repaired more efficiently, and the dream of whole-body rejuvenation becomes a reality. “This new discovery offers the potential to reverse aging with a single pill, with applications ranging from improving eyesight to effectively treating numerous age-related diseases,” Sinclair said.
Press Release: https://www.aging-us.com/news_room/NEW-STUDY-Discovery-of-Chemical-Means-to-Reverse-Aging-and-Restore-Cellular-Function
DOI: https://doi.org/10.18632/aging.204896
Corresponding Author: David A. Sinclair - david_sinclair@hms.harvard.edu
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New research continues to illuminate the far-reaching implications of the gut microbiome and its crucial role in our overall health. The term “gut dysbiosis” refers to an imbalance of healthy and unhealthy microbes in the gastrointestinal tract. Repercussions of gut dysbiosis are not only limited to innocuous discomfort—it can lead to immune dysregulation and trigger a cascade of various disease states.
In a new editorial paper, researchers Chun-Che Hung, Kristi M. Crowe-White and Ian M. McDonough from Chang Gung University and The University of Alabama discuss the relationship between gut dysbiosis and neurocognitive disorders such as Alzheimer’s disease (AD). Their editorial was published in Aging’s Volume 15, Issue 12, on June 19, 2023, entitled, “A seed and soil model of gut dysbiosis in Alzheimer’s disease.”
“[…] recent research has demonstrated a crucial role of gut microbiota in the etiopathogenesis of AD [Alzheimer’s disease] that offers a new window into possible origins and consequences of AD through interactions between gut microbiota and the central nervous system, known as the ‘microbiota-gutbrain axis’ [1].”
Full blog - https://aging-us.org/2023/07/can-a-leaky-gut-lead-to-alzheimers-disease/
Paper DOI - https://doi.org/10.18632/aging.204840
Corresponding author - Ian M. McDonough - immcdonough@ua.edu
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Keywords - aging, Alzheimer’s disease, neurocognitive disorders, gut-brain axis, gut microbiota, dysbiosis
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 12, entitled, “Hepatic hydrogen sulfide levels are reduced in mouse model of Hutchinson-Gilford progeria syndrome.”
Hutchinson-Gilford progeria syndrome (HGPS) is a rare human disease characterized by accelerated biological aging. Current treatments are limited, and most patients die before 15 years of age. Hydrogen sulfide (H2S) is an important gaseous signaling molecule that is central to multiple cellular homeostasis mechanisms. Dysregulation of tissue H2S levels is thought to contribute to an aging phenotype in many tissues across animal models. Whether H2S is altered in HGPS is unknown.
In a new study, researchers Stephen E. Wilkie, Diana E. Marcu, Roderick N. Carter, Nicholas M. Morton, Susana Gonzalo, and Colin Selman from the University of Glasgow, University of Edinburgh, Saint Louis University, and Karolinska Institute investigated hepatic H2S production capacity and transcript, protein and enzymatic activity of proteins that regulate hepatic H2S production and disposal in a mouse model of HGPS (G609G mice, mutated Lmna gene equivalent to a causative mutation in HGPS patients).
“This study was designed and undertaken due to the lack of understanding in the mechanistic targets of known treatments against HGPS and considering the positive association between H2S and longevity in model organisms.”
Here, the researchers employed the HGPS mouse model G609G to test the hypothesis that, in contrast to anti-aging increases in H2S production, the accelerated aging typical of progeroid mice is associated with reduced hepatic H2S production. G609G mice were maintained on either regular chow (RC) or high fat diet (HFD). HFD has been previously shown to significantly extend lifespan of G609G mice, and compared to wild type (WT) mice maintained on RC.
RC-fed G609G mice had significantly reduced hepatic H2S production capacity relative to WT mice, with a compensatory elevation in mRNA transcripts associated with several H2S production enzymes, including cystathionine-γ-lyase (CSE). H2S levels and CSE protein were partially rescued in HFD fed G609G mice. The data acquired here confirmed some aspects of the relevance of H2S in HGPS but raises more questions about the specific mechanisms at play.
“Regardless, the work presented here addresses an area of research that remains critically understudied and provides new evidence that the accelerated ageing phenotype observed in HGPS may be partially explained by a reduction in hepatic H2S levels.”
DOI - https://doi.org/10.18632/aging.204835
Corresponding authors - Colin Selman - colin.selman@glasgow.ac.uk, and Stephen E. Wilkie - stephen.wilkie@ki.se
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Keywords - aging, progeria, hydrogen sulfide, high-fat diet, ageing, lamin A
About Aging-US:
Launched in 2009, Aging publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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A new research paper was published in Aging (Aging-US) Volume 15, Issue 12, entitled, “A novel peptide ‘T14’ reflects age and photo-aging in human skin.”
T14 is a 14mer peptide derived from the C-terminus of acetylcholinesterase (AChE). Once cleaved, it is independently bioactive of the parent molecule and enhances calcium influx in different cell types, in a range of scenarios: it binds to an allosteric site selectively on the alpha-7 receptor, where it modulates calcium influx and is thus a potential trophic agent, as already reported in a range of normal developmental scenarios. However, if inappropriately activated, this erstwhile beneficial effect converts to a toxic one, resulting in pathologies as disparate as Alzheimer’s and various metastatic cancers.
In this new study, given that epidermal keratinocyte cells have the same ectodermal origin as brain cells, as well as expressing AChE and the alpha-7 receptor, researchers Sheila Rocha, Sara Garcia Ratés, Tumisang Moswete, Kristopher Kalleberg, Anna Villa, Jason P. Harcup, and Susan A. Greenfield from Unilever Research and Development and Neuro-Bio explored whether T14 plays a comparable role.
“The first aim of this study was therefore to see if T14-ir could be detected in keratinocytes using an antibody that would not recognize the parent AChE itself, and thus be readily differentiated from it. [...] Hence the second aim of the study was to investigate the possibility that T14 was not only present in keratinocytes but could be regarded as an index reflecting not just age but also photo-induced aging.”
The team reports that the T14 immunoreactivity is detectable in human keratinocytes with levels inversely related to age: this decrease is even more apparent with chronic photo-exposure and thus accelerated skin aging. They concluded that T14, an agent promoting cell growth and renewal in other parts of the body, also operates in skin. Moreover, monitoring of keratinocyte T14 levels might offer further insights into the now well reported link between degenerative diseases and epidermal cell profile.
“Hence further exploration of the T14 system in the epidermis might prompt new insights into the treatment of hyperproliferative skin disorders, as well as into the mechanisms of normal skin age and ageing.”
DOI - https://doi.org/10.18632/aging.204844
Corresponding author - Sara Garcia Ratés - sara.garciarates@neuro-bio.com
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Keywords - aging, skin, photo-aging, acetylcholinesterase peptide, keratinocyte
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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A new research paper was published on the cover of Aging (Aging-US) Volume 15, Issue 12, entitled, “Age prediction from human blood plasma using proteomic and small RNA data: a comparative analysis.”
Aging clocks, built from comprehensive molecular data, have emerged as promising tools in medicine, forensics, and ecological research. However, few studies have compared the suitability of different molecular data types to predict age in the same cohort and whether combining them would improve predictions. In this new study, researchers Jérôme Salignon, Omid R. Faridani, Tasso Miliotis, Georges E. Janssens, Ping Chen, Bader Zarrouki, Rickard Sandberg, Pia Davidsson, and Christian G. Riedel from Karolinska Institutet, University of New South Wales, Garvan Institute of Medical Research, and AstraZeneca explored this at the level of proteins and small RNAs in 103 human blood plasma samples.
“Here we expand the limited portfolio of comparisons between aging clocks built from different types of molecular data from the same cohort.”
First, the researchers used a two-step mass spectrometry approach measuring 612 proteins to select and quantify 21 proteins that changed in abundance with age. Notably, proteins increasing with age were enriched for components of the complement system. Next, they used small RNA sequencing to select and quantify a set of 315 small RNAs that changed in abundance with age. Most of these were microRNAs (miRNAs), downregulated with age, and predicted to target genes related to growth, cancer, and senescence. Finally, the team used the collected data to build age-predictive models.
Among the different types of molecules, proteins yielded the most accurate model (R² = 0.59 ± 0.02), followed by miRNAs as the best-performing class of small RNAs (R² = 0.54 ± 0.02). Interestingly, the use of protein and miRNA data together improved predictions (R2 = 0.70 ± 0.01). Future work using larger sample sizes and a validation dataset will be necessary to confirm these results.
“Nevertheless, our study suggests that combining proteomic and miRNA data yields superior age predictions, possibly by capturing a broader range of age-related physiological changes. It will be interesting to determine if combining different molecular data types works as a general strategy to improve future aging clocks.”
DOI - https://doi.org/10.18632/aging.204787
Corresponding author - Christian G. Riedel - christian.riedel@ki.se
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Keywords - aging, human blood plasma, small RNAs, proteomics, age prediction
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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A new research paper was published in Aging (Aging-US) Volume 15, Issue 11, entitled, “Senescence and senotherapies in biliary atresia and biliary cirrhosis.”
Premature senescence occurs in adult hepatobiliary diseases and worsens the prognosis through deleterious liver remodeling and hepatic dysfunction. Senescence might also arise in biliary atresia (BA), the first cause of pediatric liver transplantation. Alternatives to transplantation are needed. In this new study, researchers Giulia Jannone, Eliano Bonaccorsi Riani, Catherine de Magnée, Roberto Tambucci, Jonathan Evraerts, Joachim Ravau, Pamela Baldin, Caroline Bouzin, Axelle Loriot, Laurent Gatto, Anabelle Decottignies, Mustapha Najimi, and Etienne Marc Sokal from the Université catholique de Louvain in Brussels, Belgium, aimed to investigate premature senescence in BA and to assess senotherapies in a preclinical model of biliary cirrhosis.
“As there is a need for new therapies to avoid or delay liver transplantation in pediatric biliary cirrhosis, the aim of our work was to investigate premature senescence in BA through a multi-technical approach and to assess senotherapies in a preclinical model of biliary cirrhosis.”
BA liver tissues were prospectively obtained at hepatoportoenterostomy (n=5) and liver transplantation (n=30) and compared to controls (n=10). Senescence was investigated through spatial whole transcriptome analysis, SA-β-gal activity, p16 and p21 expression, γ-H2AX and senescence-associated secretory phenotype (SASP). Human allogenic liver-derived progenitor cells (HALPC) or dasatinib and quercetin (D+Q) were administered to two-month-old Wistar rats after bile duct ligation (BDL).
Advanced premature senescence was evidenced in BA livers from early stage and continued to progress until liver transplantation. Senescence and SASP were predominant in cholangiocytes, but also present in surrounding hepatocytes. HALPC but not D+Q reduced the early marker of senescence p21 in BDL rats and improved biliary injury (serum γGT and Sox9 expression) and hepatocytes mass loss (Hnf4a).
“BA livers displayed advanced cellular senescence at diagnosis that continued to progress until liver transplantation. HALPC reduced early senescence and improved liver disease in a preclinical model of BA, providing encouraging preliminary results regarding the use of senotherapies in pediatric biliary cirrhosis.”
DOI - https://doi.org/10.18632/aging.204700
Corresponding author - Giulia Jannone - giulia.jannone@uclouvain.be
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Keywords - aging, senescence, senotherapy, liver, biliary cirrhosis, biliary atresia
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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A new research paper was published in Aging (Aging-US) Volume 15, Issue 11, entitled, “Old-age-induced obesity reversed by a methionine-deficient diet or oral administration of recombinant methioninase-producing Escherichia coli in C57BL/6 mice.”
Obesity increases with aging. Methionine restriction affects lipid metabolism and can prevent obesity in mice. In this new study, researchers Yutaro Kubota, Qinghong Han, Jose Reynoso, Yusuke Aoki, Noriyuki Masaki, Koya Obara, Kazuyuki Hamada, Michael Bouvet, Takuya Tsunoda, and Robert M. Hoffman from AntiCancer Inc., University of California San Diego and Showa University School of Medicine observed C57BL/6 mice double their body weight from 4 to 48 weeks of age and become obese. The team then evaluated the efficacy of oral administration of recombinant-methioninase (rMETase)-producing E. coli (E. coli JM109-rMETase) or a methionine-deficient diet to reverse old-age-induced obesity in C57BL/6 mice.
“In the present study we tested a low-methionine diet to reverse old-age-induced obesity. [...] E. coli JM109-rMETase was also tested in the present study to reverse old-age-induced obesity.”
Fifteen C57BL/6 male mice aged 12–18 months with old-age-induced obesity were divided into three groups. Group 1 was given a normal diet supplemented with non-recombinant E. coli JM109 cells orally by gavage twice daily; Group 2 was given a normal diet supplemented with recombinant E. coli JM109-rMETase cells by gavage twice daily; and Group 3 was given a methionine-deficient diet without treatment.
The administration of E. coli JM109-rMETase or a methionine-deficient diet reduced the blood methionine level and reversed old-age-induced obesity with significant weight loss by 14 days. There was a negative correlation between methionine levels and negative body weight change. Although the degree of efficacy was higher in the methionine-deficient diet group than in the E. coli JM109-rMETase group, the present findings suggested that oral administration of E. coli JM109-rMETase, as well as a methionine-deficient diet, are effective in reversing old-age-induced obesity.
“In conclusion, the present study provides evidence that restricting methionine by either a low-methionine diet or E. coli JM109-rMETase has clinical potential to treat old-age-induced obesity.”
DOI - https://doi.org/10.18632/aging.204783
Corresponding author - Robert M. Hoffman - all@anticancer.com
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Keywords - aging, obesity, methionine restriction, methionine-deficient diet, recombinant methioninase (rMETase), Escherichia coli, microbiome, weight-loss
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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Telomeres are the protective caps at the ends of chromosomes that prevent DNA damage and maintain genomic stability. However, telomeres shorten with each cell division and eventually reach a critical length that triggers cellular senescence or death. Telomere length (TL) and telomerase activity (TA), the enzyme that replenishes telomeric repeats, are influenced by genetic and environmental factors and vary among tissues and individuals.
“Telomere attrition has been identified as one of the molecular determinants of aging [7].”
Telomere dysfunction has been implicated in various age-related diseases, including infertility. Ovarian aging is the main cause of infertility in women, as it leads to a decline in both the quantity and quality of oocytes. Previous studies have shown that TL and TA are reduced in oocytes and granulosa cells of women with diminished ovarian reserve or poor response to ovarian stimulation. Moreover, TL and TA have been associated with ovarian reserve markers and pregnancy outcomes in assisted reproductive technologies.
To better understand the molecular mechanisms underlying ovarian aging and infertility, researchers Alba M. Polonio, Marta Medrano, Lucía Chico-Sordo, Isabel Córdova-Oriz, Mauro Cozzolino, José Montans, Sonia Herraiz, Emre Seli, Antonio Pellicer, Juan A. García-Velasco, and Elisa Varela from The Health Research Institute La Fe (IIS La Fe), IVIRMA Rome, New Jersey and Madrid, Centro Anatomopatológico, Yale School of Medicine, University of Valencia, and Rey Juan Carlos University conducted a new study using a mouse model of accelerated aging: the Senescence-Accelerated Mouse Prone 8 (SAMP8). On May 23, 2023, their research paper was published in Aging’s Volume 15, Issue 11, entitled, “Impaired telomere pathway and fertility in Senescence-Accelerated Mice Prone 8 females with reproductive senescence.”
Full blog - https://aging-us.org/2023/06/how-telomere-dysfunction-affects-female-fertility-a-mouse-study/
Paper DOI - https://doi.org/10.18632/aging.204731
Corresponding author - Elisa Varela - Mariaelisa.Varela@ivirma.com, https://orcid.org/0000-0002-5361-3877
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Keywords - aging, telomere, telomerase, fertility, ovary, SAMP8
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 11, entitled, “Precious1GPT: multimodal transformer-based transfer learning for aging clock development and feature importance analysis for aging and age-related disease target discovery.”
Aging is a complex and multifactorial process that increases the risk of various age-related diseases and there are many aging clocks that can accurately predict chronological age, mortality, and health status. These clocks are disconnected and are rarely fit for therapeutic target discovery.
In this study, researchers Anatoly Urban, Denis Sidorenko, Diana Zagirova, Ekaterina Kozlova, Aleksandr Kalashnikov, Stefan Pushkov, Vladimir Naumov, Viktoria Sarkisova, Geoffrey Ho Duen Leung, Hoi Wing Leung, Frank W. Pun, Ivan V. Ozerov, Alex Aliper, Feng Ren, and Alex Zhavoronkov from Insilico Medicine propose a novel approach to multimodal aging clock, which they call Precious1GPT, utilizing methylation and transcriptomic data for interpretable age prediction and target discovery developed using a transformer-based model and transfer learning for case-control classification.
“To identify aging biomarkers associated with age-related diseases, in the present work, we combined the ability of aging clocks to predict biological age and thus grasp molecular changes accompanied by senescence and our target ID approach to establish genes that are related to the development of diseases.”
While the accuracy of the multimodal transformer is lower within each individual data type, compared to the state of art specialized aging clocks based on methylation or transcriptomic data separately, it may have higher practical utility for target discovery. This method provides the ability to discover novel therapeutic targets that hypothetically may be able to reverse or accelerate biological age providing a pathway for therapeutic drug discovery and validation using the aging clock. In addition, the researchers provided a list of promising targets annotated using the PandaOmics industrial target discovery platform.
“The transformer-based model allowed for the integration of multi-omics data and improved the accuracy of the aging clock, while the transfer learning approach facilitated the identification of disease-related genes in the context of aging.”
DOI - https://doi.org/10.18632/aging.204788
Corresponding author - Alex Zhavoronkov - alex@insilico.com
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Keywords - aging, transformers, deep learning, therapeutic target discovery, aging biomarkers, human aging
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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The Ride for Roswell is one of the nation’s largest cycling events—hosted by Roswell Park Comprehensive Cancer Center—to raise awareness and funds for cancer research and patient care. This charity bike ride, based out of Buffalo, New York, has brought people together for 27 years to celebrate cancer survivors, pay tribute to lives that have been lost, and to work together to support research and find a cure.
When its doors opened in Buffalo in 1898, Roswell Park Comprehensive Cancer Center was the first cancer research-focused institution in the world. Today, this institution is one of only four National Cancer Institute-designated comprehensive cancer centers in the state of New York. Roswell Park Comprehensive Cancer Center is ranked by U.S. News & World Report as one of the best cancer hospitals in the United States.
The Ride for Roswell started in 1989 when Mitch Flynn, owner of the advertising agency Flynn & Friends, met Katherine Gioia. Katherine was a four-year-old patient battling a rare form of cancer. After Katherine’s death (less than a year after her diagnosis), Katherine’s mother, Anne Gioia, and aunt, Donna Gioia, founded the Roswell Park Alliance Foundation in her memory to raise money for cancer research and treatment. On June 29, 1996, Mitch and Alliance Foundation staff launched the first Ride for Roswell.
In the 27 years since then, thanks to over 127,000 riders and thousands of volunteers, the Ride for Roswell has raised over $67 million to fund cancer research. The event has become one of the largest charity rides in the United States.
Full press release - https://aging-us.net/2023/06/19/aging-sponsors-2023-ride-for-roswell/
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About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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Drs. Alfredo Franco-Obregón and Brian H. Kennedy from the National University of Singapore detail a research paper they co-authored that was published by Aging (Aging-US) in Volume 15, Issue 6, entitled, “Brief, weekly magnetic muscle therapy improves mobility and lean body mass in older adults: a Southeast Asia community case study.”
DOI - https://doi.org/10.18632/aging.204597
Corresponding authors - Alfredo Franco-Obregón - suraf@nus.edu.sg, and Yee Kit Tai - surtaiyk@nus.edu.sg
Abstract
Brief (10 min) weekly exposure to low energy pulsed electromagnetic fields (PEMFs) has been shown to improve human muscle mitochondrial bioenergetics and attenuate systemic lipotoxicity following anterior cruciate ligament surgical reconstruction. Here we present data generated from 101 participants, 62% female, aged 38–91 years, recruited from the QuantumTx Demo Centre in Singapore, wherein 87% of participants (n = 88) presented with pre-existing mobility dysfunction and 13% (n = 13) were healthy volunteers. Participants were recruited if: (i) not pregnant; (ii) above 35 years of age and; (iii) without surgical implants. All participants completed mobility testing, pre- and post- PEMF intervention for 12 weeks, whereas bioelectrical impedance analysis was conducted in a subgroup of 42 and 33 participants at weeks 4 and 8, respectively. Weekly PEMF exposure was associated with significant improvements in mobility (Timed Up and Go, 5 times Sit-to-Stand, and 4m Normal Gait Speed) and body composition (increased skeletal muscle mass and reduced total and visceral fat mass), particularly in the older participants. Perception of pain was also significantly reduced. PEMF therapy may provide a manner to counteract age-associated mobility and metabolic disruptions and merits future investigation in randomized controlled trials to elucidate its clinical benefits in the frail and older adult populations.
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Keywords - aging, sarcopenia, intra-abdominal fat, frailty, muscle weakness, type 2 diabetes mellitus
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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A new research paper was published in Aging (Aging-US) Volume 15, Issue 10, entitled, “Key elements of cellular senescence involve transcriptional repression of mitotic and DNA repair genes through the p53-p16/RB-E2F-DREAM complex.”
Cellular senescence is a dynamic stress response process that contributes to aging. From initiation to maintenance, senescent cells continuously undergo complex molecular changes and develop an altered transcriptome. Understanding how the molecular architecture of these cells evolve to sustain their non-proliferative state will open new therapeutic avenues to alleviate or delay the consequences of aging.
In this new study, seeking to understand these molecular changes, researchers Renuka Kandhaya-Pillai, Francesc Miro-Mur, Jaume Alijotas-Reig, Tamar Tchkonia, Simo Schwartz, James L. Kirkland, and Junko Oshima from the University of Washington, Vall d’Hebron Research Institute (VHIR), Vall d’Hebron Hospital, and the Mayo Clinic studied the transcriptomic profiles of endothelial replication-induced senescence and senescence induced by the inflammatory cytokine, TNF-α. The researchers previously reported gene expressional pattern, pathways, and the mechanisms associated with upregulated genes during TNF-α induced senescence.
“Here, we extend our work and find downregulated gene signatures of both replicative and TNF-α senescence were highly overlapped, involving the decreased expression of several genes associated with cell cycle regulation, DNA replication, recombination, repair, chromatin structure, cellular assembly, and organization.”
The team identified multiple targets of p53/p16-RB-E2F-DREAM that are essential for proliferation, mitotic progression, resolving DNA damage, maintaining chromatin integrity, and DNA synthesis that were repressed in senescent cells. They show that repression of multiple target genes in the p53/p16-RB-E2F-DREAM pathway collectively contributes to the stability of the senescent arrest. Their findings show that the regulatory connection between DREAM and cellular senescence may play a potential role in the aging process.
“This study suggests that the transcriptome signature of senescent cells goes beyond cell cycle arrest, with expression of multiple genes, from cell cycle to DNA repair to chromatin structure, being coordinately repressed to stably lock cells into this essentially non-proliferative state.”
DOI - https://doi.org/10.18632/aging.204743
Corresponding author - Renuka Kandhaya-Pillai - renugene@uw.edu
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Keywords - aging, cellular senescence, cell cycle, DREAM complex, DNA repair
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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Dr. Masaya Koshizaka from the Department of Endocrinology, Hematology, and Gerontology at Chiba University Graduate School of Medicine, details a research paper he co-authored that was published by Aging (Aging-US) in Volume 15, Issue 9, entitled, “Renal dysfunction, malignant neoplasms, atherosclerotic cardiovascular diseases, and sarcopenia as key outcomes observed in a three-year follow-up study using the Werner Syndrome Registry.”
DOI - https://doi.org/10.18632/aging.204681
Corresponding authors - Masaya Koshizaka - overslope@chiba-u.jp, and Koutaro Yokote - kyokote@faculty.chiba-u.jp
Transcription - https://aging-us.net/2023/06/09/behind-the-study-key-outcomes-observed-in-follow-up-study-using-the-werner-syndrome-registrybehind-the-study/
Video - https://www.youtube.com/watch?v=HFqPvtYYTGE
Abstract
Werner syndrome is an adult-onset progeria syndrome that results in various complications. This study aimed to clarify the profile and secular variation of the disease. Fifty-one patients were enrolled and registered in the Werner Syndrome Registry. Their data were collected annually following registration. A cross-sectional analysis at registration and a longitudinal analysis between the baseline and each subsequent year was performed. Pearson's chi-squared and Wilcoxon signed-rank tests were used. Malignant neoplasms were observed from the fifth decade of life (mean onset: 49.7 years) and were observed in approximately 30% of patients during the 3-year survey period. Regarding renal function, the mean estimated glomerular filtration rate calculated from serum creatinine (eGFRcre) and eGFRcys, which were calculated from cystatin C in the first year, were 98.3 and 83.2 mL/min/1.73 m2, respectively, and differed depending on the index used. In longitudinal analysis, the average eGFRcre for the first and fourth years was 74.8 and 63.4 mL/min/1.73 m2, showing a rapid decline. Secular changes in Werner syndrome in multiple patients were identified. The prevalence of malignant neoplasms is high, and renal function may decline rapidly. It is, therefore, necessary to carry out active and detailed examinations and pay attention to the type and dose of the drugs used.
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Keywords - aging, disease profile, long-term follow-up, malignant neoplasm, renal function, Werner syndrome
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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As we age, our immune system undergoes changes that influence our susceptibility to various diseases. Certain factors, such as smoking, viruses, age, and sex can have differential impacts on our various circulating immune cells. How changes to these immune cells contribute to cardiovascular disease and other age-related diseases is not yet fully understood. More research is needed to fully understand the underlying mechanisms and implications.
“Understanding the composition of circulating immune cells with aging and the underlying biologic mechanisms driving aging may provide molecular targets to slow the aging process and reduce age-related disease.”
In a new study, researchers Yuan Fang, Margaret F. Doyle, Jiachen Chen, Jesse Mez, Claudia L. Satizabal, Michael L. Alosco, Wei Qiao Qiu, Kathryn L. Lunetta, and Joanne M. Murabito from Boston University, Boston Medical Center, University of Vermont, and University of Texas Health Science Center aimed to characterize the circulating innate and adaptive immune system by profiling immune cell phenotypes from a community-based cohort. Their research paper was published in Aging’s Volume 15, Issue 10, on April 27, 2023, entitled, “Circulating immune cell phenotypes are associated with age, sex, CMV, and smoking status in the Framingham Heart Study offspring participants.”
“We hypothesize that we will identify immune cell phenotype and ARIP [age-related immune phenotype] measure associations with CMV serostatus, age, and sex, as well as associations with cardiovascular risk factors.”
Full blog - https://aging-us.org/2023/06/the-impact-of-age-sex-cmv-and-smoking-on-circulating-immune-cells/
Paper DOI - https://doi.org/10.18632/aging.204686
Corresponding author - Yuan Fang - yfang8@binghamton.edu
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Keywords - aging, immune cell, CMV, T cells, smoking
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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A new research paper was published in Aging (Aging-US) Volume 15, Issue 10, entitled, “DNAmFitAge: biological age indicator incorporating physical fitness.”
Physical fitness is a well-known correlate of health and the aging process and DNA methylation (DNAm) data can capture aging via epigenetic clocks. However, current epigenetic clocks did not yet use measures of mobility, strength, lung, or endurance fitness in their construction.
In this new study, researchers develop blood-based DNAm biomarkers for fitness parameters including gait speed (walking speed), maximum handgrip strength, forced expiratory volume in one second (FEV1), and maximal oxygen uptake (VO2max) which have modest correlation with fitness parameters in five large-scale validation datasets (average r between 0.16–0.48).
“These parameters were chosen because handgrip strength and VO2max provide insight into the two main categories of fitness: strength and endurance [23], and gait speed and FEV1 provide insight into fitness-related organ function: mobility and lung function [8, 24].”
The researchers then used these DNAm fitness parameter biomarkers with DNAmGrimAge, a DNAm mortality risk estimate, to construct DNAmFitAge, a new biological age indicator that incorporates physical fitness. DNAmFitAge was associated with low-intermediate physical activity levels across validation datasets (p = 6.4E-13), and younger/fitter DNAmFitAge corresponds to stronger DNAm fitness parameters in both males and females.
DNAmFitAge was lower (p = 0.046) and DNAmVO2max is higher (p = 0.023) in male body builders compared to controls. Physically fit people had a younger DNAmFitAge and experienced better age-related outcomes: lower mortality risk (p = 7.2E-51), coronary heart disease risk (p = 2.6E-8), and increased disease-free status (p = 1.1E-7). These new DNAm biomarkers provide researchers a new method to incorporate physical fitness into epigenetic clocks.
“Our newly constructed DNAm biomarkers and DNAmFitAge provide researchers and physicians a new method to incorporate physical fitness into epigenetic clocks and emphasizes the effect lifestyle has on the aging methylome.”
DOI - https://doi.org/10.18632/aging.204538
Corresponding authors - Kristen M. McGreevy - kristenmae@ucla.edu, Zsolt Radak - radak.zsolt@tf.hu, and Steve Horvath - shorvath@mednet.ucla.edu
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Keywords - aging, epigenetics, physical fitness, biological age, DNA methylation
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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A new research paper was published in Aging (Aging-US) Volume 15, Issue 9, entitled, “Exogenous exposures shape genetic predisposition to lipids, Alzheimer’s, and coronary heart disease in the MLXIPL gene locus.”In this new study, researchers Yury Loika, Elena Loiko, Fan Feng, Eric Stallard, Anatoliy I. Yashin, Konstantin Arbeev, Allison L. Kuipers, Mary F. Feitosa, Michael A. Province, and Alexander M. Kulminski from Duke University, University of Pittsburgh and Washington University School of Medicine examined associations of single nucleotide polymorphisms (SNPs) of the MLXIPL lipid gene with Alzheimer’s (AD) and coronary heart disease (CHD) and potentially causal mediation effects of their risk factors, high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG) in two samples of European ancestry from the United States (US) (22,712 individuals 587/2,608 AD/CHD cases) and the United Kingdom Biobank (UKB) (232,341 individuals; 809/15,269 AD/CHD cases).“Our results suggest that these associations can be regulated by several biological mechanisms and shaped by exogenous exposures.”Two patterns of associations (represented by rs17145750 and rs6967028) were identified. Minor alleles of rs17145750 and rs6967028 demonstrated primary (secondary) association with high TG (lower HDL-C) and high HDL-C (lower TG) levels, respectively. The primary association explained ~50% of the secondary one suggesting partly independent mechanisms of TG and HDL-C regulation. The magnitude of the association of rs17145750 with HDL-C was significantly higher in the US vs. UKB sample and likely related to differences in exogenous exposures in the two countries. rs17145750 demonstrated a significant detrimental indirect effect through TG on AD risk in the UKB only (βIE = 0.015, pIE = 1.9 × 10−3), which suggests protective effects of high TG levels against AD, likely shaped by exogenous exposures. Also, rs17145750 demonstrated significant protective indirect effects through TG and HDL-C in the associations with CHD in both samples. In contrast, rs6967028 demonstrated an adverse mediation effect through HDL-C on CHD risk in the US sample only (βIE = 0.019, pIE = 8.6 × 10−4). This trade-off suggests different roles of triglyceride mediated mechanisms in the pathogenesis of AD and CHD.“Finally, the results of this study suggest that genetic associations of SNPs from the MLXIPL gene locus with lipids, AD, and CHD are shaped by exogenous exposures. Further study of the related biological mechanisms can help to elucidate the related, modifiable risk factors.”DOI - https://doi.org/10.18632/aging.204665Corresponding authors - Yury Loika - yury.loika@duke.edu, and Alexander M. Kulminski - alexander.kulminski@duke.eduKeywords - aging, MLXIPL, lipids, triglycerides, coronary heart disease, Alzheimer’s diseaseAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
A new research paper was published in Aging (Aging-US) Volume 15, Issue 9, entitled, “Highly multiplexed immune profiling throughout adulthood reveals kinetics of lymphocyte infiltration in the aging mouse prostate.”Aging is a significant risk factor for disease in several tissues, including the prostate. Defining the kinetics of age-related changes in these tissues is critical for identifying regulators of aging and evaluating interventions to slow the aging process and reduce disease risk. An altered immune microenvironment is characteristic of prostatic aging in mice, but whether features of aging in the prostate emerge predominantly in old age or earlier in adulthood has not previously been established.In this study, researchers Jonathan J. Fox, Takao Hashimoto, Héctor I. Navarro, Alejandro J. Garcia, Benjamin L. Shou, and Andrew S. Goldstein from the University of California Los Angeles tracked the abundance of 29 immune cell clusters in the aging mouse prostate using highly multiplexed immune profiling and time-course analysis. “In this study, we characterized how the inflammatory microenvironment of the adult mouse prostate changes during aging using highly-multiplexed single-cell mass cytometry.”Early in adulthood, myeloid cells comprise the vast majority of immune cells in the 3-month-old mouse prostate. Between 6 and 12 months of age, there is a profound shift towards a T and B lymphocyte-dominant mouse prostate immune microenvironment. Comparing the prostate to other urogenital tissues, the researchers found similar features of age-related inflammation in the mouse bladder but not the kidney. “In summary, our study offers new insight into the kinetics of prostatic inflammaging and the window when interventions to slow down age-related changes may be most effective.”DOI - https://doi.org/10.18632/aging.204708Corresponding author - Andrew S. Goldstein - AGoldstein@mednet.ucla.eduSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204708Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, prostate, immune microenvironment, mass cytometry, inflammation, lymphocyteAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
Blog summary: "Proteostatic modulation in brain aging without associated Alzheimer’s disease-and age-related neuropathological changes."______________________________________________A healthy brain continuously produces new proteins to support synaptic plasticity, maintain neuronal health, facilitate signaling pathways, produce neurotransmitters, enable neuroplasticity and adaptation, and meet its metabolic demands. These processes are essential for normal brain function, learning, memory, and overall cognitive abilities. Researchers believe that the dysregulation of proteins is at the core of brain aging. However, the exact recipe for protein dysregulation that leads to accelerated brain aging and neurodegenerative disorders has yet to be brought to light. Previous brain proteostasis (referring to the maintenance of protein homeostasis in brain cells) studies in individuals with Alzheimer’s disease (AD) pathology and age-related neuropathological changes have shown protein dysregulation leading to a buildup of amyloid plaques and neurofibrillary tangles. While these studies have greatly enhanced our knowledge of brain aging, gaps in our understanding remain. What proteomic characteristics do healthy brain aging individuals—without neurodegenerative disorders—have in common?“To our knowledge, whole phosphoproteomes centered on the human brain aging without AD pathology are unavailable.”In a new study, researchers Pol Andrés-Benito, Ignacio Íñigo-Marco, Marta Brullas, Margarita Carmona, José Antonio del Rio, Joaquín Fernández-Irigoyen, Enrique Santamaría, Mónica Povedano, and Isidro Ferrer from Bellvitge Institute for Biomedical Research, Universidad Pública de Navarra, Barcelona Institute for Science and Technology, and University of Barcelona aimed to shed light on the mechanisms underlying brain aging in the absence of AD pathology and age-related neuropathological changes. Their research paper was published on May 13, 2023, in Aging’s Volume 15, Issue 9, and entitled, “Proteostatic modulation in brain aging without associated Alzheimer’s disease-and age-related neuropathological changes.”Full blog - https://aging-us.org/2023/05/brain-aging-insights-from-individuals-without-neurodegeneration/Paper DOI - https://doi.org/10.18632/aging.204698Corresponding authors - Isidro Ferrer - 8082ifa@gmail.com, and Pol Andrés-Benito - pandres@idibell.catSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204698Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, brain aging, cytoskeleton, membranes, synapsis, mitochondria, kinases, (phospho)proteomics, proteomeAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
Impact Journals (Aging's publisher) will be participating as an exhibitor at the Society for Scholarly Publishing (SSP) 45th Annual Meeting, which convenes on May 31–June 2, 2023, at the Oregon Convention Center & Hyatt Regency Portland in Portland, Oregon, USA. This year, the SSP’s meeting theme is: “Transformation, Trust, and Transparency.”“The pace of change in our industry continues unabated, with seismic shifts in areas such as the dissemination of research, business models, and the nature of the workplace. And yet, while pressure for change has become the new normal, fundamental change has proved more elusive. We invite you to join us in highlighting the Trust and Transparency issues that underlie many of the challenges we face and exploring what it takes to create more meaningful Transformation in scholarly publishing.” (Source: sspnet.org)Visit booth No. 216 at the SSP 45th Annual Meeting to connect with members of the Impact Journals team.About Impact Journals:Impact Journals publishes scholarly journals in the biomedical sciences with a focus on all areas of cancer and aging research. Our mission is to provide scientists with the opportunity to share their exceptional discoveries, to offer services that enable rapid dissemination of results, and to present vital findings from the many fields of biomedical science. Our goal is life without disease.To learn more about Impact Journals, visit www.ImpactJournals.com.Connect with us on social media to stay updated on journals published by Impact Journals: Oncotarget Twitter – https://twitter.com/Oncotarget Aging Twitter – https://twitter.com/AgingJrnl Oncotarget Facebook – https://www.facebook.com/Oncotarget Aging Facebook – https://www.facebook.com/AgingUS Oncotarget YouTube – https://www.youtube.com/@OncotargetJournal Aging YouTube – https://www.youtube.com/@AgingJournal Oncotarget LinkedIn – https://www.linkedin.com/company/oncotarget/ Aging LinkedIn – https://www.linkedin.com/company/agingFor media requests, please contact media@impactjournals.com.
Dean Bunnell, PhD candidate from the Department of Biological Sciences at the University of Alabama, describes a research paper he co-authored that was published by Aging (Aging-US) in Volume 15, Issue 6, entitled, “RNA virus-mediated changes in organismal oxygen consumption rate in young and old Drosophila melanogaster males.”DOI - https://doi.org/10.18632/aging.204593Corresponding author - Stanislava Chtarbanova - schtarbanova@ua.eduAbstractAging is accompanied by increased susceptibility to infections including with viral pathogens resulting in higher morbidity and mortality among the elderly. Significant changes in host metabolism can take place following virus infection. Efficient immune responses are energetically costly, and viruses divert host molecular resources to promote their own replication. Virus-induced metabolic reprogramming could impact infection outcomes, however, how this is affected by aging and impacts organismal survival remains poorly understood. RNA virus infection of Drosophila melanogaster with Flock House virus (FHV) is an effective model to study antiviral responses with age, where older flies die faster than younger flies due to impaired disease tolerance. Using this aged host-virus model, we conducted longitudinal, single-fly respirometry studies to determine if metabolism impacts infection outcomes. Analysis using linear mixed models on Oxygen Consumption Rate (OCR) following the first 72-hours post-infection showed that FHV modulates respiration, but age has no significant effect on OCR. However, the longitudinal assessment revealed that OCR in young flies progressively and significantly decreases, while OCR in aged flies remains constant throughout the three days of the experiment. Furthermore, we found that the OCR signature at 24-hours varied in response to both experimental treatment and survival status. FHV-injected flies that died prior to 48- or 72-hours measurements had a lower OCR compared to survivors at 48-hours. Our findings suggest the host’s metabolic profile could influence the outcome of viral infections.Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204593Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, Drosophila melanogaster, virus infection, single-fly respirometry, metabolismAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 9, entitled, “Increased expression of musashi 1 on breast cancer cells has implication to understand dormancy and survival in bone marrow.”Breast cancer (BC) stem cells (CSCs) resist treatment and can exist as dormant cells in tissues such as the bone marrow (BM). Years before clinical diagnosis, BC cells (BCCs) could migrate from the primary site where the BM niche cells facilitate dedifferentiation into CSCs. Additionally, dedifferentiation could occur by cell autonomous methods. In this new study, researchers George R. Nahas, Lauren S. Sherman, Garima Sinha, Markos H. El Far, Andrew Petryna, Steven M. Munoz, Kimberly A. Silverio, Maran Shaker, Pujan Neopane, Veronica Mariotti, and Pranela Rameshwar from Rutgers New Jersey Medical School studied the role of the RNA-binding protein, Musashi I (Msi 1). They also analyzed its relationship with the T-cell inhibitory molecule programmed death-ligand 1 (PD-L1) in CSCs.“We validated the link between Msi 1 and PD-L1 in CSCs [cancer stem cells] based on significant reduction of CSCs following Msi 1 knockdown.”PD-L1 is expressed on triple negative BC and other cancers. Therefore, PD-L1 is an immune checkpoint that is a target in immune therapy for cancers. Msi 1 can support BCC growth through stabilization of oncogenic transcripts and modulation of stem cell-related gene expression. The researchers reported on a role for Msi 1 to maintain CSCs. They found that it seemed to occur by the differentiation of CSCs to more matured BCCs. This correlated with increased transition from cycling quiescence and reduced expression of stem cell-linked genes. CSCs co-expressed Msi 1 and PD-L1. Msi 1 knockdown led to a significant decrease in CSCs with undetectable PD-L1. “This study has implications for Msi 1 as a therapeutic target, in combination with [an] immune checkpoint inhibitor. Such treatment could also prevent dedifferentiation of breast cancer to CSCs, and to reverse tumor dormancy. The proposed combined treatment might be appropriate for other solid tumors.”DOI - https://doi.org/10.18632/aging.204620Corresponding author - Pranela Rameshwar - rameshwa@njms.rutgers.eduSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204620Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, cancer stem cell, breast cancer, musashi 1, bone marrow, dormancyAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
A new research paper was published on the cover of Aging (Aging-US) Volume 15, Issue 9, entitled, “In vitro and in vivo effects of zoledronic acid on senescence and senescence-associated secretory phenotype markers.”Zoledronic acid has been found to reduce fracture risk and, in some studies, to decrease mortality in humans and extend lifespan and healthspan in animals. Because senescent cells accumulate with aging and contribute to multiple comorbidities, the non-skeletal actions of zoledronic acid could be due to senolytic (killing of senescent cells) or senomorphic (inhibition of the secretion of the senescence-associated secretory phenotype (SASP)) actions.In this new study, researchers Parinya Samakkarnthai, Dominik Saul, Lei Zhang, Zaira Aversa, Madison L. Doolittle, Jad G. Sfeir, Japneet Kaur, Elizabeth J. Atkinson, James R. Edwards, Graham G. Russell, Robert J. Pignolo, James L. Kirkland, Tamar Tchkonia, Laura J. Niedernhofer, David G. Monroe, Nathan K. Lebrasseur, Joshua N. Farr, Paul D. Robbins, and Sundeep Khosla from the Mayo Clinic, Phramongkutklao Hospital and College of Medicine, Eberhard Karls University, University of Minnesota, University of Oxford, and University of Sheffield tested the above hypothesis using multiple complementary approaches (in vitro, in vivo, and in silico) to evaluate possible effects of zoledronic acid on modulating cellular senescence.The researchers first performed in vitro senescence assays using human lung fibroblasts and DNA repair-deficient mouse embryonic fibroblasts, which demonstrated that zoledronic acid killed senescent cells with minimal effects on non-senescent cells. Next, in aged mice treated with zoledronic acid or vehicle for 8 weeks, zoledronic acid significantly reduced circulating SASP factors, including CCL7, IL-1β, TNFRSF1A, and TGFβ1 and improved grip strength. Analysis of publicly available RNAseq data from CD115+ (CSF1R/c-fms+) pre-osteoclastic cells isolated from mice treated with zoledronic acid demonstrated a significant downregulation of senescence/SASP genes (SenMayo). To establish that these cells are potential senolytic/senomorphic targets of zoledronic acid, the team used single cell proteomic analysis (cytometry by time of flight [CyTOF]) and demonstrated that zoledronic acid significantly reduced the number of pre-osteoclastic (CD115+/CD3e-/Ly6G-/CD45R-) cells and decreased protein levels of p16, p21, and SASP markers in these cells without affecting other immune cell populations. “Collectively, our findings demonstrate that zoledronic acid has senolytic effects in vitro and modulates senescence/SASP biomarkers in vivo. These data point to the need for additional studies testing zoledronic acid and/or other bisphosphonate derivatives for senotherapeutic efficacy.”DOI - https://doi.org/10.18632/aging.204701Corresponding author - Sundeep Khosla - khosla.sundeep@mayo.eduAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
A new editorial paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 8, entitled, “The senescence-associated secretory phenotype induces neuroendocrine transdifferentiation.”In this editorial, researchers Anda Huna, Nadine Martin and David Bernard from the Université de Lyon discuss the senescence-associated secretory phenotype (SASP). SASP, in addition to stable proliferation arrest, is one of the most remarkable characteristics of senescent cells. Indeed, these cells secrete a variety of factors including cytokines, growth factors and matrix metalloproteases among others. In response to stress, through their SASP, senescent cells are able to modify and instruct their microenvironment. “The SASP is known to have several, sometimes contradictory, effects on phenotypes, including the induction or reinforcement of senescence in neighboring cells, promotion or inhibition of stemness, modification of extracellular matrix, activation or inhibition of immune responses and induction of epithelial-mesenchymal transition and cell migration.” Although cellular senescence and its SASP can initially display some beneficial effects, for instance favoring wound healing or blocking tumor initiation, accumulation of senescent cells and their secretome during aging or chronic stresses (tobacco, obesity, alcohol among others) plays a significant role in promoting aging-associated features and pathologies, like fibrosis, steatosis, chronic inflammation or cancer. In the context of cancer, senescence initially has an antitumoral role, as it promotes proliferation arrest and favors an anti-tumoral immune surveillance in response to oncogenic stress or DNA damage accumulation. However, SASP plays a dual role in tumor initiation and progression, as it first has a tumor suppressive action by reinforcing senescence in neighboring cells and recruiting immune cells, but also plays a tumor promoting role by promoting stemness, epithelial-mesenchymal transition and cell migration and by inhibiting immune responses. “Overall our work reveals a new effect of senescent cells and their SASP in tumors and offers new insights into NED [neuroendocrine transdifferentiation] in breast and prostate cancer biology. It also provides a new vision of the contribution of senescent cells and their SASP to aging-related pathologies, which could involve NED induction in some contexts.”DOI - https://doi.org/10.18632/aging.204669Corresponding author - David Bernard - david.bernard@lyon.unicancer.frSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204669Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, cellular senescence, aging, cancer, NF-κB, calcium signalingAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
A new review paper was published in Aging (Aging-US) Volume 15, Issue 8, entitled, “How can we modulate aging through nutrition and physical exercise? An epigenetic approach.”The World Health Organization predicts that by 2050, 2.1 billion people worldwide will be over 60 years old, a drastic increase from only 1 billion in 2019. Considering these numbers, strategies to ensure an extended “healthspan” or healthy longevity are urgently needed.In this new review, researchers Ana Teresa Rajado, Nádia Silva, Filipa Esteves, David Brito, Alexandra Binnie, Inês M. Araújo, Clévio Nóbrega, José Bragança, and Pedro Castelo-Branco from the ALFA Score Consortium, University of Algarve Campus Gambelas, William Osler Health System, and Champalimaud Centre for the Unknown discuss their present study that approaches the promotion of healthspan from an epigenetic perspective. Epigenetic phenomena are modifiable in response to an individual’s environmental exposures, and therefore link an individual’s environment to their gene expression pattern. Epigenetic studies demonstrate that aging is associated with decondensation of the chromatin, leading to an altered heterochromatin structure, which promotes the accumulation of errors.“In this article we explore aging and its associated epigenetic changes as well as how these changes may be delayed or reversed through nutrition, caloric restriction and sustained physical activity, as schematized in Figure 2.”Canonical histones are replaced by histone variants, concomitant with an increase in histone post-translational modifications (PTMs). A slight increase in DNA methylation at promoters has been observed, which represses transcription of previously active genes, in parallel with global genome hypomethylation. Aging is also associated with deregulation of gene expression - usually provided by non-coding RNAs - leading to both the repression of previously transcribed genes and to the transcription of previously repressed genes.“Age-associated epigenetic events are less common in individuals with a healthy lifestyle, including balanced nutrition, caloric restriction and physical exercise. Healthy aging is associated with more tightly condensed chromatin, fewer PTMs and greater regulation by ncRNAs.”DOI: https://doi.org/10.18632/aging.204668 Corresponding Author: Pedro Castelo-Branco - pjbranco@ualg.ptSign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204666Subscribe for free publication alerts from Aging: https://www.aging-us.com/subscribe-to-toc-alertsKeywords: epigenetics, aging, nutrition, caloric restriction, physical exerciseAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
A new research paper was published in Aging (Aging-US) Volume 15, Issue 8, entitled, “Single-cell transcriptomic analysis uncovers diverse and dynamic senescent cell populations.”Senescence is a state of enduring growth arrest triggered by sublethal cell damage. Given that senescent cells actively secrete proinflammatory and matrix-remodeling proteins, their accumulation in tissues of older persons has been linked to many diseases of aging. Despite intense interest in identifying robust markers of senescence, the highly heterogeneous and dynamic nature of the senescent phenotype has made this task difficult.In this new study, researchers Noah Wechter, Martina Rossi, Carlos Anerillas, Dimitrios Tsitsipatis, Yulan Piao, Jinshui Fan, Jennifer L. Martindale, Supriyo De, Krystyna Mazan-Mamczarz, and Myriam Gorospe from the National Institute on Aging set out to comprehensively analyze the senescent transcriptome of human diploid fibroblasts at the individual-cell scale by performing single-cell RNA-sequencing analysis through two approaches. “Here, we used single-cell RNA sequencing (scRNA-seq) analysis to document both the diverse transcriptomes of human senescent fibroblasts at an individual-cell scale, and the changes in the transcriptome over time during etoposide-triggered senescence.”First, the researchers characterized the different cell states in cultures undergoing senescence triggered by different stresses, and found distinct cell subpopulations that expressed mRNAs encoding proteins with roles in growth arrest, survival and the secretory phenotype. Second, they characterized the dynamic changes in the transcriptomes of cells as they developed etoposide-induced senescence; by tracking cell transitions across this process, the researchers found two different senescence programs that developed divergently, one in which cells expressed traditional senescence markers such as p16 (CDKN2A) mRNA, and another in which cells expressed long noncoding RNAs and splicing was dysregulated. Finally, they obtained evidence that the proliferation status at the time of senescence initiation affected the path of senescence, as determined based on the expressed RNAs. “We propose that a deeper understanding of the transcriptomes during the progression of different senescent cell phenotypes will help develop more effective interventions directed at this detrimental cell population.”DOI - https://doi.org/10.18632/aging.204666Corresponding authors - Krystyna Mazan-Mamczarz - krystyna.mazan-mamczarz@nih.gov, and Myriam Gorospe - myriam-gorospe@nih.govSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204666Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, senescence, single-cell analysis, transcriptomeAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
Geoffrey Leung and Dr. Doris Leung, Senior Application Scientists from Insilico Medicine Hong Kong Ltd., detail a research paper they co-authored that was published by Aging (Aging-US) in Volume 15, Issue 8, entitled, "Identification of dual-purpose therapeutic targets implicated in aging and glioblastoma multiforme using PandaOmics - an AI-enabled biological target discovery platform.”#openaccess #aging #glioblastoma #research #ai #artificialintelligence #peerreview #openscience #researchpaper #journal #publication #meded #targetdiscovery #gbmDOI - https://doi.org/10.18632/aging.204678Corresponding author - Mikhail Korzinkin - mike@insilicomedicine.comAbstractGlioblastoma Multiforme (GBM) is the most aggressive and most common primary malignant brain tumor. The age of GBM patients is considered as one of the disease's negative prognostic factors and the mean age of diagnosis is 62 years. A promising approach to preventing both GBM and aging is to identify new potential therapeutic targets that are associated with both conditions as concurrent drivers. In this work, we present a multi-angled approach of identifying targets, which takes into account not only the disease-related genes but also the ones important in aging. For this purpose, we developed three strategies of target identification using the results of correlation analysis augmented with survival data, differences in expression levels and previously published information of aging-related genes. Several studies have recently validated the robustness and applicability of AI-driven computational methods for target identification in both cancer and aging-related diseases. Therefore, we leveraged the AI predictive power of the PandaOmics TargetID engine in order to rank the resulting target hypotheses and prioritize the most promising therapeutic gene targets. We propose cyclic nucleotide gated channel subunit alpha 3 (CNGA3), glutamate dehydrogenase 1 (GLUD1) and sirtuin 1 (SIRT1) as potential novel dual-purpose therapeutic targets to treat aging and GBM.Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204678Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, target discovery, GBM, glioblastoma, PandaOmicsAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
Blog summary of an editorial published in Aging’s Volume 15, Issue 8, on April 3, 2023, entitled, “Artificial intelligence and the aging mind.”_________________________________________Aging is a risk factor for many diseases, including Alzheimer’s disease (AD). While scientists have made some progress in understanding the physiology of aging and its relationship to AD and related disorders, our understanding remains incomplete (to say the least). It is possible that civilization is currently in the midst of an artificial intelligence (AI) and machine learning (ML) “boom.” Researchers are now using AI and ML technologies to elevate our comprehension of aging and aging-related diseases.“Artificial intelligence (AI) and machine learning (ML) technologies can help us better understand these diseases and aging itself by using biological data from the brain or other sources to create a mapping between age and biological data.”In a new editorial paper, researchers Jeyeon Lee, Leland R. Barnard and David T. Jones from the Mayo Clinic in Rochester, Minnesota, discuss a recent study they conducted and explore the potential of AI to revolutionize the field of geriatrics. Their editorial was published in Aging’s Volume 15, Issue 8, on April 3, 2023, entitled, “Artificial intelligence and the aging mind.”Full blog - https://aging-us.org/2023/05/the-brain-age-gap/Paper DOI - https://doi.org/10.18632/aging.204644 (PDF)Corresponding author - David T. Jones - Jones.David@mayo.eduSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204644Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, brain age, artificial intelligence, Alzheimer’s dementia, neurodegenerative disease, biomarkerAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
Blog summary of a research paper published by Aging (Aging-US) in Volume 15, Issue 8: "Identification of dual-purpose therapeutic targets implicated in aging and glioblastoma multiforme using PandaOmics – an AI-enabled biological target discovery platform.”_____________________________________________________Glioblastoma multiforme (GBM) is one of the most aggressive and fatal malignant brain tumors. With a median survival time of 15 months, only about 25% of patients survive for one year and less than 5% survive for five years. As people get older, the risk of developing GBM increases. The discovery of new drug targets for GBM is of paramount importance.The good news here is that high school students, Zachary Harpaz, Andrea Olsen and Christopher Ren, and researchers Anastasia Shneyderman, Alexander Veviorskiy, Maria Dralkina, Simon Konnov, Olga Shcheglova, Frank W. Pun, Geoffrey Ho Duen Leung, Hoi Wing Leung, Ivan V. Ozerov, Alex Aliper, Mikhail Korzinkin, and Alex Zhavoronkov have recently made remarkable strides in the joint field of aging and glioblastoma research. The team used a generative artificial intelligence (AI) engine from Insilico Medicine (founded by Dr. Alex Zhavoronkov) called PandaOmics, to identify new therapeutic targets for both GBM and aging. On April 26, 2023, their research paper was published in Aging’s Volume 15, Issue 8, entitled, “Identification of dual-purpose therapeutic targets implicated in aging and glioblastoma multiforme using PandaOmics – an AI-enabled biological target discovery platform.”Full blog - https://aging-us.org/2023/05/high-school-students-use-ai-to-make-aging-and-glioblastoma-discoveries/Research paper DOI - https://doi.org/10.18632/aging.204678Corresponding author - Mikhail Korzinkin - mike@insilicomedicine.comSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204678Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, target discovery, GBM, glioblastoma, PandaOmicsAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
A new research paper was published in Aging (Aging-US) Volume 15, Issue 8, entitled, “Identification of dual-purpose therapeutic targets implicated in aging and glioblastoma multiforme using PandaOmics - an AI-enabled biological target discovery platform.”Glioblastoma Multiforme (GBM) is the most aggressive and most common primary malignant brain tumor. The age of GBM patients is considered as one of the disease's negative prognostic factors and the mean age of diagnosis is 62 years. A promising approach to preventing both GBM and aging is to identify new potential therapeutic targets that are associated with both conditions as concurrent drivers.In this new study, researchers Anastasia Shneyderman, Alexander Veviorskiy, Maria Dralkina, Simon Konnov, Olga Shcheglova, Frank W. Pun, Geoffrey Ho Duen Leung, Hoi Wing Leung, Ivan V. Ozerov, Alex Aliper, Mikhail Korzinkin, and Alex Zhavoronkov from The Youth Longevity Association, Pine Crest School Science Research Department, Shanghai High School International Division, and Insilico Medicine present a multi-angled approach of identifying targets, which takes into account not only the disease-related genes but also the ones important in aging. “For this purpose, we developed three strategies of target identification using the results of correlation analysis augmented with survival data, differences in expression levels and previously published information of aging-related genes.”Several studies have recently validated the robustness and applicability of AI-driven computational methods for target identification in both cancer and aging-related diseases. Therefore, the researchers leveraged the AI predictive power of the PandaOmics TargetID engine in order to rank the resulting target hypotheses and prioritize the most promising therapeutic gene targets. They propose three potentially novel dual-purpose therapeutic targets to treat aging and GBM: cyclic nucleotide gated channel subunit alpha 3 (CNGA3), glutamate dehydrogenase 1 (GLUD1) and sirtuin 1 (SIRT1).“The next steps towards implementation of the identified therapeutic targets into the clinic would involve a generation of small molecules and their optimisation with further validation and preclinical testing to determine their safety, efficacy, and potential side effects.”DOI: https://doi.org/10.18632/aging.204678Corresponding author - Mikhail Korzinkin - mike@insilicomedicine.comSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204678Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, target discovery, GBM, glioblastoma, PandaOmicsAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
A new research paper was published on the cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 8, entitled, “A chronic wound model to investigate skin cellular senescence.”Wound healing is an essential physiological process for restoring normal skin structure and function post-injury. The role of cellular senescence, an essentially irreversible cell cycle state in response to damaging stimuli, has emerged as a critical mechanism in wound remodeling. Transiently-induced senescence during tissue remodeling has been shown to be beneficial in the acute wound healing phase. In contrast, persistent senescence, as observed in chronic wounds, contributes to delayed closure. In this new study, researchers Saranya P. Wyles, Parisa Dashti, Tamar Pirtskhalava, Burak Tekin, Christina Inman, Lilian Sales Gomez, Anthony B. Lagnado, Larissa Prata, Diana Jurk, João F. Passos, Tamar Tchkonia, and James L. Kirkland from the Mayo Clinic in Rochester, Minnesota, describe a chronic wound murine model and its cellular senescence profile, including the senescence-associated secretory phenotype.“Herein we hypothesize that persistent senescent cell accumulation contributes to delayed healing in chronic wounds.” This study presents a novel oxidative stress-induced chronic murine wound mouse model in which there is capacity to target aberrant senescent cell expression. Pharmacological manipulation of oxidative stress can influence wound healing and result in delayed wound closure, which offers the opportunity to characterize cellular senescence in late stages of wound healing. The molecular and histological profiles of senescent cells in the epidermis and dermis demonstrate the adverse influence of SASP factors in the chronic wound bed, a new avenue for root-cause, targeted therapeutic interventions.“To our knowledge, this study is the first chronic wound murine model to profile the effects of the chronic cellular senescence that is linked to delayed wound healing. This may have implications for developing interventions that target cellular senescence for chronic or stalled wounds as a root cause-driven therapeutic strategy.”DOI: https://doi.org/10.18632/aging.204667 Corresponding Authors: James L. Kirkland - kirkland.james@mayo.edu, and Tamar Tchkonia - tchkonia.tamar@mayo.eduSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204667Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, wound healing, cellular senescence, chronic wound, re-epithelization, skinAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
A new research paper was published in Aging (Aging-US) Volume 15, Issue 7, entitled, “Effect of deferoxamine and ferrostatin-1 on salivary gland dysfunction in ovariectomized rats.”Xerostomia can be defined as a subjective sensation associated with reduction of lubrication and dehydration of the oral mucosa. Xerostomia is known to be common in elderly people, especially women, and its prevalence is thought to range from 5.5% to 46%. The mechanism underlying xerostomia after menopause has not yet been fully elucidated. In this new study, researchers Yong-Il Cheon, Ji Min Kim, Sung-Chan Shin, Hyung-Sik Kim, Jin-Choon Lee, Gi Cheol Park, Eui-Suk Sung, Minhyung Lee, and Byung-Joo Lee from Pusan National University and Sungkyunkwan University School of Medicine aimed to investigate the mechanism of xerostomia and the effect of the ferroptosis inhibitors deferoxamine (DFO) and ferrostatin-1 (FER) on salivary gland dysfunction in a postmenopausal animal model. “Recently, it was reported that ferroptosis in the salivary gland may be related to the xerostomia that occurs after menopause [30]. However, no studies to date have used anti-ferroptosis drugs to investigate the mechanisms underlying postmenopausal salivary gland dysfunction.”Twenty-four female Sprague–Dawley rats were randomly divided into four groups: a SHAM group (n = 6, sham-operated rats), an OVX group (n = 6, ovariectomized rats), an FER group (n = 6, ovariectomized rats injected intraperitoneally with FER), and a DFO group (n = 6, ovariectomized rats injected intraperitoneally with DFO). GPX4 activity, iron accumulation, lipid peroxidation, inflammation, fibrosis, and salivary gland function were analyzed.Recovery of GPX4 activity and a decrease in iron accumulation and cytosolic MDA + HAE were observed in the DFO group. In addition, collagen I, collagen III, TGF-β, IL-6, TNF-α, and TGF-β levels were decreased in the DFO group compared to the OVX group. Recovery of GPX4 activity and the morphology of mitochondria, and reduction of cytosolic MDA + HAE were also observed in the FER group. In addition, decreased expression of inflammatory cytokines and fibrosis markers and increased expression of AQP5 were observed in both the DFO and FER groups. Postmenopausal salivary gland dysfunction is associated with ferroptosis. This is the first study to investigate the effect of ferroptosis inhibitors (DFO and FER) on the salivary glands of ovariectomized rats. DFO and FER are considered promising treatments for postmenopausal xerostomia.“In the absence of a standard treatment for postmenopausal dry mouth, this study is expected to be helpful in understanding the mechanism of postmenopausal salivary gland dysfunction and developing a treatment for postmenopausal dry mouth.”DOI: https://doi.org/10.18632/aging.204641Corresponding author - Byung-Joo Lee - voicelee@pusan.ac.krKeywords - aging, menopause, ferroptosis, xerostomia, deferoxamine, ferrostatin-1About Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/MEDIA@IMPACTJOURNALS.COM
A new research paper was published in Aging (Aging-US) Volume 15, Issue 7, entitled, “Characterization of the HDAC/PI3K inhibitor CUDC-907 as a novel senolytic.”The accumulation of senescent cells has an important role in the phenotypical changes observed in aging and in many age-related pathologies. Thus, the strategies designed to prevent these effects, collectively known as senotherapies, have a strong clinical potential. Senolytics are a type of senotherapy aimed at specifically eliminating senescent cells from tissues. Several small molecule compounds with senolytic properties have already been identified, but their specificity and range of action are variable. Because of this, potential novel senolytics are being actively investigated. Given the involvement of HDACs and the PI3K pathway in senescence, researchers Fares Al-Mansour, Abdullah Alraddadi, Buwei He, Anes Saleh, Marta Poblocka, Wael Alzahrani, Shaun Cowley, and Salvador Macip from the University of Leicester, Najran University and Universitat Oberta de Catalunya hypothesized that the dual inhibitor CUDC-907, a drug already in clinical trials for its antineoplastic effects, could have senolytic effects. “Here, we show that CUDC-907 was indeed able to selectively induce apoptosis in cells driven to senesce by p53 expression, but not when senescence happened in the absence of p53.” Consistent with this, CUDC-907 showed senolytic properties in different models of stress-induced senescence. Their results also indicate that the senolytic functions of CUDC-907 depend on the inhibitory effects of both HDACs and PI3K, which leads to an increase in p53 and a reduction in BH3 pro-survival proteins. Taken together, their results show that CUDC-907 has the potential to be a clinically relevant senolytic in pathological conditions in which stress-induced senescence is involved.“According to our results, CUDC-907 could be an interesting drug to be used as a senolytic, alone or as part of a targeted approach.”DOI: https://doi.org/10.18632/aging.204616Corresponding author - Salvador Macip - sm460@le.ac.ukSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204616Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, senescence, senolytics, HDAC, PI3K, CUDC-907About Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
A new research paper was published in Aging (Aging-US) Volume 15, Issue 7, entitled, “Viral vector-mediated upregulation of serine racemase expression in medial prefrontal cortex improves learning and synaptic function in middle age rats.”An age-associated decrease in N-methyl-D-aspartate receptor (NMDAR)-mediated synaptic function contributes to impaired synaptic plasticity and is associated with cognitive impairments. Levels of serine racemase (SR), an enzyme that synthesizes D-serine, an NMDAR co-agonist, decline with age. In this new study, researchers Brittney Yegla, Asha Rani and Ashok Kumar from the University of Florida’s McKnight Brain Institute predicted that enhancing NMDAR function via increased SR expression in middle age (when subtle declines in cognition emerge) may enhance performance on a prefrontal cortex-mediated task sensitive to aging. “We hypothesized that augmenting SR expression within mPFC glutamatergic neurons would improve attention and cognitive flexibility in middle-aged rats and facilitate synaptic responses in the mPFC. Thus, for this study, SR expression was upregulated in pyramidal neurons of the mPFC through lenti-viral technology to enhance NMDAR function and evaluate its impact on cognitive flexibility and NMDAR-mediated synaptic transmission in middle-age rats.”Middle-aged (~12 mo) male Fischer-344 rats were injected bilaterally in the medial prefrontal cortex (mPFC) with viral vector (LV), SR (LV-SR) or control (LV-GFP). Rats were trained on the operant attentional set-shift task (AST) to examine cognitive flexibility and attentional function. LV-SR rats exhibited a faster rate of learning compared to controls during visual discrimination of the AST.Extradimensional set shifting and reversal were not impacted. Immunohistochemical analyses demonstrated that LV-SR significantly increased SR expression in the mPFC. Electrophysiological characterization of synaptic transmission in the mPFC slices obtained from LV-GFP and LV-SR animals indicated a significant increase in isolated NMDAR-mediated synaptic responses in LV-SR slices. Thus, results of the current study demonstrated that prefrontal SR upregulation in middle age rats can improve learning of task contingencies for visual discrimination and increase glutamatergic synaptic transmission, including NMDAR activity.“The results from this study support the beneficial effects of the D-serine pathway involvement in NMDAR-mediated transmission and cognitive function, expanding the literature to emphasize its role in not only the hippocampus but also the PFC. Thus, targeting this pathway could pose a potential route in reversing age-related cognitive decline and should be considered for future research.”DOI: https://doi.org/10.18632/aging.204652 Corresponding Author: Ashok Kumar - kash@ufl.eduKeywords - aging, medial prefrontal cortex, serine racemase, D-serine, NMDA receptor, cognitive flexibilityAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/MEDIA@IMPACTJOURNALS.COM
A new research paper was published on the cover of Aging (Aging-US) Volume 15, Issue 7, entitled, “p21 facilitates chronic lung inflammation via epithelial and endothelial cells.”Cellular senescence is a stable state of cell cycle arrest that regulates tissue integrity and protects the organism from tumorigenesis. However, the accumulation of senescent cells during aging contributes to age-related pathologies. One such pathology is chronic lung inflammation. p21 (CDKN1A) regulates cellular senescence via inhibition of cyclin-dependent kinases (CDKs). However, its role in chronic lung inflammation and functional impact on chronic lung disease, where senescent cells accumulate, is less understood. In this new study, researchers Naama Levi, Nurit Papismadov, Julia Majewska, Lior Roitman, Noa Wigoda, Raya Eilam, Michael Tsoory, Ron Rotkopf, Yossi Ovadya, Hagay Akiva, Ofer Regev, and Valery Krizhanovsky from the Weizmann Institute of Science aimed to elucidate the role of p21 in chronic lung inflammation.“[...] we subjected p21 knockout (p21-/-) mice to repetitive inhalations of lipopolysaccharide (LPS), an exposure that leads to chronic bronchitis and accumulation of senescent cells.” The researchers utilized a lipopolysaccharide (LPS) inhalation-induced chronic bronchitis procedure to study the effects of repetitive LPS exposure on p21 knockout (p21-/-) mice. Furthermore, the team aimed to examine the specific contribution of the epithelial, endothelial and immune compartments to chronic bronchitis pathology. They found that p21 knockout led to a reduced presence of senescent cells, alleviated the pathological manifestations of chronic lung inflammation, and improved the fitness of the mice. The expression profiling of the lung cells revealed that resident epithelial and endothelial cells, but not immune cells, play a significant role in mediating the p21-dependent inflammatory response following chronic LPS exposure. “Therefore, we suggest that p21-dependent elimination of senescent cells may limit the damage induced by the pro-inflammatory presence of senescent cells, but also promote tissue regeneration. Therefore, inhibition of p21 represents a promising strategy for limiting age-related inflammatory disorders in general and obstructive lung diseases in particular.”DOI: https://doi.org/10.18632/aging.204622 Corresponding Author: Valery Krizhanovsky - valery.krizhanovsky@weizmann.ac.il Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204622Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, cellular senescence, chronic lung inflammation, p21 (CDKN1A)About Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 6, entitled, “Selenium as a predictor of metabolic syndrome in middle age women.”Metabolic syndrome (MetS) is a widespread clinical entity that has become almost a global epidemic. Selenium plays an important role in metabolic homeostasis. It has been suggested that it may also affect the expression and activity of PPAR-γ—an important mediator in energy balance and cell differentiation. In this new study, researchers Daria Schneider-Matyka, Anna Maria Cybulska, Małgorzata Szkup, Bogumiła Pilarczyk, Mariusz Panczyk, Agnieszka Tomza-Marciniak, and Elżbieta Grochans from Pomeranian Medical University in Szczecin, West Pomeranian University of Technology and Medical University of Warsaw aimed to analyze the relationships between these variables in the context of the health of women, for whom the risk of MetS increases with age.“The aim of this study was to search for a relationship between selenium concentrations and MetS, and to assess the impact of PPAR-γ on the incidence of MetS with regard to the moderating role of selenium.”The study involved 390 women in middle age. The stages of study: a survey-based part; anthropometric measurements; analysis of biological material (blood) in terms of glycemia, triglyceride, HDL, and selenium levels, as well as genetic analysis of the PPAR-γ polymorphisms. The researchers found that selenium may moderate the effect of the G allele of the PPAR-γ gene on the occurrence of elevated waist circumference (OR=1.030, 95%CI 1.005-1.057, p=0.020); and the effect of the C (OR=1.077, 95%CI 1.009-1.149, p=0.026) and the G alleles (OR=1.052, 95%CI 1.025-1.080, p<0.000) on the odds of elevated blood pressure. Women in whom HDL levels were not significantly reduced, had higher selenium levels (p=0.007).This study lead the team to 4 distinct conclusions: 1-The effect of selenium on MetS and its components has not been demonstrated. 2-The effect of individual alleles of the PPAR-γ gene on MetS and its components was not demonstrated. 3-The concentration of selenium may affect waist circumference in carriers of the G allele, and arterial hypertension in carriers of the C and G alleles by affecting the expression of PPAR-γ. 4-Higher selenium concentrations increased the odds of higher HDL levels in the group of subjects meeting the MetS criteria.“Recently, optimizing selenium intake in the population to prevent diseases associated with selenium deficiency or excess has been an important issue in modern health care worldwide. Our study suggests the influence of selenium levels on some components of MetS, such as waist circumference, blood pressure and HDL concentration. Thus, serum selenium concentration could be considered as one of the factors affecting some components of MetS.”DOI: https://doi.org/10.18632/aging.204590 Corresponding Author: Daria Schneider-Matyka - daria.schneider-matyka@pum.edu.plSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204590Keywords - aging, selenium, metabolic syndrome, middle aged womenAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Visit https://www.Aging-US.com for more about Aging (Aging-US).MEDIA@IMPACTJOURNALS.COM
A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 6, entitled, “Knockout of AMD-associated gene POLDIP2 reduces mitochondrial superoxide in human retinal pigment epithelial cells.”Genetic and epidemiologic studies have significantly advanced our understanding of the genetic factors contributing to age-related macular degeneration (AMD). In particular, recent expression quantitative trait loci (eQTL) studies have highlighted POLDIP2 as a significant gene that confers risk of developing AMD. However, the role of POLDIP2 in retinal cells such as retinal pigment epithelium (RPE) and how it contributes to AMD pathology are unknown. In this new study, researchers Tu Nguyen, Daniel Urrutia-Cabrera, Luozixian Wang, Jarmon G. Lees, Jiang-Hui Wang, Sandy S.C. Hung, Alex W. Hewitt, Thomas L. Edwards, Sam McLenachan, Fred K. Chen, Shiang Y. Lim, Chi D. Luu, Robyn Guymer, and Raymond C.B. Wong from Royal Victorian Eye and Ear Hospital, University of Melbourne, St Vincent’s Institute of Medical Research, University of Tasmania, and The University of Western Australia report the generation of a stable human RPE cell line ARPE-19 with POLDIP2 knockout using CRISPR/Cas, providing an in vitro model to investigate the functions of POLDIP2. “We conducted functional studies on the POLDIP2 knockout cell line and showed that it retained normal levels of cell proliferation, cell viability, phagocytosis and autophagy. Also, we performed RNA sequencing to profile the transcriptome of POLDIP2 knockout cells.”Their results highlighted significant changes in genes involved in immune response, complement activation, oxidative damage and vascular development. They showed that loss of POLDIP2 caused a reduction in mitochondrial superoxide levels, which is consistent with the upregulation of the mitochondrial superoxide dismutase SOD2. In conclusion, this study demonstrates a novel link between POLDIP2 and SOD2 in ARPE-19, which supports a potential role of POLDIP2 in regulating oxidative stress in AMD pathology.“In summary, we have generated a POLDIP2 knockout ARPE-19 cell line using CRISPR/Cas9 and studied the biological functions of POLDIP2. To our knowledge, this is the first functional study of POLDIP2 in retinal cells to understand its potential role in AMD.”DOI: https://doi.org/10.18632/aging.204522 Corresponding Author: Raymond C.B. Wong - wongcb@unimelb.edu.au Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204522Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, age-related macular degeneration, retina, CRISPR/Cas, mitochondria superoxide, POLDIP2About Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
Blog summary of a research paper published by Aging (Aging-US) in Volume 15, Issue 6: “RNA virus-mediated changes in organismal oxygen consumption rate in young and old Drosophila melanogaster males.”_________________________________________RNA viruses are responsible for approximately 70% of emerging infectious diseases in humans, according to a 2020 report by the National Academy of Medicine. Examples of RNA viruses include: influenza, hepatitis C, HIV, measles, zika, ebola, poliovirus, rhinovirus, rabies, and SARS-CoV-2—the virus responsible for the COVID-19 pandemic. After infection with an RNA virus, significant changes can take place in the host’s metabolism. While it is clear that disease tolerance declines as humans age, it is not yet clear how aging affects virus-induced changes in metabolism.“Virus-induced metabolic reprogramming could impact infection outcomes, however, how this is affected by aging and impacts organismal survival remains poorly understood.”In a new study, researchers Eli Hagedorn, Dean Bunnell, Beate Henschel, Daniel L. Smith Jr., Stephanie Dickinson, Andrew W. Brown, Maria De Luca, Ashley N. Turner, and Stanislava Chtarbanova from the University of Alabama, Indiana University, University of Arkansas for Medical Sciences, Arkansas Children’s Research Institute, and Jacksonville State University examined how an RNA virus can affect the respiration rate in male fruit flies (Drosophila melanogaster), both young and old. On March 22, 2023, their research paper was published in Aging’s Volume 15, Issue 6, entitled, “RNA virus-mediated changes in organismal oxygen consumption rate in young and old Drosophila melanogaster males.”Full blog - https://aging-us.org/2023/04/rna-virus-fruit-fly-model-first-study-to-measure-single-fly-respiration/DOI - https://doi.org/10.18632/aging.204593Corresponding author - Stanislava Chtarbanova - schtarbanova@ua.eduSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204593Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, Drosophila melanogaster, virus infection, single-fly respirometry, metabolismAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
Impact Journals (Aging's publisher) will be participating as an exhibitor at the American Association for Cancer Research (AACR) Annual Meeting 2023 from April 14-19 at the Orange County Convention Center in Orlando, Florida. This year, the AACR meeting theme is: “Advancing the Frontiers of Cancer Science and Medicine.”Impact Journals publishes scholarly journals in the biomedical sciences with a focus on all areas of cancer and aging research. Aging is one of the most prominent journals published by Impact Journals. Aging’s 2021 Impact Factor is 5.955. This number has increased from 2020’s 5.682.Visit booth No. 2642 at the AACR Annual Meeting 2023 to connect with members of the Aging team.Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, aacr, conference, meeting, annual meeting, cancer researchAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
A new research paper was published in Aging (Aging-US) Volume 15, Issue 6, entitled, “Potential reversal of biological age in women following an 8-week methylation-supportive diet and lifestyle program: a case series.”In this new study, researchers Kara N. Fitzgerald, Tish Campbell, Suzanne Makarem, and Romilly Hodges from the Institute for Functional Medicine, Virginia Commonwealth University and the American Nutrition Association reported on a case series of six women who completed a methylation-supportive diet and lifestyle program designed to impact DNA methylation and measures of biological aging. “The modifiable lifestyle intervention used by participants in this case series was first investigated in a pilot clinical trial in which participants (all men between the ages of 50-72 years) reduced their biological age by an average of 3.23 years as compared to controls [7]. The case series reported on herein was conducted to further the investigation of a modifiable lifestyle intervention that was largely the same in other populations; importantly in women.”The team carried out an intervention consisting of an eight-week program. This program included guidance on diet, sleep, exercise, and relaxation, supplemental probiotics and phytonutrients and nutritional coaching. DNA methylation and biological age analysis (Horvath DNAmAge clock (2013), normalized using the SeSAMe pipeline [a]) was conducted on blood samples at baseline and at the end of the eight-week period. Five of the six participants exhibited a biological age reduction of between 1.22 and 11.01 years from their baseline biological age. There was a statistically significant (p=.039) difference in the participants' mean biological age before (55.83 years) and after (51.23 years) the 8-week diet and lifestyle intervention, with an average decrease of 4.60 years. The average chronological age at the start of the program was 57.9 years and all but one participant had a biological age younger than their chronological age at the start of the program, suggesting that biological age changes were unrelated to disease improvement and instead might be attributed to underlying aging mechanisms.“This case series of women participants extends the previous pilot study of this intervention in men, indicating that favorable biological age changes may be achievable in both sexes. In addition, the investigation of otherwise-healthy individuals, rather than those with diagnosed disease, suggests an influence directly on underlying mechanisms of aging instead of disease-driven aging.”DOI: https://doi.org/10.18632/aging.204602 Corresponding Author: Kara N. Fitzgerald - kf@drkarafitzgerald.com Keywords: DNA methylation, epigenetic aging, lifestyle, biological clockSign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204602About Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
A new research paper was published on the cover of Aging (Aging-US) Volume 15, Issue 6, entitled, “Cellular senescence and disrupted proteostasis induced by myotube atrophy are prevented with low-dose metformin and leucine cocktail.”Aging coincides with the accumulation of senescent cells within skeletal muscle that produce inflammatory products, known as the senescence-associated secretory phenotype, but the relationship of senescent cells to muscle atrophy is unclear. Previously, researchers found that a metformin + leucine (MET+LEU) treatment had synergistic effects in aged mice to improve skeletal muscle structure and function during disuse atrophy. In this new study, researchers Jonathan J. Petrocelli, Naomi M.M.P. de Hart, Marisa J. Lang, Elena M. Yee, Patrick J. Ferrara, Dennis K. Fix, Amandine Chaix, Katsuhiko Funai, and Micah J. Drummond from the University of Utah aimed to determine the mechanisms by which MET+LEU exhibits muscle atrophy protection in vitro and if this occurs through cellular senescence. “The purpose of this study was to identify the skeletal muscle cell-intrinsic effects of MET+LEU during an atrophy stimulus. Secondarily, we sought to determine the possible mechanisms underlying MET+LEU action on skeletal muscle cells with an emphasis on cellular senescence.”C2C12 myoblasts differentiated into myotubes were used to determine MET+LEU mechanisms during atrophy. Additionally, aged mouse single myofibers and older human donor primary myoblasts were individually isolated to determine the translational potential of MET+LEU on muscle cells. MET+LEU (25 + 125 μM) treatment increased myotube differentiation and prevented myotube atrophy. Low concentration (0.1 + 0.5 μM) MET+LEU had unique effects to prevent muscle atrophy and increase transcripts related to protein synthesis and decrease transcripts related to protein breakdown. Myotube atrophy resulted in dysregulated proteostasis that was reversed with MET+LEU and individually with proteasome inhibition (MG-132). Inflammatory and cellular senescence transcriptional pathways and respective transcripts were increased following myotube atrophy yet reversed with MET+LEU treatment. Dasatinib + quercetin (D+Q) senolytic prevented myotube atrophy similar to MET+LEU. Finally, MET+LEU prevented loss in myotube size in alternate in vitro models of muscle atrophy as well as in aged myofibers while, in human primary myotubes, MET+LEU prevented reductions in myonuclei fusion. These data support that MET+LEU has skeletal muscle cell-autonomous properties to prevent atrophy by reversing senescence and improving proteostasis.“In conclusion, this study provides evidence of a possible link between cellular senescence and disrupted proteostasis that is targeted by MET+LEU in muscle cells to reverse the muscle atrophy phenotype.”DOI: https://doi.org/10.18632/aging.204600 Corresponding Author: Micah J. Drummond - micah.drummond@hsc.utah.edu Keywords: skeletal muscle atrophy, inflammation, senolytic, AMPK, protein breakdownAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Visit our website at https://www.Aging-US.com and connect with us:Facebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/MEDIA@IMPACTJOURNALS.COM
A new editorial paper was published in Aging (Aging-US) Volume 15, Issue 5, entitled, “Senescence and extracellular vesicles: novel partners in vascular amyloidosis.”In their editorial, researchers Meredith Whitehead, Marco Antonazzi and Catherine M. Shanahan from King’s College London discussed amyloidosis—a prevalent age-associated pathology caused by the accumulation of fibrous, insoluble protein fibrils in tissues. The most common human amyloid is aortic medial amyloid (AMA), caused by aggregation of a 50-amino acid peptide called medin, which is cleaved by an unknown mechanism from its parent protein, milk fat globulin EGF-factor 8 (MFGE8). Medin is present in the vessel wall of 97% of Caucasians aged over 50- years ,yet despite its prevalence in the ageing population there is a very limited understanding of the mechanisms driving AMA.“Despite several forms of amyloidosis, including AMA and Alzheimer’s disease (AD), being frequently associated with ageing, there has been limited research to date on the effect of cellular ‘ageing’, termed senescence, on amyloidosis.”The novel data presented in the paper by Whitehead et al. provides evidence that vascular smooth muscle cell (VSMC)-derived small extracellular vesicles (sEVs) are key mediators of medin accumulation in the vessel wall. In addition, the authors identify, for the first time, a role for cellular senescence in triggering amyloidosis via changes in sEVs and extracellular matrix (ECM) composition. Thus, this study not only advances our understanding of how AMA is formed but uncovers potential therapeutic targets for mitigating the detrimental effects of amyloidosis on tissue function.“Further work is now required to understand the relationships between cellular ageing pathways, different forms of amyloidosis and potentially other ageing pathologies with shared mechanisms, such as vascular calcification, that often occur concomitantly within the aged ECM.”Full Editorial: DOI: https://doi.org/10.18632/aging.204571 Corresponding Author: Catherine M. Shanahan -cathy.shanahan@kcl.ac.uk Keywords: amyloid, smooth muscle cells, senescence,extracellular vesicles, medinSign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204571About Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
A new editorial paper was published in Aging (Aging-US) Volume 15, Issue 5, entitled, “Parsing chronological and biological age effects on vaccine responses.”Researchers Chris P. Verschoor and George A. Kuchel from Health Sciences North Research Institute in Ontario, Canada, began this editorial by writing that the COVID-19 pandemic illustrated that older age, particularly when accompanied by common chronic illnesses of aging, is arguably the most significant population attributable factor for severe outcomes of acute respiratory infection, including the risk of hospitalization, disability and death.“In the absence of widely available and highly effective treatments, vaccines remain our most powerful tool to help overcome this vulnerability through the prevention of primary infection, and far more importantly, by improving clinical outcomes once infection does take place.”In the case of SARS-CoV-2, vaccine effectiveness (VE) against hospitalization was remarkable for dominant strains prior to omicron, whereas for influenza or Streptococcus pneumoniae VE ranges from 80% to <10%, depending on the season and infecting strain/serotype. Nonetheless, for all three pathogens VE decreases with age, which is caused by deficiencies in the capacity of older adults’ immune systems to mount productive and persistent antibody and/or cell-mediated responses to the vaccine. Given that extremely large, costly and typically lengthy clinical trials are often required to estimate VE reliably, the vast majority of human vaccine studies assess immune correlates of protection as a proxy to VE. For these studies, antibody related parameters such as neutralization capacity are most commonly employed since they are generally simpler from a technical standpoint and many have been rigorously standardized.“Although informative, cross-sectional studies comparing immune parameters across age groups to understand ‘immune aging’ risk ignore the degree to which departures from healthy aging might contribute.”Full Editorial: DOI: https://doi.org/10.18632/aging.204572 Corresponding Author: Chris P. Verschoor - cverschoor@hsnri.ca Keywords: biological age, frailty, vaccination, influenzaSign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204572Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
Blog summary of a research paper published in Volume 15, Issue 5 of Aging (Aging-US): “Cellular senescence with SASP in periodontal ligament cells triggers inflammation in aging periodontal tissue.”_____________________________________________Repercussions of poor dental health aren’t limited to mere social stigmas. Poor dental health can impart serious consequences on an individual’s overall health. Periodontal disease broadly refers to any disease that affects the gums and the surrounding tissues that support the teeth, including the periodontal ligament (PDL) and alveolar bone. Periodontal disease can increase the risk of heart disease, stroke and diabetes by allowing bacteria to enter the bloodstream, causing inflammation and organ damage. Periodontitis is a more advanced stage of periodontal disease. It is thought to be the most common infectious disease in the United States—affecting more than 40% of adults over 30 years old. Previous research has suggested that aging is a significant risk factor for periodontitis, although the underlying mechanisms are unclear.“The direct cause of periodontitis is periodontopathic bacteria, while various environmental factors affect the severity of periodontitis. Previous epidemiological studies have shown positive correlations between aging and periodontitis. However, whether and how aging is linked to periodontal health and disease in biological processes is poorly understood.”Full blog - https://aging-us.org/2023/03/a-promising-approach-to-preventing-periodontitis/DOI - https://doi.org/10.18632/aging.204569Corresponding author - Motozo Yamashita - yamashita.motozou.dent@osaka-u.ac.jpSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204569Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, cellular senescence, periodontitis, periodontal ligament, SASP, microRNAs, SIRT1About Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
A new research paper was published in Aging (Aging-US) Volume 15, Issue 5, entitled, “Age-related methylation changes in the human sperm epigenome.”Advanced paternal age is associated with increased risks for reproductive and offspring medical problems. Accumulating evidence suggests age-related changes in the sperm epigenome as one underlying mechanism. In a recent study, researchers Laura Bernhardt, Marcus Dittrich, Andreas Prell, Ramya Potabattula, Charis Drummer, Rüdiger Behr, Thomas Hahn, Martin Schorsch, Tobias Müller, and Thomas Haaf from Julius Maximilians University, Partner Site Göttingen and Fertility Center Wiesbaden performed reduced representation bisulfite sequencing (RRBS) on 73 sperm samples of males attending a fertility center in Germany.“[...] we identified 1,162 (74%) regions which were significantly (FDR-adjusted) hypomethylated and 403 regions (26%) being hypermethylated with age.” There were no significant correlations with paternal BMI, semen quality, or ART outcome. The majority (1,152 of 1,565; 74%) of age-related differentially methylated regions (ageDMRs) were located within genic regions, including 1,002 genes with symbols. Hypomethylated ageDMRs were closer to transcription start sites than hypermethylated DMRs, half of which reside in gene-distal regions. In this and conceptually related genome-wide studies, so far 2,355 genes have been reported with significant sperm ageDMRs, however most (90%) of them in only one study. The 241 genes which have been replicated at least once showed significant functional enrichments in 41 biological processes associated with development and the nervous system and in 10 cellular components associated with synapses and neurons. This supports the hypothesis that paternal age effects on the sperm methylome affect offspring behavior and neurodevelopment. The researchers found it interesting to note that sperm ageDMRs were not randomly distributed throughout the human genome; chromosome 19 showed a highly significant twofold enrichment with sperm ageDMRs. Although the high gene density and CpG content have been conserved, the orthologous marmoset chromosome 22 did not appear to exhibit an increased regulatory potential by age-related DNA methylation changes.“Collectively, our data support the conclusion that age-induced methylation changes in the sperm epigenome contribute to the increased offspring disease susceptibility for neurodevelopmental disorders.”DOI: https://doi.org/10.18632/aging.204546 Corresponding Author: Thomas Haaf - thomas.haaf@uni-wuerzburg.de Keywords: ART outcome, DNA methylation, male germ cells, paternal age effect, human sperm epigenomeSign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204546Keywords - aging, ART outcome, DNA methylation, male germ cells, paternal age effect, human sperm epigenomeAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/MEDIA@IMPACTJOURNALS.COM
Ariel K. Frame, PhD Candidate in the Neuroscience program at Western University, London, Canada, discusses a research paper he co-authored that was published by Aging (Aging-US) in Volume 15, Issue 4, entitled, “Aging and memory are altered by genetically manipulating lactate dehydrogenase in the neurons or glia of flies.”DOI - https://doi.org/10.18632/aging.204565Corresponding authors - Ariel K. Frame - aframe@uwo.ca, and Robert C. Cumming - rcummin5@uwo.caAbstractThe astrocyte-neuron lactate shuttle hypothesis posits that glial-generated lactate is transported to neurons to fuel metabolic processes required for long-term memory. Although studies in vertebrates have revealed that lactate shuttling is important for cognitive function, it is uncertain if this form of metabolic coupling is conserved in invertebrates or is influenced by age. Lactate dehydrogenase (Ldh) is a rate limiting enzyme that interconverts lactate and pyruvate. Here we genetically manipulated expression of Drosophila melanogaster lactate dehydrogenase (dLdh) in neurons or glia to assess the impact of altered lactate metabolism on invertebrate aging and long-term courtship memory at different ages. We also assessed survival, negative geotaxis, brain neutral lipids (the core component of lipid droplets) and brain metabolites. Both upregulation and downregulation of dLdh in neurons resulted in decreased survival and memory impairment with age. Glial downregulation of dLdh expression caused age-related memory impairment without altering survival, while upregulated glial dLdh expression lowered survival without disrupting memory. Both neuronal and glial dLdh upregulation increased neutral lipid accumulation. We provide evidence that altered lactate metabolism with age affects the tricarboxylic acid (TCA) cycle, 2-hydroxyglutarate (2HG), and neutral lipid accumulation. Collectively, our findings indicate that the direct alteration of lactate metabolism in either glia or neurons affects memory and survival but only in an age-dependent manner.Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204565Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsKeywords - aging, astrocyte-neuron lactate shuttle (ANLS), lactate, lactate dehydrogenase, dLdh, Drosophila melanogaster, glia, long-term memory, courtship conditioningAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
A new research paper was published in Aging (Aging-US) Volume 15, Issue 5, entitled, “Senescence-associated exosomes transfer miRNA-induced fibrosis to neighboring cells.”Radiation-induced fibrosis is a common side effect of radiotherapy, which is the most common treatment for cancer. However, radiation also causes p53-mediated cell cycle arrest, prolonged expression of p21, and the development of senescence in normal cells that reside in irradiated tissues. Bone marrow-derived mesenchymal stem cells (MSCs) accumulate in primary tumor sites because of their natural tropism for inflammatory and fibrotic tissues. MSCs are extremely sensitive to low doses of ionizing radiation and acquire senescence as a result of bystander radiation effects. Senescent cells remain metabolically active but develop a potent senescence-associated secretory phenotype (SASP) that correlates to hyperactive secretion of cytokines, pro-fibrotic growth factors, and exosomes (EXOs). Integrative pathway analysis has highlighted that radiation-induced senescence significantly enriched cell-cycle, extracellular matrix, transforming growth factor-β (TGF-β) signaling, and vesicle-mediated transport genes in MSCs. EXOs are cell-secreted nanovesicles (a subclass of small extracellular vesicles) that contain biomaterials—proteins, RNAs, microRNAs (miRNAs)—that are critical in cell-cell communication. miRNA content analysis of secreted EXOs further revealed that radiation-induced senescence uniquely altered miRNA profiles. “In fact, several of the standout miRNAs directly targeted TGF-β or downstream genes.”In this new study, researchers Amy H. Lee, Deepraj Ghosh, Ivy L. Koh, and Michelle R. Dawson from Brown University further treated normal MSCs with senescence-associated EXOs (SA-EXOs) to examine bystander effects of radiation-induced senescence. The researchers found that these modulated genes were related to TGF-β pathway and elevated both alpha smooth muscle actin (protein increased in senescent, activated cells) and Ki-67 (proliferative marker) expression in SA-EXO treated MSCs compared to untreated MSCs. They revealed that SA-EXOs possess unique miRNA content that influence myofibroblast phenotypes via TGF-β pathway activation. This highlights that SA-EXOs are potent SASP factors that play a large role in cancer-related fibrosis.“Our integrated omics and EXO microarray analyses show that senescent MSCs possess differential transcriptional genes and secrete vesicles that contain unique post-transcriptional cargo. We subsequently demonstrated that these EXO miRNAs can play important roles in cell-cell communication during disease progression.”Paper: DOI: https://doi.org/10.18632/aging.204539 Corresponding Author: Michelle R. Dawson - michelle_dawson@brown.eduKeywords: radiation-induced senescence, exosomes (EXOs), microRNA (miRNA), transforming growth factor-β (TGF-β), mesenchymal stem cells (MSCs) About Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
A new research paper was published on the cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 5, entitled, “AAV1.NT-3 gene therapy prevents age-related sarcopenia.”Sarcopenia is progressive loss of muscle mass and strength occurring during normal aging with significant consequences on the quality of life for elderly. Neurotrophin 3 (NT-3) is an important autocrine factor supporting Schwann cell survival and differentiation and stimulating axon regeneration and myelination. NT-3 is involved in the maintenance of neuromuscular junction (NMJ) integrity, restoration of impaired radial growth of muscle fibers through activation of the Akt/mTOR pathway.In this new study, researchers Burcak Ozes, Lingying Tong, Morgan Myers, Kyle Moss, Alicia Ridgley, and Zarife Sahenk from Nationwide Children’s Hospital and The Ohio State University used a triple muscle-specific creatine kinase (tMCK) promoter to restrict NT-3 expression to the skeletal muscle and self-complimentary adeno-associated virus serotype 1 (scAAV1) as vector to assess the therapeutic efficacy of AAV1.NT-3 in wild type-aged C57BL/6J mice, a model for natural aging and sarcopenia.“Quantitative histopathologic parameters served to address age-related changes in muscle, peripheral nerve and NMJ.”The treatment efficacy was assessed at 6 months post-injection using run to exhaustion and rotarod tests, in vivo muscle contractility assay, and histopathological studies of the peripheral nervous system, including NMJ connectivity and muscle. AAV1.NT-3 gene therapy in WT-aged C57BL/6 mice resulted in functional and in vivo muscle physiology improvements, supported by quantitative histology from muscle, peripheral nerves and NMJ. Hindlimb and forelimb muscles in the untreated cohort showed the presence of a muscle- and sex-dependent remodeling and fiber size decrease with aging, which was normalized toward values obtained from 10 months old WT mice with treatment. The molecular studies assessing the NT-3 effect on the oxidative state of distal hindlimb muscles, accompanied by western blot analyses for mTORC1 activation were in accordance with the histological findings. “When considering the burden of sarcopenia on the lifestyle of elderly, and on the healthcare system, we believe this preclinical study is providing strong support for AAV.NT-3 gene therapy in the successful management of sarcopenia, as a serious and plausible option in the future.”DOI: https://doi.org/10.18632/aging.204577 Corresponding Author: Zarife Sahenk - zarife.sahenk@nationwidechildrens.org Keywords: sarcopenia, gene therapy, aging, NT-3, muscle remodelingSign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204577About Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
Aging (Aging-US) published a new editorial paper in Volume 15, Issue 4, entitled, “Cognitive aging and dementia prevention: the time for psychology?”Modifiable risk and protective factors (e.g. engaging in active lifestyles and avoiding alcohol or smoking amongst others) are seen as key agents for dementia prevention, and they also exert an important effect on cognitive trajectories of non-demented older adults. In this new editorial, researchers David Bartrés-Faz, Cristina Solé-Padullés and Natalie L. Marchant from the University of Barcelona discuss recent research that has begun to identify psychological processes that confer relative risk and protection. “For example, repetitive negative thinking (RNT), a cognitive process defined by selfrelevant, persistent thoughts that elaborate on negative themes, has been associated with greater burden of typical Alzheimer’s disease (AD) pathological brain markers and accelerated cognitive decline over time [3].”In contrast, self-reflection, as well as purpose in life and other components of psychological well being, may help to maintain cognition and boost cognitive resilience against neuropathological burden. The possibility of incorporating psychological elements as key players in affecting one of the most important public health issues of the century opens a window of great therapeutic opportunity, particularly because fundamental psychological processes are at the core of cognitive-behavioral interventions that may help reduce dementia risk. However, for this emergent area to develop and wield maximum benefit, major unanswered questions need to be addressed. In their editorial, the researchers highlight three main areas for future research. “In summary, we propose that with momentum gathering, now is the time for psychology to make important contributions to cognitive ageing and dementia prevention research.”Full Paper: DOI: https://doi.org/10.18632/aging.204562 Corresponding Author: David Bartrés-Faz - dbartres@ub.edu Keywords: cognitive aging, psychological factors, dementia, preventionSign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204562Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
Blog summary of a research paper published in Aging (Aging-US) Volume 15, Issue 4: "Aging and memory are altered by genetically manipulating lactate dehydrogenase in the neurons or glia of flies."__________________________________________________________The brain is a complex organ responsible for many critical functions, including the formation and retrieval of our memories. As we age, the brain undergoes changes that can affect cognitive abilities, including our memory. Understanding the mechanisms that underlie these changes is critical for developing therapies for age-related cognitive decline. “Over the last two decades there has been growing recognition that lactate, the end product of glycolysis, serves many functions, including acting as a source of energy, a signaling molecule, and even as an epigenetic regulator.”Lactate is a molecule that is produced during the metabolism of glucose in the body. It is a byproduct of anaerobic metabolism, which occurs when there is insufficient oxygen supply to meet the energy demands of the body. Lactate can be used as an energy source by some cells, such as the heart and skeletal muscles, and it can also be transported to the liver where it can be converted back into glucose.Lactate dehydrogenase (LDH), on the other hand, is an enzyme that catalyzes the conversion of pyruvate to lactate (the reverse reaction of lactate production) and is also involved in other metabolic processes. This enzyme is found in many tissues of the body, including the heart, liver and skeletal muscles, and is released into the bloodstream when tissues are damaged. LDH is often used as a diagnostic marker for various medical conditions, such as heart attacks, liver disease and certain cancers. High levels of LDH in the blood may indicate tissue damage or cell death, while low levels may indicate a deficiency in the enzyme.Blog - https://aging-us.org/2023/03/fruit-flies-shed-new-light-on-memory-and-aging/DOI - https://doi.org/10.18632/aging.204565Corresponding authors - Ariel K. Frame - aframe@uwo.ca, and Robert C. Cumming - rcummin5@uwo.caSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204565Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alertsAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/MEDIA@IMPACTJOURNALS.COM
Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) published a new research paper in Volume 15, Issue 4, entitled, “Isoform-specific effects of neuronal repression of the AMPK catalytic subunit on cognitive function in aged mice.”AMP-activated protein kinase (AMPK) functions as a molecular sensor that plays a critical role in maintaining cellular energy homeostasis. Dysregulation of the AMPK signaling has been linked to synaptic failure and cognitive impairments. In a recent study, researchers Xueyan Zhou, Wenzhong Yang, Xin Wang, and Tao Ma from Wake Forest University School of Medicine demonstrated abnormally increased AMPK activity in the hippocampus of aged mice. The kinase catalytic subunit of AMPK exists in two isoforms α1 and α2, and their specific roles in aging-related cognitive deficits are unknown. “Taking advantage of the unique transgenic mice (AMPKα1/α2 cKO) recently developed by our group, we investigated how isoform-specific suppression of the neuronal AMPKα may contribute to the regulation of cognitive and synaptic function associated with aging.” The team found that aging-related impairment of long-term object recognition memory was improved with suppression of AMPKα1 but not AMPKα2 isoform. Moreover, aging-related spatial memory deficits were unaltered with suppression of either AMPKα isoform. Biochemical experiments showed that the phosphorylation levels of the eukaryotic initiation factor 2 α subunit (eIF2α) were specifically decreased in the hippocampus of the AMPKα1 cKO mice. They further performed large-scale unbiased proteomics analysis and revealed identities of proteins whose expression is differentially regulated with AMPKα isoform suppression. These novel findings may provide insights into the roles of AMPK signaling pathway in cognitive aging.“In summary, the current study reported that suppression of neuronal AMPKα1 isoform can improve aging-related impairments of long-term recognition memory.”Full Paper: DOI: https://doi.org/10.18632/aging.204554 Corresponding Author: Tao Ma - tma@wakehealth.edu Keywords: AMPK, aging, protein synthesis, learning and memory, proteomicsSign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204554About Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
Aging (listed as "Aging (Albany NY)" by MEDLINE/PubMed and "Aging-US" by Web of Science) published a new review paper in Volume 15, Issue 4, entitled, “Cellular senescence: when growth stimulation meets cell cycle arrest.”In this review, researcher Mikhail V. Blagosklonny, M.D., Ph.D., from Roswell Park Comprehensive Cancer Center discusses cellular senescence—a natural process that occurs as cells age and eventually stop dividing. Recent research has revealed that cellular senescence can also be triggered by hypertrophy and hyperfunctions.“At the very moment of cell-cycle arrest, the cell is not senescent yet. For several days in cell culture, the arrested cell is acquiring a senescent phenotype. What is happening during this geroconversion? Cellular enlargement (hypertrophy) and hyperfunctions (lysosomal and hyper-secretory) are hallmarks of geroconversion.”In his comprehensive review paper, Dr. Blagosklonny explores the complex relationship between growth stimulation and cell cycle arrest in cellular senescence. He discusses the various mechanisms that can lead to senescence, markers of senescence and geroconversion, and the importance of understanding these mechanisms and markers in the development of anti-aging drugs.“The same pathways that drive geroconversion are involved in organismal aging and age-related diseases. The same drugs that slow down geroconversion also extend lifespan, as tested in animals so far. Targets of gerostatics (e.g., mTOR, PI3K) are involved in aging of animals from worms to mammals. Therefore, gerostatics are anti-aging drugs. The model of geroconversion is useful to discover anti-aging drugs.”Dr. Blagosklonny is a renowned expert in the field of aging research. He has focused on the molecular mechanisms of aging, the hyperfunction theory of aging and the development of new drugs to combat age-related diseases. Dr. Blagosklonny’s research, perspectives and reviews have made significant contributions to our understanding of aging.Full Paper: DOI: https://doi.org/10.18632/aging.204543 Corresponding Author: Mikhail V. Blagosklonny - Blagosklonny@oncotarget.com, Blagosklonny@rapalogs.com Keywords: rapamycin, mTOR, hyperfunction theory of aging, cell volume and enlargement, gerogenic conversionSign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204543
A new research paper was published on the cover of Aging (Aging-US) Volume 15, Issue 4, entitled, “Relationship between telomere shortening and early subjective depressive symptoms and cognitive complaints in older adults.”Telomere length (TL) has been reported to be associated with depression and cognitive impairment in elderly. Early detection of depression and cognitive impairment is important to delay disease progression. Therefore, in this new study, researchers Myung-Hoon Han, Eun-Hye Lee2, Hyun-Hee Park, Seong Hye Choi, and Seong-Ho Koh from Hanyang University and Inha University aimed to identify whether TL is associated with early subjective depressive symptoms and cognitive complaints among healthy elderly subjects. “Several hypotheses have been proposed to explain the emergence of a prematurely aged phenotype in late-life depression, such as glucocorticoid cascade dysregulation, increased allostatic load, and telomere shortening [10, 12].”This study was a multicenter, outcome assessor-blinded, 24-week, randomized controlled trial (RCT). Measurement of questionnaire and physical activity scores and blood sample analyses were performed at baseline and after six months of follow-up in all study participants. Linear regression analyses were performed to identify whether early subjective depressive symptoms, cognitive complaints, and several blood biomarkers are associated with TL. Altogether, 137 relatively healthy elderly individuals (60–79 years old) were enrolled in this prospective RCT. The team observed an approximate decrease of 0.06 and 0.11−0.14 kbps of TL per one point increase in the geriatric depression scale and cognitive complaint interview scores, respectively, at baseline and after six months of follow-up. They also found an approximate decrease of 0.08−0.09 kbps of TL per one point increase in interleukin (IL)-6 levels at baseline and after six months of follow-up. “In conclusion, we showed that both early subjective depressive symptoms and cognitive complaints in relatively healthy elderly individuals were associated with a relatively shorter TL in the randomized controlled prospective SUPERBRAIN study. In addition, a shorter TL was associated with increased IL-6 levels in our study participants. We believe that IL-6, an inflammatory cytokine, plays an important role in the relationship of shortening TL with early subjective depressive mood and cognitive complaints. Although the results will need to be verified through a large-scale RCT in the future, we believe that our findings will help prevent and treat depression and cognitive impairment in the healthy elderly.”DOI: https://doi.org/10.18632/aging.204533 Corresponding Authors: Seong Hye Choi - seonghye@inha.ac.kr, Seong-Ho Koh - ksh213@hanyang.ac.kr Sign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204533Keywords - aging, telomere length, cognitive complaint, depressive symptom, interleukin-6About Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/MEDIA@IMPACTJOURNALS.COM
Listen to a blog summary of a trending research paper published in Volume 15, Issue 3 of Aging (Aging-US), entitled, "The lipidomes of C. elegans with mutations in asm-3/acid sphingomyelinase and hyl-2/ceramide synthase show distinct lipid profiles during aging."__________________________________________________Lipids are a diverse group of biomolecules that are essential for life, including fats, oils, waxes, and steroids, and play crucial roles in cell membrane structure, energy storage and signaling. Lipidomics is the comprehensive analysis of lipids and their interactions in biological systems, with an aim to understand the role of lipids in cellular processes and their association with diseases. As we age, our cells undergo complex changes, including alterations in cellular lipid profiles. These changes are not only confined to humans; organisms such as the nematode Caenorhabditis elegans (C. elegans) are also subject to changes in lipid composition during aging. “For example, lipid classes including fatty acids (FA), triacylglycerols (TAG), sphingolipids (SL), and phospholipids (PL) have been identified as targets in lipid signatures related to aging [2, 3]. Furthermore, specific signatures are detected in the lipid profiles of those with age-related diseases, such as Alzheimer’s Disease [4–9]. In addition, the abundance of many fatty acid subtypes differs between the youth, elderly, and centenarians [10, 11].”In a recent study, researchers Trisha A. Staab, Grace McIntyre, Lu Wang, Joycelyn Radeny, Lisa Bettcher, Melissa Guillen, Margaret P. Peck, Azia P. Kalil, Samantha P. Bromley, Daniel Raftery, and Jason P. Chan from Marian University, the University of Washington and Juniata College investigate the lipid profiles of C. elegans with mutations in the genes asm-3/acid sphingomyelinase and hyl-2/ceramide synthase during aging. On February 13, 2023, their research paper was published in Aging’s Volume 15, Issue 3, entitled, “The lipidomes of C. elegans with mutations in asm-3/acid sphingomyelinase and hyl-2/ceramide synthase show distinct lipid profiles during aging.”Full blog - https://aging-us.org/2023/02/the-role-of-lipids-in-aging-insights-from-c-elegans/DOI - https://doi.org/10.18632/aging.204515Corresponding author - Jason P. Chan - jpchan@me.comKeywords - lipidomics, aging, sphingolipid metabolism, C. elegans, fatty acid metabolismAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
A new research paper was published in Aging (listed as "Aging (Albany NY)" by MEDLINE/PubMed and "Aging-US" by Web of Science) Volume 15, Issue 3, entitled, “Metformin use history and genome-wide DNA methylation profile: potential molecular mechanism for aging and longevity.”Metformin, a commonly prescribed anti-diabetic medication, has repeatedly been shown to hinder aging in pre-clinical models and to be associated with lower mortality for humans. It is, however, not well understood how metformin can potentially prolong lifespan from a biological standpoint. In this recent study, researchers Pedro S. Marra, Takehiko Yamanashi, Kaitlyn J. Crutchley, Nadia E. Wahba, Zoe-Ella M. Anderson, Manisha Modukuri, Gloria Chang, Tammy Tran, Masaaki Iwata, Hyunkeun Ryan Cho, and Gen Shinozaki from Stanford University School of Medicine, University of Iowa, Tottori University Faculty of Medicine, University of Nebraska Medical Center College of Medicine, and Oregon Health and Science University School of Medicine hypothesized that metformin’s potential mechanism of action for longevity is through its epigenetic modifications.“To test our hypothesis, we conducted a post-hoc analysis of available genome-wide DNA methylation (DNAm) data obtained from whole blood collected from inpatients with and without a history of metformin use.”The researchers assessed the methylation profile of 171 patients (first run) and only among 63 diabetic patients (second run) and compared the DNAm rates between metformin users and nonusers. Enrichment analysis from the Kyoto Encyclopedia of Genes and Genome (KEGG) showed pathways relevant to metformin’s mechanism of action, such as longevity, AMPK and inflammatory pathways. They also identified several pathways related to delirium whose risk factor is aging. Moreover, top hits from the Gene Ontology (GO) included HIF-1α pathways. However, no individual CpG site showed genome-wide statistical significance (p < 5E-08).“This study may elucidate metformin’s potential role in longevity through epigenetic modifications and other possible mechanisms of action.”Read the Full Paper: DOI: https://doi.org/10.18632/aging.204498 Corresponding Author: Gen Shinozaki - gens@stanford.edu Keywords: metformin, longevity, diabetes, epigenetics, aging, inflammation, methylationSign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204498About Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/agingusLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
Crossref is a non-profit organization that logs and updates citations for scientific publications. Below are Crossref’s Top 10 Aging DOIs in 2022.10: DNA- and telomere-damage does not limit lifespan: evidence from rapamycinDOI: https://doi.org/10.18632/aging.202674Author: Mikhail V. Blagosklonny9: Psychological factors substantially contribute to biological aging: evidence from the aging rate in Chinese older adultsDOI: https://doi.org/10.18632/aging.204264Authors: Fedor Galkin, Kirill Kochetov, Diana Koldasbayeva, Manuel Faria, Helene H. Fung, Amber X. Chen, and Alex Zhavoronkov8: DNA methylation GrimAge strongly predicts lifespan and healthspanDOI: https://doi.org/10.18632/aging.101684Authors: Ake T. Lu, Austin Quach, James G. Wilson, Alex P. Reiner, Abraham Aviv, Kenneth Raj, Lifang Hou, Andrea A. Baccarelli, Yun Li, James D. Stewart, Eric A. Whitsel, Themistocles L. Assimes, Luigi Ferrucci, and Steve Horvath7: Hallmarks of aging-based dual-purpose disease and age-associated targets predicted using PandaOmics AI-powered discovery engineDOI: https://doi.org/10.18632/aging.203960Authors: Frank W. Pun, Geoffrey Ho Duen Leung, Hoi Wing Leung, Bonnie Hei Man Liu, Xi Long, Ivan V. Ozerov, Ju Wang, Feng Ren, Alexander Aliper, Evgeny Izumchenko, Alexey Moskalev, João Pedro de Magalhães, and Alex Zhavoronkov6: CircRNA_100367 regulated the radiation sensitivity of esophageal squamous cell carcinomas through miR-217/Wnt3 pathwayDOI: https://doi.org/10.18632/aging.102580Authors: Junqi Liu, Nannan Xue, Yuexin Guo, Kerun Niu, Liang Gao, Song Zhang, Hao Gu, Xin Wang, Di Zhao, and Ruitai Fan5: Five years of exercise intervention at different intensities and development of white matter hyperintensities in community dwelling older adults, a Generation 100 sub-studyDOI: https://doi.org/10.18632/aging.203843Authors: Anette Arild, Torgil Vangberg, Hanne Nikkels, Stian Lydersen, Ulrik Wisløff, Dorthe Stensvold, and Asta K. Håberg4: The aging-related risk signature in colorectal cancerDOI: https://doi.org/10.18632/aging.202589Authors: Taohua Yue, Shanwen Chen, Jing Zhu, Shihao Guo, Zhihao Huang, Pengyuan Wang, Shuai Zuo, and Yucun Liu3: An epigenetic biomarker of aging for lifespan and healthspanDOI: https://doi.org/10.18632/aging.101414Authors: Morgan E. Levine, Ake T. Lu, Austin Quach, Brian H. Chen, Themistocles L. Assimes, Stefania Bandinelli, Lifang Hou, Andrea A. Baccarelli, James D. Stewart, Yun Li, Eric A. Whitsel, James G Wilson, Alex P Reiner, Abraham Aviv, Kurt Lohman, Yongmei Liu, Luigi Ferrucci, and Steve Horvath2: Nrf2 inhibits ferroptosis and protects against acute lung injury due to intestinal ischemia reperfusion via regulating SLC7A11 and HO-1DOI: https://doi.org/10.18632/aging.103378Authors: Hui Dong, Zhuanzhuan Qiang, Dongdong Chai, Jiali Peng, Yangyang Xia, Rong Hu, and Hong Jiang1: Optimizing future well-being with artificial intelligence: self-organizing maps (SOMs) for the identification of islands of emotional stabilityDOI: https://doi.org/10.18632/aging.204061Authors: Fedor Galkin, Kirill Kochetov, Michelle Keller, Alex Zhavoronkov, and Nancy Etcoff____________________About Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com.
A new research paper was published in Aging (listed as "Aging (Albany NY)" by MEDLINE/PubMed and "Aging-US" by Web of Science) Volume 15, Issue 3, entitled, “Epigenetic age and lung cancer risk in the CLUE II prospective cohort study.”Epigenetic age, a robust marker of biological aging, has been associated with obesity, low-grade inflammation and metabolic diseases. However, few studies have examined associations between different epigenetic age measures and risk of lung cancer, despite great interest in finding biomarkers to assist in risk stratification for lung cancer screening.In a recent study, researchers Dominique S. Michaud, Mei Chung, Naisi Zhao, Devin C. Koestler, Jiayun Lu, Elizabeth A. Platz, and Karl T. Kelsey from Tufts University, University of Kansas Medical Center, Johns Hopkins Bloomberg School of Public Health, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, and Brown University conducted a nested case-control analysis of 208 lung cancer cases and 208 matched controls with archived pre-diagnostic blood samples (from 1989). The case-control study is nested in the CLUE II cohort study, a predominantly White cohort of men and women, based in Maryland, USA.“It is important to examine whether epigenetic age is associated with lung cancer risk across multiple prospective studies to determine its utility as a potential biomarker to be considered for risk stratification in the selection of high-risk individuals for lung cancer screening.”Prediagnostic blood samples were collected in 1989 (CLUE II study baseline) and stored at −70°C. DNA was extracted from buffy coat and DNA methylation levels were measured using Illumina MethylationEPIC BeadChip Arrays. Three epigenetic age acceleration (i.e., biological age is greater than chronological age) measurements (Horvath, Hannum and PhenoAge) were examined in relation to lung cancer risk using conditional logistic regression. The researchers did not observe associations between the three epigenetic age acceleration measurements and risk of lung cancer overall; however, inverse associations for the two Hannum age acceleration measures (intrinsic and extrinsic) were observed in men and among younger participants, but not in women or older participants. Additionally, they did not observe effect modification by time from blood draw to diagnosis.“Findings from this study do not support a positive association between three different biological age acceleration measures and risk of lung cancer. Additional studies are needed to address whether epigenetic age is associated with lung cancer in never smokers.”Read the Full Paper: DOI: https://doi.org/10.18632/aging.204501 Corresponding Author: Dominique S. Michaud - Dominique.Michaud@tufts.edu Keywords: DNA methylation, epigenetic clocks, lung cancer, cohort studySign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204501About Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/
A new research paper was published on the cover of Aging (listed as "Aging (Albany NY)" by Medline/PubMed and "Aging-US" by Web of Science) Volume 15, Issue 3, entitled, “Immune-mediated platelet depletion augments Alzheimer’s disease neuropathological hallmarks in APP-PS1 mice.”In Alzheimer’s disease (AD), platelets become dysfunctional and might contribute to amyloid beta deposition. In a recent study, researchers Diana M. Bessa de Sousa, Ariane Benedetti, Barbara Altendorfer, Heike Mrowetz, Michael S. Unger, Katharina Schallmoser, Ludwig Aigner, and Kathrin Maria Kniewallner from Paracelsus Medical University and Austrian Cluster for Tissue Regeneration in Austria depleted platelets in one-year-old APP Swedish PS1 dE9 (APP-PS1) transgenic mice for five days, using intraperitoneal injections of an anti-CD42b antibody, and assessed changes in cerebral amyloidosis, plaque-associated neuritic dystrophy and gliosis. “The potential role of platelets in amyloid beta deposition led to the hypothesis that reducing platelet numbers might ameliorate AD pathology [30]. Here, we performed immune-mediated platelet depletion in APP-PS1 mice with an already fully developed amyloidosis and investigated its effects on classical hallmarks of AD: amyloid plaque pathology, plaque-associated neuritic dystrophy and gliosis.”In APP-PS1 female mice, platelet depletion shifted amyloid plaque size distribution towards bigger plaques and increased neuritic dystrophy in the hippocampus. In platelet-depleted females, plaque-associated Iba1+ microglia had lower amounts of fibrillar amyloid beta cargo and GFAP+ astrocytic processes showed a higher overlap with thioflavin S+ amyloid plaques. In contrast to the popular hypothesis that platelets foster plaque pathology, data from this study suggest that platelets might limit plaque growth and attenuate plaque-related neuritic dystrophy at advanced stages of amyloid plaque pathology in APP-PS1 female mice. Whether the changes in amyloid plaque pathology are due to a direct effect on amyloid beta deposition or are a consequence of altered glial function needs to be further elucidated.“In APP-PS1 females, acute thrombocytopenia aggravates AD neuropathology, suggesting that platelets might have a protective function in AD. However, the underlying molecular mechanisms by which platelets modulate amyloid plaque deposition remain elusive and need to be investigated in future experiments.”DOI: https://doi.org/10.18632/aging.204502Corresponding Author: Kathrin Maria Kniewallner - kathrin.drerup@pmu.ac.at Keywords: Alzheimer’s disease, platelets, amyloid-beta, microglia, astrocytesSign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204502About Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/@AgingJournalLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
Blog summary of "Epigenetic age acceleration correlates with BMI in young adults" published in Volume 15, Issue 2 of Aging (Aging-US).___________________________________________While the study of genetics focuses on heredity and alterations in the genetic code itself, epigenetics refers to the changes in gene expression that occur as a result of environmental or lifestyle factors. Advances in epigenetic research have allowed measures of DNA methylation (DNAm) (epigenetic clocks) to illustrate clear links between obesity, accelerated epigenetic aging and a variety of negative health outcomes in older adults. Despite these advances, there is a lack of research about these correlations and sex-based variations among young adults. The ability to detect accelerated epigenetic aging in young adulthood could potentially be used to prevent the onset of chronic diseases and improve health outcomes later in life.“Moreover, few studies have included replication across measures of obesity and epigenetic aging to examine the robustness or specificity of these effects. Finally, little is known about sex differences in the links between obesity and epigenetic aging, despite evidence of substantial sex dimorphism in both physiological and epigenetic aging [20].”In a recent study, researchers Christy Anne Foster, Malcolm Barker-Kamps, Marlon Goering, Amit Patki, Hemant K. Tiwari, and Sylvie Mrug from the University of Alabama at Birmingham’s Department of Pediatrics examined the relationship between obesity and measures of DNAm in young adults. They also investigated whether there is a sex-dependant correlation between obesity and DNAm in young adults. On January 18, 2023, their research paper was published in Aging’s Volume 15, Issue 2, and entitled, “Epigenetic age acceleration correlates with BMI in young adults.”Full blog - https://aging-us.org/2023/02/bmi-correlates-with-accelerated-epigenetic-aging-in-young-adults/DOI - https://doi.org/10.18632/aging.204492Corresponding author - Christy Anne Foster - cafoster@uabmc.eduSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204492Keywords - obesity, epigenetic aging, young adult, DNA methylation, epigenetic accelerationAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://youtube.com/Aging-USLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
A new research paper was published in Aging (listed as "Aging (Albany NY)" by MEDLINE/PubMed and "Aging-US" by Web of Science) Volume 15, Issue 2, entitled, “Body weight influences musculoskeletal adaptation to long-term voluntary wheel running during aging in female mice.”Aging increases the prevalence of sarcopenia and osteoporosis that are often both components of a musculoskeletal syndrome, osteosarcopenia. Osteosarcopenia is highly associated with frailty, falls, fractures, and disability, leading to decreased quality of life and increased morbidity and mortality. Frailty is the hallmark of aging that can be delayed with exercise. In this new research paper, researchers Yukiko Kitase, Julian A. Vallejo, Sarah L. Dallas, Yixia Xie, Mark Dallas, LeAnn Tiede-Lewis, David Moore, Anthony Meljanac, Corrine Kumar, Carrie Zhao, Jennifer Rosser, Marco Brotto, Mark L. Johnson, Ziyue Liu, Michael J. Wacker, and Lynda Bonewald from Indiana University, University of Missouri and University of Texas wrote that the present studies were initiated based on the hypothesis that long-term voluntary wheel running (VWR) in female mice from 12 to 18 or 22 months of age would have beneficial effects on the musculoskeletal system. “Frequently osteoporosis and sarcopenia occur concurrently. It is not known if one precedes the other or if one condition influences disease progression of the other condition [26, 27]. We hypothesized that long-term voluntary exercise started later in life (12 months of age) would improve both skeletal muscle and bone parameters in aging female mice up to 22 months.”Mice were separated into high (HBW) and low (LBW) body weight based on final body weights upon termination of experiments. Bone marrow fat was significantly higher in HBW than LBW under sedentary conditions, but not with VWR. HBW was more protective for soleus size and function than LBW under sedentary conditions, however VWR increased soleus size and function regardless of body weight. VWR plus HBW was more protective against muscle loss with aging. Similar effects of VWR plus HBW were observed with the extensor digitorum longus, EDL, however, LBW with VWR was beneficial in improving EDL fatigue resistance in 18 mo mice and was more beneficial with regards to muscle production of bone protective factors. VWR plus HBW maintained bone in aged animals. In summary, HBW had a more beneficial effect on muscle and bone with aging especially in combination with exercise. These effects were independent of bone marrow fat, suggesting that intrinsic musculoskeletal adaptions were responsible for these beneficial effects.”“Collectively, VWR has beneficial effects on bone health during advanced aging regardless of body weight, but VWR differentially alters bone parameters depending on body weight, with modifications in mechanical properties in LBW but structural modifications in HBW contributing to the prevention of osteopenia.”Full Paper: DOI: https://doi.org/10.18632/aging.204390 Corresponding Authors: Lynda Bonewald -bonewal@iu.edu, Michael J. Wacker - wackerm@umkc.edu About Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Website - https://www.Aging-US.comSoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://youtube.com/Aging-USLinkedIn - https://www.linkedin.com/company/aging/
A new research perspective was published in Aging (listed as "Aging (Albany NY)" by MEDLINE/PubMed and "Aging-US" by Web of Science) Volume 15, Issue 2, entitled, “Are menopause, aging and prostate cancer diseases?”In this new research perspective, researcher Mikhail (Misha) Blagosklonny M.D., Ph.D., from Roswell Park Comprehensive Cancer Center wrote in the abstract: “There is no doubt that prostate cancer is a disease. Then, according to hyperfunction theory, menopause is also a disease. Like all age-related diseases, it is a natural process, but is also purely harmful, aimless and unintended by nature. But exactly because these diseases (menopause, prostate enlargement, obesity, atherosclerosis, hypertension, diabetes, presbyopia and thousands of others) are partially quasi-programmed, they can be delayed by slowing aging. Is aging a disease? Aging is a quasi-programmed disease that is partially treatable by rapamycin. On the other hand, aging is an abstraction, a sum of all quasi-programmed diseases and processes. In analogy, the zoo consists of animals and does not exist without animals, but the zoo is not an animal.”Read the Full Paper: DOI: https://doi.org/10.18632/aging.204499 Corresponding Author: Mikhail V. BlagosklonnyCorresponding Emails: Blagosklonny@oncotarget.com, Blagosklonny@rapalogs.com Keywords: geroscience, mTOR, hyperfunction theory of aging, lifespan, healthspanSign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204499About Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://youtube.com/Aging-USLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
A new research paper was published on the cover of Aging (Aging-US)) Volume 15, Issue 2, entitled, “Clearance of p16Ink4a-positive cells in a mouse transgenic model does not change β-cell mass and has limited effects on their proliferative capacity.”Type 2 diabetes is partly characterized by decreased β-cell mass and function which have been linked to cellular senescence. Despite a low basal proliferative rate of adult β-cells, they can respond to growth stimuli, but this proliferative capacity decreases with age and correlates with increased expression of senescence effector, p16Ink4a. In a new study, researchers Nadine Bahour, Lucia Bleichmar, Cristian Abarca, Emeline Wilmann, Stephanie Sanjines, and Cristina Aguayo-Mazzucato from the Joslin Diabetes Center at Harvard Medical School hypothesized that selective deletion of p16Ink4a-positive cells would enhance the proliferative capacity of the remaining β-cells due to the elimination of the local senescence-associated secretory phenotype (SASP). “We aimed to investigate the effects of p16Ink4a-positive cell removal on the mass and proliferative capacity of remaining β-cells using INK-ATTAC mice as a transgenic model of senolysis.”Clearance of p16Ink4a-positive subpopulation was tested in mice of different ages, males and females, and with two different insulin resistance models: high-fat diet (HFD) and insulin receptor antagonist (S961). Clearance of p16Ink4a-positive cells did not affect the overall β-cell mass. β-cell proliferative capacity negatively correlated with cellular senescence load and clearance of p16Ink4a positive cells in 1-year-old HFD mice improved β-cell function and increased proliferative capacity in a subset of animals. Single-cell sequencing revealed that the targeted p16Ink4a subpopulation of β-cells is non-proliferative and non-SASP producing whereas additional senescent subpopulations remained contributing to continued local SASP secretion. “In conclusion, deletion of p16Ink4a cells did not negatively impact beta-cell mass and blood glucose under basal and HFD conditions and proliferation was restored in a subset of HFD mice opening further therapeutic targets in the treatment of diabetes.”DOI: https://doi.org/10.18632/aging.204483 Corresponding Author: Cristina Aguayo-Mazzucato - cristina.aguayo-mazzucato@joslin.harvard.edu Keywords: beta cells, mass, proliferation, senolysis, senescenceSign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204483About Aging-US:Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://youtube.com/Aging-USLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
Blog summary of a recent research paper published by Aging: "A case-control study coupling with meta-analysis elaborates decisive association between IGF-1 rs35767 and osteoporosis in Asian postmenopausal females."____________________________________________________Osteoporosis is characterized by the loss of bone density and an increased risk of fractures. This serious health condition is a major public health concern, particularly among older women. According to the National Osteoporosis Foundation, approximately 80% of the estimated 10 million Americans with osteoporosis are women. Additionally, roughly one in two women over the age of 50 will break a bone due to osteoporosis. “Osteoporosis (OP) is prevalent in postmenopausal women. Several studies investigated the association between IGF-1 polymorphisms and OP among postmenopausal females with conflicting outcomes.”While the main risk factor for osteoporosis is undeniably aging, the causes of osteoporosis are more complex—involving a combination of genetic and environmental factors. The insulin-like growth factor 1 (IGF-1) gene plays a critical role in bone growth and development, and previous studies have suggested that variations in this gene may be associated with osteoporosis. Some genetic variants have been found to be associated with decreased IGF-1 levels, which may contribute to the development of osteoporosis.In a recent study, researchers Sui-Lung Su, Yung-Hsun Huang, Yu-Hsuan Chen, Pi-Shao Ko, Wen Su, Chih-Chien Wang, and Meng-Chang Lee from the Tri-Service General Hospital and National Defense Medical Center in Taipei, Taiwan, explored the relationship between IGF-1 polymorphisms rs35767, rs2288377 and rs5742612 and the development of osteoporosis in postmenopausal Asian women. Their new research paper was published in Aging’s Volume 15, Issue 1, entitled, “A case-control study coupling with meta-analysis elaborates decisive association between IGF-1 rs35767 and osteoporosis in Asian postmenopausal females.”Full blog - https://aging-us.org/2023/01/gene-linked-to-osteoporosis-risk-in-postmenopausal-asian-women/DOI - https://doi.org/10.18632/aging.204464Corresponding author - Meng-Chang Lee - apply0710@yahoo.com.twKeywords - osteoporosis, postmenopausal, insulin-like growth factor-1, single nucleotide polymorphism, meta-analysisAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://youtube.com/Aging-USLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/For media inquiries, please contact: media@impactjournals.com.
A new research paper was published in Aging (listed as "Aging (Albany NY)" by MEDLINE/PubMed and "Aging-US" by Web of Science) Volume 15, Issue 1, entitled, “The innate immune signaling component FBXC-58 mediates dietary restriction effects on healthy aging in Caenorhabditis elegans.”Dietary restriction (DR) is a highly effective and reproducible intervention that prolongs longevity in many organisms. The molecular mechanism of action of DR is tightly connected with the immune system; however, the detailed mechanisms and effective downstream factors of immunity that mediate the beneficial effects of DR on aging remain unknown.In this new study, researchers Jeong-Hoon Hahm, Farida S. Nirmala, Pyeong Geun Choi, Hyo-Deok Seo, Tae Youl Ha, Chang Hwa Jung, and Jiyun Ahn from the Korea Food Research Institute and the University of Science and Technology (in Daejeon, South Korea) investigated the immune signaling that mediates DR effects. The team used Caenorhabditis elegans (C. elegans) to understand the underlying molecular mechanisms of aging and immunity. “We found that the F-box gene, fbxc-58, a regulator of the innate immune response, is a novel mediator of DR effects on extending the health span of C. elegans.”Fbxc-58 is upregulated by DR and is necessary for DR-induced lifespan extension and physical health improvement in C. elegans. Furthermore, through DR, fbxc-58 prevents disintegration of the mitochondrial network in body wall muscle during aging. The researchers found that fbxc-58 is a downstream target of the ZIP-2 and PHA-4 transcription factors, the well-known DR mediator, and fbxc-58 extends longevity in DR through an S6 kinase-dependent pathway. Thus, the team proposed that fbxc-58 may provide a new mechanistic understanding of the effects of DR on healthy aging and elucidate the signaling mechanisms that link immunity and DR effects with aging.“Thus, we propose that investigating the molecular mechanism of action of F-box proteins, including fbxc-58, in DR will shed light on means to prevent sarcopenia and offer a potentially practical means of encouraging healthy aging via DR.”DOI: https://doi.org/10.18632/aging.204477 Corresponding Authors: Jeong-Hoon Hahm - hahmjh@kfri.re.kr, Jiyun Ahn - jyan@kfri.re.kr Keywords: dietary restriction, aging, innate immunity, F-box protein, Caenorhabditis elegansSign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204477About Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://youtube.com/Aging-USLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/For media inquiries, please contact: media@impactjournals.com
A new research paper was published in Aging (listed as "Aging (Albany NY)" by MEDLINE/PubMed and "Aging-US" by Web of Science) Volume 15, Issue 1, entitled, “Genetic deficiency and pharmacological modulation of RORα regulate laser-induced choroidal neovascularization.”Choroidal neovascularization (CNV) causes acute vision loss in neovascular age-related macular degeneration (AMD). Genetic variations of the nuclear receptor RAR-related orphan receptor alpha (RORα) have been linked with neovascular AMD, yet its specific role in pathological CNV development is not entirely clear.In this new study, researchers Chi-Hsiu Liu, Felix Yemanyi, Kiran Bora, Neetu Kushwah, Alexandra K. Blomfield, Theodore M. Kamenecka, John Paul SanGiovanni, Ye Sun, Laura A. Solt, and Jing Chen from Harvard Medical School, UF Scripps Biomedical Research and University of Arizona showed that Rora was highly expressed in the mouse choroid compared with the retina, and genetic loss of RORα in Staggerer mice (Rorasg/sg) led to increased expression levels of Vegfr2 and Tnfa in the choroid and retinal pigment epithelium (RPE) complex. “Here, we investigated whether RORα regulates CNV using a mouse model of laser-induced CNV, mimicking the neovascular features of wet AMD. We found that expression of RORα was enriched in the mouse choroid/RPE complex and upregulated in laser-induced CNV.”In a mouse model of laser-induced CNV, RORα expression was highly increased in the choroidal/RPE complex post-laser, and loss of RORα in Rorasg/sg eyes significantly worsened CNV with increased lesion size and vascular leakage, associated with increased levels of VEGFR2 and TNFα proteins. Pharmacological inhibition of RORα also worsened CNV. In addition, both genetic deficiency and inhibition of RORα substantially increased vascular growth in isolated mouse choroidal explants ex vivo. RORα inhibition also promoted angiogenic function of human choroidal endothelial cell culture. “Together, our results suggest that RORα negatively regulates pathological CNV development in part by modulating angiogenic response of the choroidal endothelium and inflammatory environment in the choroid/RPE complex.”DOI: https://doi.org/10.18632/aging.204480 Corresponding Author: Jing Chen - jing.chen@childrens.harvard.edu Keywords: age-related macular degeneration, angiogenesis, choroidal neovascularization, inflammation, nuclear receptors, RORα, VEGFR2, TNFαSign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204480About Aging-US:Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at www.Aging-US.com and connect with us:SoundCloud – https://soundcloud.com/Aging-UsFacebook – https://www.facebook.com/AgingUS/Twitter – https://twitter.com/AgingJrnlInstagram – https://www.instagram.com/agingjrnl/YouTube – https://www.youtube.com/agingusLinkedIn – https://www.linkedin.com/company/aging/Reddit – https://www.reddit.com/user/AgingUSPinterest – https://www.pinterest.com/AgingUS/For media inquiries, please contact media@impactjournals.com.
A new research paper was published on the cover of Aging (listed as "Aging (Albany NY)" by Medline/PubMed and "Aging-US" by Web of Science) Volume 15, Issue 1, entitled, “Single-cell transcriptomics of peripheral blood in the aging mouse.”Compositional and transcriptional changes in the hematopoietic system have been used as biomarkers of immunosenescence and aging. In this new study, researchers Yee Voan Teo, Samuel J. Hinthorn, Ashley E. Webb, and Nicola Neretti from Brown University used single-cell RNA-sequencing to study the aging peripheral blood in mice and characterize the changes in cell-type composition and transcriptional profiles associated with age.“Here, we applied scRNA-seq on young and old mice to dissect the transcriptional and cell composition changes of all cell types in the peripheral blood with age.”The team identified 17 clusters from a total of 14,588 single cells. They detected a general upregulation of antigen processing and presentation and chemokine signaling pathways and a downregulation of genes involved in ribosome pathways with age. In old peripheral blood, the researchers also observed an increased percentage of cells expressing senescence markers (Cdkn1a, and Cdkn2a). In addition, a cluster of activated T cells exclusively found in old blood was detected, with lower expression of Cd28 and higher expression of Bcl2 and Cdkn2a, suggesting that the cells are senescent and resistant to apoptosis.“Finally, targeting senescent cells using genetic approaches has been shown to ameliorate the aging phenotype [34, 35]. More recently, senolytics drugs are being identified or developed to target apoptotic pathways because senescent cells are known to be apoptosis-resistant [34]. Therefore, the Bcl2+ old T cells that we identified in old mice can potentially be targeted pharmacologically to ameliorate the phenotypes associated with the aging of the immune system.”DOI: https://doi.org/10.18632/aging.204471 Corresponding Author: Nicola Neretti - nicola_neretti@brown.edu Keywords: aging, single-cell transcriptomics, senescence, peripheral bloodSign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204471About Aging-US:Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at www.Aging-US.com and connect with us: SoundCloud – https://soundcloud.com/Aging-UsFacebook – https://www.facebook.com/AgingUS/Twitter – https://twitter.com/AgingJrnlInstagram – https://www.instagram.com/agingjrnl/YouTube – https://www.youtube.com/agingusLinkedIn – https://www.linkedin.com/company/aging/Reddit – https://www.reddit.com/user/AgingUSPinterest – https://www.pinterest.com/AgingUS/For media inquiries, please contact media@impactjournals.com.
A new research paper was published in Aging (Aging-US) Volume 14, Issue 24, entitled, “Transcriptomic analysis of human ALS skeletal muscle reveals a disease-specific pattern of dysregulated circRNAs.”Circular RNAs are abundant, covalently closed transcripts that arise in cells through back-splicing and display distinct expression patterns across cells and developmental stages. While their functions are largely unknown, their intrinsic stability has made them valuable biomarkers in many diseases.In this new study, researchers Dimitrios Tsitsipatis, Krystyna Mazan-Mamczarz, Ying Si, Allison B. Herman, Jen-Hao Yang, Abhishek Guha, Yulan Piao, Jinshui Fan, Jennifer L. Martindale, Rachel Munk, Xiaoling Yang, Supriyo De, Brijesh K. Singh, Ritchie Ho, Myriam Gorospez, and Peter H. King from the National Institutes of Health’s National Institute on Aging, The University of Alabama at Birmingham, Birmingham Veterans Affairs Medical Center, and Cedars-Sinai Medical Center set out to examine circRNA patterns in amyotrophic lateral sclerosis (ALS). By RNA-sequencing analysis, the researchers first identified circRNAs and linear RNAs that were differentially abundant in skeletal muscle biopsies from ALS compared to normal individuals. “By RT-qPCR analysis, we confirmed that 8 circRNAs were significantly elevated and 10 were significantly reduced in ALS, while the linear mRNA counterparts, arising from shared precursor RNAs, generally did not change.” Several of these circRNAs were also differentially abundant in motor neurons derived from human induced pluripotent stem cells (iPSCs) bearing ALS mutations, and across different disease stages in skeletal muscle from a mouse model of ALS (SOD1G93A). Interestingly, a subset of the circRNAs significantly elevated in ALS muscle biopsies were significantly reduced in the spinal cord samples from ALS patients and ALS (SOD1G93A) mice. In sum, the researchers identified differentially abundant circRNAs in ALS-relevant tissues (muscle and spinal cord) that could inform about neuromuscular molecular programs in ALS and guide the development of therapies.“As our studies advance, we will investigate the function of the most promising and abundant circRNAs, among the 18 circRNAs reported here. We are especially interested in those that appeared to be specific for ALS (Figure 2), as they may help to characterize disease-associated molecular pathways that could be targeted therapeutically.”DOI: https://doi.org/10.18632/aging.204450 Corresponding Authors: Myriam Gorospe - GorospeM@grc.nia.nih.gov, Dimitrios Tsitsipatis - dimitrios.tsitsipatis@nih.gov, Peter H. King - phking@uabmc.eduKeywords: amyotrophic lateral sclerosis, circular RNAs, neurodegenerative disease, human skeletal muscle, human spinal cord tissueAbout Aging-US:Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at www.Aging-US.com and connect with us:SoundCloud – https://soundcloud.com/Aging-UsFacebook – https://www.facebook.com/AgingUS/Twitter – https://twitter.com/AgingJrnlInstagram – https://www.instagram.com/agingjrnl/YouTube – https://www.youtube.com/agingusLinkedIn – https://www.linkedin.com/company/aging/Reddit – https://www.reddit.com/user/AgingUSPinterest – https://www.pinterest.com/AgingUS/For media inquiries, please contact media@impactjournals.com.
Listen to a blog summary of a research paper published by Aging in Volume 14, Issue 24, entitled, "12-year evolution of multimorbidity patterns among older adults based on Hidden Markov Models."_______________________________________Multimorbidity is a term that refers to living with two or more chronic diseases at the same time, and the prevalence of this phenomenon increases with age. In addition, humans tend to evolve and transition into distinct patterns of multimorbidity. These still ill-defined patterns of multimorbidity may offer a window of opportunity for researchers. Since the aging population continues to grow in many parts of the world, researchers are motivated to better understand these patterns and how they evolve and transition over time in order to develop interventions and therapeutics for healthier aging. However, this is a challenging task for several reasons.“Multimorbidity is associated with a higher risk of polypharmacy and decreased quality of life, and challenges the decision-making of clinicians that lack effective guidelines for the management and treatment of patients with cohexisting complex diseases [4].”While researchers have investigated multimorbidity, not all studies are created equal—rendering meta-analyses largely incongruent (thus far). One reason the evolution of multimorbidity patterns is so challenging to study is because most study designs are not powered to account for the dynamic nature of multimorbidity in old age. Another reason is that various studies use different lists of diseases. (Some studies include ten conditions or less and others include 200+ conditions.) Finally, most statistical methods used to organize data are not able to properly handle the complexity of multimorbidity.“Exploring how multimorbidity patterns evolve throughout people’s lives and the time subjects remain within specific patterns is still an under-researched area [7, 8]. The understanding of how diseases cluster longitudinally in specific age groups would pave the way to the design of new prognostic tools, as well as new preventive and, eventually, therapeutic approaches.”Full blog - https://aging-us.org/2023/01/how-hidden-markov-models-can-help-elucidate-multimorbidity-in-aging/DOI - https://doi.org/10.18632/aging.204395Corresponding authors - Albert Roso-Llorach - aroso@idiapjgol.org, Amaia Calderón-Larrañaga - amaia.calderon.larranaga@ki.seKeywords - multimorbidity, older adults, longitudinal population-based study, aging, Hidden Markov ModelsAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/agingusLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/For media inquiries, please contact media@impactjournals.com.
A new research paper was published in Aging (Aging-US) Volume 14, Issue 24, entitled, “Epigenetic aging is associated with aberrant neural oscillatory dynamics serving visuospatial processing in people with HIV.”Despite effective antiretroviral therapy, cognitive impairment and other aging-related comorbidities are more prevalent in people with HIV (PWH) than in the general population. Previous research examining DNA methylation has shown PWH exhibit accelerated biological aging. However, it is unclear how accelerated biological aging may affect neural oscillatory activity in virally suppressed PWH, and more broadly how such aberrant neural activity may impact neuropsychological performance.Participants (n = 134) between the ages of 23 – 72 years underwent a neuropsychological assessment, a blood draw to determine biological age via DNA methylation, and a visuospatial processing task during magnetoencephalography (MEG). Researchers Mikki Schantell, Brittany K. Taylor, Rachel K. Spooner, Pamela E. May, Jennifer O’Neill, Brenda M. Morsey, Tina Wang, Trey Ideker, Sara H. Bares, Howard S. Fox, and Tony W. Wilson from the Boys Town National Research Hospital, University of Nebraska Medical Center, Creighton University, Heinrich-Heine University, and the University of California San Diego focused their analyses on the relationship between biological age and oscillatory theta (4-8 Hz) and alpha (10 - 16 Hz) activity among PWH (n=65) and seronegative controls (n = 69).“To our knowledge, no study to date has directly linked accelerated biological aging in PWH to the neuro-functional changes that occur in cognitively impaired PWH, which include deficits in visuospatial processing, attention, working memory, and motor function networks.”PWH had significantly elevated biological age when controlling for chronological age relative to controls. Biological age was differentially associated with theta oscillations in the left posterior cingulate cortex (PCC) and with alpha oscillations in the right medial prefrontal cortex (mPFC) among PWH and seronegative controls. Stronger alpha oscillations in the mPFC were associated with lower CD4 nadir and lower current CD4 counts, suggesting such responses were compensatory. Participants who were on combination antiretroviral therapy for longer had weaker theta oscillations in the PCC.Full press release - https://www.aging-us.com/news_room/Aging-Epigenetic-aging-associated-with-aberrant-neural-oscillatory-dynamics-serving-visuospatial-processing-in-people-with-HIVDOI: https://doi.org/10.18632/aging.204437 Corresponding Author: Tony W. Wilson - tony.wilson@boystown.org Keywords: HIV, epigenetics, biological age, visuospatial discrimination, oscillations About Aging-US:Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Visit our website at www.Aging-US.com and connect with us: SoundCloud – https://soundcloud.com/Aging-UsFacebook – https://www.facebook.com/AgingUS/Twitter – https://twitter.com/AgingJrnlInstagram – https://www.instagram.com/agingjrnl/YouTube – https://www.youtube.com/agingusLinkedIn – https://www.linkedin.com/company/aging/For media inquiries, contact media@impactjournals.com.
A new research paper was published on the cover of Aging (listed as "Aging (Albany NY)" by Medline/PubMed and "Aging-US" by Web of Science) Volume 14, Issue 24, entitled, “Associations of the APOE ε2 and ε4 alleles and polygenic profiles comprising APOE-TOMM40-APOC1 variants with Alzheimer’s disease biomarkers.”Capturing the genetic architecture of Alzheimer’s disease (AD) is challenging because of the complex interplay of genetic and non-genetic factors in its etiology. It has been suggested that AD biomarkers may improve the characterization of AD pathology and its genetic architecture. Most studies have focused on connections of individual genetic variants with AD biomarkers, whereas the role of combinations of genetic variants is substantially underexplored.In this new study for the Alzheimer’s Disease Neuroimaging Initiative, researchers, from Alexander M. Kulminski, Ethan Jain-Washburn, Elena Loiko, Yury Loika, Fan Feng, and Irina Culminskaya from Duke University and University of California examined the associations of the APOE ε2 and ε4 alleles and polygenic profiles comprising the ε4-encoding rs429358, TOMM40 rs2075650, and APOC1 rs12721046 polymorphisms with cerebrospinal fluid (CSF) and plasma amyloid β (Aβ40 and Aβ42) and tau biomarkers. “Here, we examine the associations of the APOE ε2 and ε4 alleles and the AD-risk-differentiating compound genotypes comprising rs429358, rs2075650, and rs12721046 SNPs with Aβ40, Aβ42, and tau AD biomarkers measured in CSF and plasma using data from three studies: the AD Neuroimaging Initiative (ADNI), the Atherosclerosis Risk in Communities (ARIC) study, and the Framingham Heart Study (FHS).”Findings from this study support associations of the ε4 alleles with both plasma and CSF Aβ42 and CSF tau, and the ε2 alleles with baseline, but not longitudinal, CSF Aβ42 measurements. The researchers found that the ε4-bearing polygenic profiles conferring higher and lower AD risks are differentially associated with tau but not Aβ42. Modulation of the effect of the ε4 alleles by TOMM40 and APOC1 variants indicates the potential genetic mechanism of differential roles of Aβ and tau in AD pathogenesis.“Our primary finding is that the ε4-bearing polygenic profiles conferring higher and lower AD risks are differently associated with tau but not Aβ42. The other main results of our work are characterizations of the associations of the APOE ε2 and ε4 alleles with Aβ40, Aβ42, and tau biomarkers in ADNI-1, ADNI-2/GO, ARIC, and three FHS cohorts.”DOI: https://doi.org/10.18632/aging.204384 Corresponding Author: Alexander M. Kulminski - kulminsk@duke.edu Keywords: aging, apolipoprotein E polymorphism, Alzheimer’s disease, haplotypes, Alzheimer’s disease biomarkersSign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204384About Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/agingusLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
A new research paper was published in Aging (Aging-US) Volume 14, Issue 23, entitled, “DNA methylation-based measures of biological aging and cognitive decline over 16-years: preliminary longitudinal findings in midlife.”DNA methylation-based (DNAm) measures of biological aging associate with increased risk of morbidity and mortality, but their links with cognitive decline are less established. In this new study, researchers Rebecca G. Reed, Judith E. Carroll, Anna L. Marsland, and Stephen B. Manuck from University of Pittsburgh and University of California examined changes over a 16-year interval in epigenetic clocks (the traditional and principal components [PC]-based Horvath, Hannum, PhenoAge, GrimAge) and pace of aging measures (Dunedin PoAm, Dunedin PACE) in 48 midlife adults enrolled in the longitudinal arm of the Adult Health and Behavior project (56% Female, baseline AgeM = 44.7 years), selected for discrepant cognitive trajectories. “We hypothesized that overall, cognitive Decliners would be biologically older compared to cognitive Maintainers.”Cognitive Decliners (N = 24) were selected based on declines in a composite score derived from neuropsychological tests and matched with participants who did not show any decline, Maintainers (N = 24). Multilevel models with repeated DNAm measures within person tested the main effects of time, group, and group by time interactions. DNAm measures significantly increased over time generally consistent with elapsed time between study visits. There were also group differences: overall, Cognitive Decliners had an older PC-GrimAge and faster pace of aging (Dunedin PoAm, Dunedin PACE) than Cognitive Maintainers. There were no significant group by time interactions, suggesting accelerated epigenetic aging in Decliners remained constant over time. Older PC-GrimAge and faster pace of aging may be particularly sensitive to cognitive decline in midlife.“In conclusion, these preliminary results suggest PC-GrimAge and DNAm based pace of aging measures (Dunedin PoAm and PACE) associate with 16-year, neuropsychologically-validated cognitive decline in midlife. The results warrant a larger-scale study to better examine longitudinal associations between changes in DNAm measures and changes across multiple cognitive domains. Ultimately, establishing DNAm measures as biomarkers of cognitive function in midlife may offer pre-clinical markers of a molecular aging mechanism that can help identify individuals at increased risk for cognitive impairment and dementia in later life.”DOI: https://doi.org/10.18632/aging.204376 Corresponding Author: Rebecca G. Reed - rebecca.reed@pitt.edu Keywords: epigenetic age, aging biomarker, pace of aging, geroscience, cognitive agingSign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204376About Aging-US:Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at www.Aging-US.com and connect with us:SoundCloud – https://soundcloud.com/Aging-UsFacebook – https://www.facebook.com/AgingUS/Twitter – https://twitter.com/AgingJrnlInstagram – https://www.instagram.com/agingjrnl/YouTube – https://www.youtube.com/agingusLinkedIn – https://www.linkedin.com/company/aging/Reddit – https://www.reddit.com/user/AgingUSPinterest – https://www.pinterest.com/AgingUS/For media inquiries, please contact media@impactjournals.com.
Listen to a blog summary about a recent research perspective published in Volume 14, Issue 23, entitled, “Reduce, Reuse, Recycle, Run ! : 4 Rs to improve cardiac health in advanced age.”_____________________________________________Cardiac dysfunction is a major public health concern. While it can occur for various reasons at any age, the prevalence of cardiac dysfunction dramatically increases with advancing age. Unfortunately, the underlying mechanisms of age-related cardiac decline are still largely unknown. Thus, it is essential for researchers to uncover novel strategies to improve cardiac health at advanced ages.AUTOPHAGIC FLUXAn important physiological process involved in maintaining cardiovascular homeostasis is autophagic flux. Autophagic flux is the process by which cells break down and recycle their own cellular components after they have become damaged or unnecessary. This process is essential for maintaining healthy cardiac function, as it slows age-related oxidative damage, reduces the accumulation of toxic lipid and protein aggregates, and improves energy metabolism. However, the efficiency of autophagic flux decreases with age, resulting in declined cardiac function.Given its crucial role and fading functioning, the search for strategies to improve autophagic flux may be essential for improving cardiovascular health as humans age. Researchers Jae Min Cho, Rajeshwary Ghosh, Sohom Mookherjee, Sihem Boudina, and J. David Symons from the University of Utah authored a new research perspective about nutraceutical, lifestyle and pharmacological interventions that can reduce age-associated cardiac dysfunction. On December 1, 2022, their research perspective was published in Aging’s Volume 14, Issue 23, entitled, “Reduce, Reuse, Recycle, Run ! : 4 Rs to improve cardiac health in advanced age.”“In the following sections we review evidence that age-associated cardiac dysfunction can be Reduced by boosting cardiomyocyte autophagy (i.e., the ability to Reuse and Recycle damaged/dysfunctional proteins) via spermidine, rapamycin, and caloric-restriction. In addition, we highlight a new report indicating that a physiological intervention i.e., Running, rejuvenates cardiomyocyte autophagic flux to an extent that lessens age-associated cardiac dysfunction.”Full blog - https://aging-us.org/2022/12/late-in-life-interventions-to-improve-cardiac-health/DOI - https://doi.org/10.18632/aging.204415Corresponding authors - Sihem Boudina: sihem.boudina@u2m2.utah.edu, and J. David Symons: J.David.Symons@hsc.utah.eduSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204415Keywords - aging, authophagy, exercise training, heart, cardiac functionAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/agingusLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/For media inquiries, please contact media@impactjournals.com
A new research paper was published in Aging (listed as "Aging (Albany NY)" by MEDLINE/PubMed and "Aging-US" by Web of Science) Volume 14, Issue 23, entitled, “White matter hyperintensity load is associated with premature brain aging.”Brain age is an MRI-derived estimate of brain tissue loss that has a similar pattern to aging-related atrophy. White matter hyperintensities (WMHs) are neuroimaging markers of small vessel disease and may represent subtle signs of brain compromise. In this new study, researchers Natalie Busby, Sarah Newman-Norlund, Sara Sayers, Roger Newman-Norlund, Sarah Wilson, Samaneh Nemati, Chris Rorden, Janina Wilmskoetter, Nicholas Riccardi, Rebecca Roth, Julius Fridriksson, and Leonardo Bonilha from University of South Carolina, Medical University of South Carolina and Emory University tested the hypothesis that WMHs are independently associated with premature brain age in an original aging cohort.“We hypothesized that a higher WMH load is linearly associated with premature brain aging controlling for chronological age.”Brain age was calculated using machine-learning on whole-brain tissue estimates from T1-weighted images using the BrainAgeR analysis pipeline in 166 healthy adult participants. WMHs were manually delineated on FLAIR images. WMH load was defined as the cumulative volume of WMHs. A positive difference between estimated brain age and chronological age (BrainGAP) was used as a measure of premature brain aging. Then, partial Pearson correlations between BrainGAP and volume of WMHs were calculated (accounting for chronological age).Brain and chronological age were strongly correlated (r(163)=0.932, p<0.001). There was significant negative correlation between BrainGAP scores and chronological age (r(163)=-0.244, p<0.001) indicating that younger participants had higher BrainGAP (premature brain aging). Chronological age also showed a positive correlation with WMH load (r(163)=0.506, p<0.001) indicating older participants had increased WMH load. Controlling for chronological age, there was a statistically significant relationship between premature brain aging and WMHs load (r(163)=0.216, p=0.003). Each additional year in brain age beyond chronological age corresponded to an additional 1.1mm3 in WMH load.“WMHs are an independent factor associated with premature brain aging. This finding underscores the impact of white matter disease on global brain integrity and progressive age-like brain atrophy.”DOI: https://doi.org/10.18632/aging.204397 Corresponding Author: Natalie Busby - hethern@mailbox.sc.edu Keywords: brain age, white matter hyperintensity, brain health, aging, healthSign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204397About Aging-US:Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at www.Aging-US.com and connect with us:SoundCloud – https://soundcloud.com/Aging-UsFacebook – https://www.facebook.com/AgingUS/Twitter – https://twitter.com/AgingJrnlInstagram – https://www.instagram.com/agingjrnl/YouTube – https://www.youtube.com/agingusLinkedIn – https://www.linkedin.com/company/aging/Reddit – https://www.reddit.com/user/AgingUSPinterest – https://www.pinterest.com/AgingUS/For media inquiries, please contact media@impactjournals.com.
A new research paper was published in Aging (listed as “Aging (Albany NY)” by MEDLINE/PubMed and “Aging-US” by Web of Science) Volume 14, Issue 23, entitled, “DNA methylation GrimAge version 2.”Researchers Ake T. Lu, Alexandra M. Binder, Joshua Zhang, Qi Yan, Alex P. Reiner, Simon R. Cox, Janie Corley, Sarah E. Harris, Pei-Lun Kuo, Ann Z. Moore, Stefania Bandinelli, James D. Stewart, Cuicui Wang, Elissa J. Hamlat, Elissa S. Epel, Joel D. Schwartz, Eric A. Whitsel, Adolfo Correa, Luigi Ferrucci, Riccardo E. Marioni, and Steve Horvath from the University of California Los Angeles, Altos Labs, University of Hawaii at Manoa, Fred Hutchinson Cancer Research Center, University of Edinburgh, National Institute on Aging, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Harvard T.H. Chan School of Public Health, University of California – San Francisco, and the University of Mississippi Medical Center previously described a DNA methylation (DNAm) based biomarker of human mortality risk DNAm GrimAge. In their current study, the researchers describe version 2 of GrimAge (trained on individuals aged between 40 and 92) which leverages two new DNAm based estimators of (log transformed) plasma proteins: high sensitivity C-reactive protein (logCRP) and hemoglobin A1C (logA1C).“To arrive at version 2 of GrimAge, we developed two additional DNAm based surrogates for plasma proteins that are widely used in the clinic (DNAm logCRP and DNAm logA1C).”The team evaluated GrimAge2 in 13,399 blood samples across nine study cohorts. After adjustment for age and sex, GrimAge2 outperforms GrimAge in predicting mortality across multiple racial/ethnic groups (meta P=3.6×10-167 versus P=2.6×10-144) and in terms of associations with age related conditions such as coronary heart disease, lung function measurement FEV1 (correlation= -0.31, P=1.1×10-136), computed tomography based measurements of fatty liver disease. The researchers presented evidence that GrimAge version 2 also applies to younger individuals and to saliva samples where it tracks markers of metabolic syndrome. DNAm logCRP is positively correlated with morbidity count (P=1.3×10-54). DNAm logA1C is highly associated with type 2 diabetes (P=5.8×10-155). DNAm PAI-1 outperforms the other age-adjusted DNAm biomarkers including GrimAge2 in correlating with triglyceride (cor=0.34, P=9.6×10-267) and visceral fat (cor=0.41, P=4.7×10-41). Overall, the team demonstrated that GrimAge version 2 is an attractive epigenetic biomarker of human mortality and morbidity risk.“GrimAge2 will not replace existing clinical biomarkers. Rather, GrimAge2 complements existing clinical biomarkers when evaluating an individual’s aging rate.”DOI: https://doi.org/10.18632/aging.204434Corresponding Author: Steve Horvath - shorvath@mednet.ucla.edu About Aging-US:Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at www.Aging-US.com and connect with us:SoundCloud – https://soundcloud.com/Aging-UsFacebook – https://www.facebook.com/AgingUS/Twitter – https://twitter.com/AgingJrnlInstagram – https://www.instagram.com/agingjrnl/YouTube – https://www.youtube.com/agingusLinkedIn – https://www.linkedin.com/company/aging/Reddit – https://www.reddit.com/user/AgingUSPinterest – https://www.pinterest.com/AgingUS/For media inquiries, please contact media@impactjournals.com.
Listen to a blog summary of a trending research paper published by Aging (Aging-US) in Volume 14, Issue 22, entitled, “Denervation induces mitochondrial decline and exacerbates lysosome dysfunction in middle-aged mice.”________________________________________________________A hallmark characteristic of aging is the progressive loss of skeletal muscle mass, known as sarcopenia. A process called motor neuron denervation (Den)—when nerve signals to muscles are blocked or reduced—leads to muscle atrophy, fatigue and eventually muscle loss. Determining how and when Den events influence older muscles is crucially important for developing interventions to stop or reverse age-related muscle wasting.“Further, aged muscle exhibits reduced plasticity to both enhanced and suppressed contractile activity. It remains unclear when the onset of this blunted response occurs, and how middle-aged muscle adapts to denervation.”Dysfunctional mitochondria in muscle tissue are known to increase with age. Lysosomes are responsible for the recycling of damaged mitochondria. However, as muscles age, lysosomal function in muscle tissue also declines.In a new study, researchers Matthew Triolo, Debasmita Bhattacharya and David A. Hood from York University in Toronto, Canada, aimed to characterize the time-dependent changes in denervated skeletal muscle from middle-aged mice. The team focussed on how mitochondrial turnover is impacted. On November 4, 2022, their research paper was published in Aging’s Volume 14, Issue 22, entitled, “Denervation induces mitochondrial decline and exacerbates lysosome dysfunction in middle-aged mice.”Full blog - https://aging-us.org/2022/12/new-insights-into-the-mechanisms-of-sarcopenia/DOI - https://doi.org/10.18632/aging.204365Corresponding author - David A. Hood - dhood@yorku.caVideo - https://www.youtube.com/watch?v=Vcrv4KeFvsYSign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204365Keywords - mitochondrial biogenesis, autophagy, mitophagy, lysosomes, muscleAbout Aging-USLaunched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at https://www.Aging-US.com and connect with us:SoundCloud - https://soundcloud.com/Aging-UsFacebook - https://www.facebook.com/AgingUS/Twitter - https://twitter.com/AgingJrnlInstagram - https://www.instagram.com/agingjrnl/YouTube - https://www.youtube.com/agingusLinkedIn - https://www.linkedin.com/company/aging/Pinterest - https://www.pinterest.com/AgingUS/Media Contact18009220957MEDIA@IMPACTJOURNALS.COM
A new research paper was published in Aging (listed as “Aging (Albany NY)” by MEDLINE/PubMed and “Aging-US” by Web of Science) Volume 14, Issue 22, entitled, “The potential benefit of metformin to reduce delirium risk and mortality: a retrospective cohort study.”Metformin has been reported to improve age-related disorders, including dementia, and to lower mortality. This study was conducted to investigate whether metformin use lowers delirium risk, as well as long-term mortality.In the current retrospective cohort study, researchers Takehiko Yamanashi, Zoe-Ella EM Anderson, Manisha Modukuri, Gloria Chang, Tammy Tran, Pedro S. Marra, Nadia E. Wahba, Kaitlyn J. Crutchley, Eleanor J. Sullivan, Sydney S. Jellison, Katie R. Comp, Cade C. Akers, Alissa A. Meyer, Sangil Lee, Masaaki Iwata, Hyunkeun R. Cho, Eri Shinozaki, and Gen Shinozaki from Stanford University School of Medicine, University of Iowa Carver College of Medicine, University of Iowa College of Public Health, and Tottori University Faculty of Medicine analyzed 1,404 previously recruited subjects. The relationship between metformin use and delirium, and the relationship between metformin use and 3-year mortality were investigated.“Thus, in this report we aimed to investigate the relationship between DM [diabetes mellitus] and delirium risk with a focus on the influence from metformin. We hypothesized that history of metformin use is associated with lower risk for delirium. We were also interested in testing if history of metformin use can alter one of the most important patient outcomes, mortality.”242 subjects were categorized into a type 2 diabetes mellitus (DM)-without-metformin group, and 264 subjects were categorized into a DM-with-metformin group. Prevalence of delirium was 36.0% in the DM-without-metformin group, and 29.2% in the DM-with-metformin group. A history of metformin use reduced the risk of delirium in patients with DM (OR, 0.50 [95% CI, 0.32 to 0.79]) after controlling for confounding factors. The 3-year mortality in the DM-without-metformin group (survival rate, 0.595 [95% CI, 0.512 to 0.669]) was higher than in the DM-with-metformin group (survival rate, 0.695 [95% CI, 0.604 to 0.770]) (p=0.035). A history of metformin use decreased the risk of 3-year mortality after adjustment for confounding factors (HR, 0.69 [95% CI, 0.48 to 0.98]). The researchers concluded that metformin use may lower the risk of delirium and mortality in DM patients.“In this report, we showed the potential benefit of metformin in decreasing the risk of delirium and mortality in DM subjects.”DOI: https://doi.org/10.18632/aging.204393Corresponding Author: Gen Shinozaki - gens@stanford.edu Keywords: delirium, metformin, diabetes mellitus, mortality, agingAbout Aging-US:Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.Please visit our website at www.Aging-US.com and connect with us:SoundCloud – https://soundcloud.com/Aging-UsFacebook – https://www.facebook.com/AgingUS/Twitter – https://twitter.com/AgingJrnlInstagram – https://www.instagram.com/agingjrnl/YouTube – https://www.youtube.com/agingusLinkedIn – https://www.linkedin.com/company/aging/Reddit – https://www.reddit.com/user/AgingUSPinterest – https://www.pinterest.com/AgingUS/For media inquiries, please contact media@impactjournals.com.
A new research paper was published on the cover of Aging (Aging-US) Volume 14, Issue 22, entitled, “Glutaminase inhibitors rejuvenate human skin via clearance of senescent cells: a study using a mouse/human chimeric model.”
Skin aging caused by various endogenous and exogenous factors results in structural and functional changes to skin components. However, the role of senescent cells in skin aging has not been clarified.
In this new study, researchers Kento Takaya, Tatsuyuki Ishii, Toru Asou, and Kazuo Kishi, from the Department of Plastic and Reconstructive Surgery at the Keio University School of Medicine, evaluated the effects of the glutaminase inhibitor BPTES (bis-2-(5-phenylacetamido-1, 3, 4-thiadiazol-2-yl)ethyl sulfide) on human senescent dermal fibroblasts and aged human skin to elucidate the function of senescent cells in skin aging.
“[...] we utilized plastic surgery to create an experimental mouse/human chimeric model in which intraoperatively obtained human whole skin layers were transplanted into nude mice using previously described methods [25] and evaluated the anti-aging effects of BPTES on real human skin.”
Primary human dermal fibroblasts (HDFs) were induced to senescence by long-term passaging, ionizing radiation, and treatment with doxorubicin, an anticancer drug. Cell viability of HDFs was assessed after BPTES treatment. A mouse/human chimeric model was created by subcutaneously transplanting whole skin grafts from aged humans into nude mice. The model was treated intraperitoneally with BPTES or vehicle for 30 days. Skin samples were collected and subjected to reverse transcription-quantitative polymerase chain reaction (RT-qPCR), western blotting, and histological analysis.
BPTES selectively eliminated senescent dermal fibroblasts regardless of the method used to induce senescence; aged human skin grafts treated with BPTES exhibited increased collagen density, increased cell proliferation in the dermis, and decreased aging-related secretory phenotypes, such as matrix metalloprotease and interleukin. These effects were maintained in the grafts 1 month after termination of the treatment. In conclusion, selective removal of senescent dermal fibroblasts can improve the skin aging phenotype, indicating that BPTES may be an effective novel therapeutic agent for skin aging.
“In summary, our results indicate that selective clearance of aging dermal fibroblasts by BPTES ameliorates skin senescence-related changes and that aging dermal fibroblasts may play an important role in the skin aging process. Therefore, senescent cell eliminators for aging skin cells may be an effective option for treating skin aging.”
DOI: https://doi.org/10.18632/aging.204391
Corresponding Author: Kento Takaya - kento-takaya312@keio.jp
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About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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A new research paper was published in Aging (listed as "Aging (Albany NY)" by MEDLINE/PubMed and "Aging-US" by Web of Science) Volume 14, Issue 21, entitled, “Krill oil protects dopaminergic neurons from age-related degeneration through temporal transcriptome rewiring and suppression of several hallmarks of aging.”
There is accumulating evidence that interfering with the basic aging mechanisms can enhance healthy longevity. The interventional/therapeutic strategies targeting multiple aging hallmarks could be more effective than targeting one hallmark. While health-promoting qualities of marine oils have been extensively studied, the underlying molecular mechanisms are not fully understood.
Lipid extracts from Antarctic krill are rich in long-chain omega-3 fatty acids choline, and astaxanthin. In this new study, researchers Tanima SenGupta, Yohan Lefol, Lisa Lirussi, Veronica Suaste, Torben Luders, Swapnil Gupta, Yahyah Aman, Kulbhushan Sharma, Evandro Fei Fang, and Hilde Nilsen from the University of Oslo, Oslo University Hospital and Akershus University Hospital used C. elegans and human cells to investigate whether krill oil promotes healthy aging.
“In a C. elegans model of Parkinson's disease, we show that krill oil protects dopaminergic neurons from aging-related degeneration, decreases alpha-synuclein aggregation, and improves dopamine-dependent behavior and cognition”
Krill oil rewires distinct gene expression programs that contribute to attenuating several aging hallmarks, including oxidative stress, proteotoxic stress, senescence, genomic instability, and mitochondrial dysfunction. Mechanistically, krill oil increases neuronal resilience through temporal transcriptome rewiring to promote anti-oxidative stress and anti-inflammation via healthspan regulating transcription factors such as SNK-1. Moreover, krill oil promotes dopaminergic neuron survival through regulation of synaptic transmission and neuronal functions via PBO-2 and RIM-1.
“Collectively, krill oil rewires global gene expression programs and promotes healthy aging via abrogating multiple aging hallmarks, suggesting directions for further pre-clinical and clinical explorations.”
DOI: https://doi.org/10.18632/aging.204375
Corresponding Author: Hilde Nilsen - hilde.nilsen@medisin.uio.no
Video: https://www.youtube.com/watch?v=oucZo5px1YU
Keywords: krill oil, aging, healthspan, mitochondrial health, senescence
About Aging-US:
Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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A new research paper was published in Aging (listed as “Aging (Albany NY)” by MEDLINE/PubMed and “Aging-US” by Web of Science) Volume 14, Issue 21, entitled, “The deubiquitylase USP7 is a novel cyclin F-interacting protein and regulates cyclin F protein stability.”
Orderly progression through the cell cycle is driven by the periodic oscillations in the activity of cyclin-dependent kinases (CDKs). Cyclin F, unlike canonical and transcriptional cyclins, does not bind or activate any cyclin-dependent kinases. Instead, it harbors an F-box motif and primarily functions as the substrate recognition subunit of the Skp1-Cul1-F-box E3 ubiquitin ligase complex, SCFCyclin F.
By targeting specific proteins for ubiquitin-mediated proteasomal degradation, cyclin F plays a critical role in the regulation of centrosomal duplication, DNA replication and repair, and maintenance of genomic stability. Cyclin F abundance and activity are tightly regulated throughout the cell cycle. However, the molecular mechanisms regulating cyclin F are scantily understood.
In this new study, researchers Savitha S. Sharma, W. Jack Pledger and Paturu Kondaiah from Indian Institute of Science, Sri Shankara Cancer Hospital and Research Centre and University of Utah Health’s Huntsman Cancer Institute identified the deubiquitylase USP7 as a novel cyclin F-interacting protein.
“In this study, we identify USP7 as a novel cyclin F-interacting protein and uncover novel aspects of cyclin F regulation mediated by this interaction.”
The team observed that USP7 stabilizes cyclin F protein and that this function is independent of the deubiquitylase activity of USP7. Additionally, their data suggest that USP7 is also involved in the regulation of cyclin F mRNA. Pharmacological inhibition of the deubiquitylase activity of USP7 resulted in downregulation of cyclin F mRNA.
“In conclusion, in this study, we demonstrate a new interacting partner of cyclin F, namely USP7, and the role of USP7 in the regulation of cyclin F mRNA and protein. This study highlights a potential role for the cyclin F-USP7 axis in pathological conditions, including cancer and neurodegenerative diseases.”
DOI: https://doi.org/10.18632/aging.204372
Corresponding Author: Savitha S. Sharma - savitha.sharma@ssnccpr.org
Video: https://www.youtube.com/watch?v=NMGevJWU9Ac
Keywords: cyclin F, atypical cyclins, USP7, cell cycle, genomic integrity
About Aging-US:
Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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Listen to a blog summary of a trending research paper published by Aging (Aging-US), entitled, "ESR1 dysfunction triggers neuroinflammation as a critical upstream causative factor of the Alzheimer’s disease process.” _________________________________________________
The United States government currently has a mind-blowing annual budget of $3.5 billion designated for Alzheimer’s disease (AD) and dementia research funding. Therapeutics pushed forward thus far have been largely based on the amyloid-beta (Aβ) cascade hypothesis of AD. Surprisingly, despite decades and billions, these interventions have yielded little to no benefits for AD patients. This lack of efficacy has encouraged some researchers to rethink AD pathology and focus on discovering key triggers and mechanisms of neuroinflammation.
“There has been a lengthy and ongoing scientific debate around the causative factors of AD, and the relative importance of both senile Aβ plaques and tau tangles has been largely informed by postmortem investigations of the AD brain. For several decades, the amyloid hypothesis has dominated the field, which has brought forth many high-profile therapeutic attempts that have produced side effects but no real benefits [5].”
Women compose two-thirds of the United States Alzheimer’s population. Is this gender-specific risk a result of living longer or is it due to other causes, perhaps related to hormonal differences or gender-associated differential gene expression? Previous studies have found that estrogen may protect neurons from the damaging effects of amyloid-beta plaques and tau tangles. However, in women, estrogen levels tend to decline with age, which could be one reason why aging women are more susceptible to AD.
In a new study, researchers Junying Liu, Shouli Yuan, Xinhui Niu, Robbie Kelleher, and Helen Sheridan from Trinity College Dublin, Peking University and Jilin University examined the potential relationship between the estrogen receptor-α gene (ESR1) and neuroinflammation. Their research paper was published on November 1, 2022, in Aging’s Volume 14, Issue 21, and entitled, “ESR1 dysfunction triggers neuroinflammation as a critical upstream causative factor of the Alzheimer’s disease process.”
“AD is characterized by three major questions: Why is age the primary risk factor? Why are women more sensitive to the onset of this form of dementia? And why are neurons in areas of the brain that are essential for memory selectively targeted?”
Full blog - https://aging-us.org/2022/11/is-estrogen-dysregulation-behind-alzheimers-pathology/
DOI - https://doi.org/10.18632/aging.204359
Corresponding authors - Junying Liu - juliu@tcd.ie
Video - https://www.youtube.com/watch?v=NPWv39SJOpQ
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Keywords - ESR1, Alzheimer’s disease, CEBPB/ATF4, APOE, pyroptosis
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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A new research paper was published on the cover of Aging (listed as "Aging (Albany NY)" by Medline/PubMed and "Aging-US" by Web of Science) Volume 14, Issue 21, entitled, “IGF1 gene therapy in middle-aged female rats delays reproductive senescence through its effects on hypothalamic GnRH and kisspeptin neurons.”
The process of aging is the result of progressive loss of homeostasis and functional body impairment, including the central nervous system, where the hypothalamus plays a key role in regulating aging mechanisms. The consequences of aging include a chronic proinflammatory environment in the hypothalamus that leads to decreased secretion of gonadotropin-releasing hormone (GnRH) and impairs kisspeptin neuron functionality.
In this new study, researchers Franco Juan Cruz Dolcetti, Eugenia Falomir-Lockhart, Francisco Acuña, Macarena Lorena Herrera, Sofia Cervellini, Claudio Gustavo Barbeito, Daniela Grassi, Maria-Angeles Arevalo, and María José Bellini from Consejo Nacional de Investigaciones Científicas y Técnicas (UNC-CONICET), Universidad Nacional de La Plata, Autonomous University of Madrid, Instituto Cajal, and Instituto de Salud Carlos III investigated the effect of insulin-like growth factor 1 (IGF1) gene therapy on hypothalamic kisspeptin/GnRH neurons and on microglial cells, that mediate the inflammatory process related with the aging process.
“The aim of the present study is to investigate the effect of IGF1 gene therapy on estrous cycle, kisspeptin and GnRH neurons, and microglial cells in middle-aged female rats.”
The results show that IGF1 rats have higher kisspeptin expression in the anteroventral periventricular (AVPV) nucleus and higher immunoreactivity of GnRH in the arcuate nucleus and median eminence. In addition, IGF1-treated animals exhibit increased numbers of Iba1+ microglial cells and MHCII+/Iba1+ in the AVPV and arcuate nuclei. In conclusion, IGF1 gene therapy maintains kisspeptin production in the AVPV nucleus, induces GnRH release in the median eminence, and alters the number and reactivity of microglial cells in middle-aged female rats. The researchers suggest that IGF1 gene therapy may have a protective effect against reproductive decline.
“Based on our findings, we propose IGF1 gene therapy to delay reproductive senescence as a potential strategy to optimize lifespan and combat age-related health problems in women.”
DOI: https://doi.org/10.18632/aging.204360
Corresponding Authors: Maria-Angeles Arevalo - arevalo@cajal.csic.es, and María José Bellini - mariajosebellini@med.unlp.edu.ar
Keywords: IGF1, gene therapy, reproductive senescence, GnRH, kisspeptin, microglia
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About Aging-US:
Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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A new research paper was published in Aging (listed as “Aging (Albany NY)” by MEDLINE/PubMed and “Aging-US” by Web of Science) Volume 14, Issue 20, entitled, “Age-associated changes in microglia activation and Sirtuin-1- chromatin binding patterns.”
The aging process is associated with changes in mechanisms maintaining physiology, influenced by genetics and lifestyle, and impacting late life quality and longevity. Brain health is critical in healthy aging. Sirtuin 1 (Sirt1), a histone deacetylase with silencing properties, is one of the molecular determinants experimentally linked to health and longevity.
In this new study, researchers Liana V. Basova, Nikki Bortell, Bruno Conti, Howard S. Fox, Richard Milner, and Maria Cecilia Garibaldi Marcondes from San Diego Biomedical Research Institute, University of Nebraska Medical Center and Oncovalent Therapeutics compared brain pathogenesis and Sirt1-chromatin binding dynamics in brain pre-frontal cortex from 2 groups of elder rhesus macaques (rhesus monkeys), divided by age of necropsy: shorter-lived animals (18-20 years old (yo)), equivalent to 60-70 human yo; and longer-lived animals (23-29 yo), corresponding to 80-100 human yo and modeling successful aging. These were compared with young adult brains (4-7 yo).
“Our findings indicated drastic differences in the microglia marker Iba1, along with factors influencing Sirt1 levels and activity, such as CD38 (an enzyme limiting NAD that controls Sirt1 activity) and mir142 (a microRNA targeting Sirt1 transcription) between the elder groups.”
Iba1 was lower in shorter-lived animals than in the other groups, while CD38 was higher in both aging groups compared to young. mir142 and Sirt1 levels were inversely correlated in longer-lived brains (>23yo), but not in shorter-lived brains (18-20 yo). They also found that Sirt1 binding showed signs of better efficiency in longer-lived animals compared to shorter-lived ones, in genes associated with nuclear activity and senescence.
“Overall, differences in neuroinflammation and Sirt1 interactions with chromatin distinguished shorter- and longer-lived animals, suggesting the importance of preserving microglia and Sirt1 functional efficiency for longevity.”
DOI: https://doi.org/10.18632/aging.204329
Corresponding Author: Maria Cecilia Garibaldi Marcondes - cmarcondes@SDBRI.org
Keywords: aging, brain, rhesus macaques, microglia, Sirtuin-1
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Video: https://www.youtube.com/watch?v=Cz33TWM4so4
About Aging-US:
Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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Scientific integrity is a crucial component of scholarly publishing for any credible journal. Peer-reviewed, open-access journal Aging (listed as “Aging (Albany NY)” by Medline/PubMed and “Aging-US” by Web of Science) has recently presented its Scientific Integrity process.
Launched in 2009, Aging is an open-access biomedical journal dedicated to publishing high-quality, aging-focused research. Aging publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome.
Aging has a scientific integrity process to ensure that publications meet a number of scrupulous criteria for authenticity and integrity. Each published paper is thoroughly analyzed by diligent reviewers and services, including multiple in-house developed image forensics softwares. A growing industry of digital technologies, tools and ideas are constantly being added to Aging’s scientific integrity toolbox.
Aging’s Scientific Integrity process is built upon six critical components:
1-Easily Accessible Ethics Statements 2-Devotion to Industry Standards for Scientific Publishing 3-Rigorous and Insightful Peer Review 4-Detection and Zero-Tolerance of Plagiarism 5-Leading-Edge Image Forensics 6-Post-Publication Investigations (if needed)
The new webpage also depicts publishing statistics in a detailed graph —showcasing a visual representation of the number of post-publication corrections and retractions by Aging compared to the industry average, between 2010 and 2022. As of September 2022, Aging’s average rate of corrections/retractions since 2009 is a low 2.33%. The industry average correction/retraction rate is 3.80%.
Aging’s highly-effective scientific integrity process allows researchers to read, share and cite Aging papers with confidence.
Learn more about Aging’s Scientific Integrity Process: https://www.aging-us.com/scientific-integrity
Video: https://www.youtube.com/watch?v=5wbStfARUlI
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A new research perspective was published in Aging (listed as "Aging (Albany NY)" by MEDLINE/PubMed and "Aging-US" by Web of Science) Volume 14, Issue 20, entitled, “Rapamycin treatment early in life reprograms aging: hyperfunction theory and clinical practice.”
On October 24, 2022, Mikhail Blagosklonny, M.D., Ph.D. from Roswell Park Comprehensive Cancer Center published a riveting research perspective discussing the clinical application of early-life rapamycin treatment and its ability to reprogram aging, based on the hyperfunction theory.
“Making provocative headlines, three outstanding publications demonstrated that early-life treatment with rapamycin, including treatments during developmental growth, extends lifespan in animals, confirming predictions of hyperfunction theory, which views aging as a quasi-program (an unintended continuation of developmental growth) driven in part by mTOR.
Despite their high theoretical importance, clinical applications of two of these studies in mice, Drosophila and Daphnia cannot be implemented in humans because that would require growth retardation started at birth.
A third study demonstrated that a transient (around 20% of total lifespan in Drosophila) treatment with rapamycin early in Drosophila adult life is as effective as lifelong treatment, whereas a late-life treatment is not effective.
However, previous studies in mice demonstrated that a transient late-life treatment is highly effective.
Based on hyperfunction theory, this article attempts to reconcile conflicting results and suggests the optimal treatment strategy to extend human lifespan.”
DOI: https://doi.org/10.18632/aging.204354
Corresponding Author: Mikhail V. Blagosklonny - Corresponding Email: Blagosklonny@oncotarget.com
Video - https://www.youtube.com/watch?v=Br7iD48fKF4
Keywords: senescence, gerostatics, geroscience, sirolimus, healthspan
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About Aging-US:
Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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Dr. Ya-Jen Chiu from the Department of Life Science at National Taiwan Normal University in Taipei, discusses a research paper she co-authored that was published by Aging (Aging-US) in Volume 14, Issue 18, entitled, “Novel TRKB agonists activate TRKB and downstream ERK and AKT signaling to protect Aβ-GFP SH-SY5Y cells against Aβ toxicity.”
DOI - https://doi.org/10.18632/aging.204306
Corresponding authors - Chiung-Mei Chen - cmchen@cgmh.org.tw, Ying-Chieh Sun - sun@ntnu.edu.tw, Guey-Jen Lee-Chen - t43019@ntnu.edu.tw
Video - https://www.youtube.com/watch?v=1rT96K9VeZw
Transcript - https://aging-us.net/2022/11/01/behind-the-study-novel-trkb-agonists-activate-trkb-and-downstream-erk-and-akt-signaling/
Abstract
Decreased BDNF and impaired TRKB signaling contribute to neurodegeneration in Alzheimer's disease (AD). We have shown previously that coumarin derivative LM-031 enhanced CREB/BDNF/BCL2 pathway. In this study we explored if LM-031 analogs LMDS-1 to -4 may act as TRKB agonists to protect SH-SY5Y cells against Aβ toxicity. By docking computation for binding with TRKB using 7,8-DHF as a control, all four LMDS compounds displayed potential of binding to domain d5 of TRKB. In addition, all four LMDS compounds exhibited anti-aggregation and neuroprotective efficacy on SH-SY5Y cells with induced Aβ-GFP expression. Knock-down of TRKB significantly attenuated TRKB downstream signaling and the neurite outgrowth-promoting effects of these LMDS compounds. Among them, LMDS-1 and -2 were further examined for TRKB signaling. Treatment of ERK inhibitor U0126 or PI3K inhibitor wortmannin decreased p-CREB, BDNF and BCL2 in Aβ-GFP cells, implicating the neuroprotective effects are via activating TRKB downstream ERK, PI3K-AKT and CREB signaling. LMDS-1 and -2 are blood-brain barrier permeable as shown by parallel artificial membrane permeability assay. Our results demonstrate how LMDS-1 and -2 are likely to work as TRKB agonists to exert neuroprotection in Aβ cells, which may shed light on the potential application in therapeutics of AD.
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Keywords - aging, Alzheimer’s disease, TRKB agonists, Aβ, neuroprotection, therapeutics
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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A new research paper was published on the cover of Aging (listed as "Aging (Albany NY)" by Medline/PubMed and "Aging-US" by Web of Science) Volume 14, Issue 20, entitled, “Downregulation of senescence-associated secretory phenotype by knockdown of secreted frizzled-related protein 4 contributes to the prevention of skin aging.”
There is growing evidence that the appearance and texture of the skin that is altered during the aging process are considerably enhanced by the accumulation of senescent dermal fibroblasts. These senescent cells magnify aging via an inflammatory, histolytic, and senescence-associated secretory phenotype (SASP).
Secreted frizzled-related protein 4 (SFRP4) was previously determined to be expressed in dermal fibroblasts of aging skin, and its increased expression has been shown to promote cellular senescence. However, its role in the SASP remains unknown.
In this new study, researchers Kento Takaya, Toru Asou and Kazuo Kishi from Keio University School of Medicine’s Department of Plastic and Reconstructive Surgery investigated the classical model of skin fibroblasts based on Hayflick’s mitotic limit, the observation of SFRP4 expression in replicating senescent cells, and the effect of regulating this on the suppression of SASP and aging skin.
“These results may contribute to the development of new therapies to ameliorate skin aging.”
The researchers found that SFRP4 was significantly expressed in p16ink4a-positive human skin fibroblasts and that treatment with recombinant SFRP4 promoted SASP and senescence, whereas siRNA knockdown of SFRP4 suppressed SASP. They also found that knockdown of SFRP4 in mouse skin ameliorates age-related reduction of subcutaneous adipose tissue, panniculus carnosus muscle layer, and thinning and dispersion of collagen fibers. These findings suggest a potential candidate for the development of new skin rejuvenation therapies that suppress SASP.
“This study shows that SFRP4, which is specifically expressed in aged p16ink4a-positive skin fibroblasts, contributes to SASP, and that treatment with SFRP4 causes worsening of this phenotype. To the best of our knowledge, the present study is the first to report that the suppression of SFRP4 expression in vivo ameliorates skin aging-related phenotypes, that is, adipose tissue atrophy and collagen fiber thinning, via SASP suppression.”
DOI: https://doi.org/10.18632/aging.204273
Corresponding Author: Kento Takaya - Email: kento-takaya312@keio.jp
Keywords: skin, fibroblast, SASP, SFRP4
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About Aging-US:
Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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Dr. Takushi Namba, Associate Professor at Kochi University in Japan, discusses a research paper he co-authored that was published by Aging (Aging-US) in Volume 14, Issue 19, entitled, “Lotus germ extract rejuvenates aging fibroblasts via restoration of disrupted proteostasis by the induction of autophagy.”
DOI - https://doi.org/10.18632/aging.204303
Corresponding author - Takushi Namba - t-namba@kochi-u.ac.jp
Video - https://www.youtube.com/watch?v=sXDw80HrqzM
Abstract
Cell aging attenuates cellular functions, resulting in time-dependent disruption of cellular homeostasis, which maintains the functions of proteins and organelles. Mitochondria are important organelles responsible for cellular energy production and various metabolic processes, and their dysfunction is strongly related to the progression of cellular aging. Here we demonstrate that disruption of proteostasis attenuates mitochondrial function before the induction of DNA damage signaling by proliferative and replicative cellular aging. We found that lotus (Nelumbo nucifera Gaertn.) germ extract clears abnormal proteins and agglutinates via autophagy-mediated restoration of mitochondrial function and cellular aging phenotypes. Pharmacological analyses revealed that DAPK1 expression was suppressed in aging cells, and lotus germ extract upregulated DAPK1 expression by stimulating the acetylation of histones and then induced autophagy by activating the DAPK1-Beclin1 signaling pathway. Furthermore, treatment of aging fibroblasts with lotus germ extract stimulated collagen production and increased contractile ability in three-dimensional cell culture. Thus, time-dependent accumulation of abnormal proteins and agglutinates suppressed mitochondrial function in cells in the early stage of aging, and reactivation of mitochondrial function by restoring proteostasis rejuvenated aging cells. Lotus germ extract rejuvenates aging fibroblasts via the DAPK1-Beclin1 pathway-induced autophagy to clear abnormal proteins and agglutinates.
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Keywords - aging, mitochondria, autophagy, proteostasis
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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A new review paper was published in Aging (listed as "Aging (Albany NY)" by MEDLINE/PubMed and "Aging-US" by Web of Science) Volume 14, Issue 19, entitled, “RNA modifications in aging-associated cardiovascular diseases.”
Cardiovascular disease (CVD) is a leading cause of morbidity and mortality worldwide that bears an enormous healthcare burden. Aging is a major contributing factor to CVDs. Functional gene expression network during aging is regulated by mRNAs transcriptionally and by non-coding RNAs epi-transcriptionally. RNA modifications alter the stability and function of both mRNAs and non-coding RNAs and are involved in differentiation, development and diseases.
In this new review paper, researchers Xinyu Yang, Priyanka Gokulnath, H. Immo Lehmann, Zhitao Hou, Sun Yang, Liangzhen You, Guoxia Zhang, Yanwei Xing, Ji Lei, Guoping Li, Shuwen Guo, and Hongcai Shang from Fangshan Hospital and Dongzhimen Hospital (affiliated with Beijing University of Chinese Medicine), Massachusetts General Hospital, Harvard Medical School, Heilongjiang University of Chinese Medicine, and Chinese Academy of Chinese Medical Sciences reviewed major chemical RNA modifications on mRNAs and non-coding RNAs, including N6-adenosine methylation, N1-adenosine methylation, 5-methylcytidine, pseudouridylation, 2′ -O-ribose-methylation, and N7-methylguanosine, in the aging process with an emphasis on cardiovascular aging. They also summarize the currently available methods to detect RNA modifications and the bioinformatic tools to study RNA modifications.
“More importantly, we discussed the specific implication of the RNA modifications on mRNAs and non-coding RNAs in the pathogenesis of aging-associated CVDs, including atherosclerosis, hypertension, coronary heart diseases, congestive heart failure, atrial fibrillation, peripheral artery disease, venous insufficiency, and stroke.”
DOI: https://doi.org/10.18632/aging.204311
Corresponding Authors: Guoping Li; Shuwen Guo; Hongcai Shang - Corresponding Emails: gli21@mgh.harvard.edu; guo1163@163.com; shanghongcai@bucm.edu.cn
Keywords: RNA modifications, aging, aging-related cardiovascular diseases, epitranscriptome
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About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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Listen to a blog summary of a trending research paper published by Aging (Aging-US) in Volume 14, Issue 19, entitled, “Natural variation in macrophage polarization and function impact pneumocyte senescence and susceptibility to fibrosis.” ______________________________________
Radiation is an effective treatment for many types of cancer. Unfortunately, this treatment has the potential to cause long-term side effects in some patients, including the thickening or scarring of lung tissue, known as pulmonary fibrosis. Radiation-induced pulmonary fibrosis (RIPF) is a serious complication that can occur after radiation therapy and can lead to death. Predicting an individual’s risk of developing RIPF remains challenging for clinicians, as little is known about the underlying mechanisms that cause it.
“Differential susceptibility to lung injury from radiation and other toxic insults across mouse strains is well described but poorly understood.”
Previous studies in mouse models have shown that there are natural variations in susceptibility to RIPF among different strains of mice. The mechanism(s) underlying this difference in susceptibility is still unknown. In a new study, researchers Eun Joo Chung, Seokjoo Kwon, Uma Shankavaram, Ayla O. White, Shaoli Das, and Deborah E. Citrin from the National Institutes of Health’s National Cancer Institute investigated differences in macrophage function across mouse strains and their potential contribution to varied RIPF susceptibility. On September 28, 2022, their research paper was published in Aging’s Volume 14, Issue 19, “Natural variation in macrophage polarization and function impact pneumocyte senescence and susceptibility to fibrosis.”
Full blog - https://aging-us.org/2022/10/investigating-susceptibility-to-radiation-induced-pulmonary-fibrosis/
DOI - https://doi.org/10.18632/aging.204309
Corresponding author - Deborah E. Citrin - citrind@mail.nih.gov
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Keywords - aging, senescence, macrophage, alveolar epithelial cell Type II, strain
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at https://www.Aging-US.com and connect with us:
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Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM
Fedor Galkin, Scientific Director at Deep Longevity, Inc. in Hong Kong, discusses a research paper he co-authored that was published by Aging (Aging-US) as the cover for Volume 14, Issue 18, entitled, “Psychological factors substantially contribute to biological aging: evidence from the aging rate in Chinese older adults.”
DOI - https://doi.org/10.18632/aging.204264
Corresponding author - Fedor Galkin - fedor@deeplongevity.com
Video - https://www.youtube.com/watch?v=WBxTe1fGPxI
Abstract
We have developed a deep learning aging clock using blood test data from the China Health and Retirement Longitudinal Study, which has a mean absolute error of 5.68 years. We used the aging clock to demonstrate the connection between the physical and psychological aspects of aging. The clock detects accelerated aging in people with heart, liver, and lung conditions. We demonstrate that psychological factors, such as feeling unhappy or being lonely, add up to 1.65 years to one’s biological age, and the aggregate effect exceeds the effects of biological sex, living area, marital status, and smoking status. We conclude that the psychological component should not be ignored in aging studies due to its significant impact on biological age.
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Press release - https://www.aging-us.com/news_room/Psychological-factors-substantially-contribute-to-biological-aging-evidence-from-the-aging-rate-in-Chinese-older-adults
Keywords - aging, psychological aging, lifespan psychology, aging clocks, longevity
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at https://www.Aging-US.com and connect with us:
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Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM
A new research paper was published on the cover of Aging (listed as "Aging (Albany NY)" by Medline/PubMed and "Aging-US" by Web of Science) Volume 14, Issue 19, entitled, “Centenarians consistently present a younger epigenetic age than their chronological age with four epigenetic clocks based on a small number of CpG sites.”
Aging is a progressive time-dependent biological process affecting differentially individuals, who can sometimes present exceptional longevity. Epigenetic alterations are one of the hallmarks of aging, which comprise the epigenetic drift and clock at DNA methylation level.
In a new study, researchers Antoine Daunay, Lise M. Hardy, Yosra Bouyacoub, Mourad Sahbatou, Mathilde Touvier, Hélène Blanché, Jean-François Deleuze, and Alexandre How-Kit from Foundation Jean Dausset – CEPH, Laboratory of Excellence GenMed, Sorbonne Paris Nord University, University of Paris (CRESS), and Institut François Jacob investigated the DNA methylation-based age (DNAmage) of long-lived French individuals in the CEPH Aging Cohort using four epigenetic clocks.
“In the present study, we estimated the DNA methylation-based age (DNAmage) using four epigenetic clocks based on a small number of CpGs in French centenarians and semi-supercentenarians (CSSC, n=214) as well as nonagenarians' and centenarians' offspring (NCO, n=143) compared to individuals from the French general population (CG, n=149).”
DNA methylation analysis of the nine CpGs included in the epigenetic clocks showed high correlation with chronological age (-0.66>R>0.54) and also the presence of an epigenetic drift for four CpGs that was only visible in CSSC. DNAmage analysis showed that CSSC and to a lesser extend NCO present a younger DNAmage than their chronological age (15-28.5 years for CSSC, 4.4-11.5 years for NCO and 4.2-8.2 years for CG), which were strongly significant in CSSC compared to CG (p-values<2.2e-16).
These differences suggest that epigenetic aging and potentially biological aging are slowed in exceptionally long-lived individuals and that epigenetic clocks based on a small number of CpGs are sufficient to reveal alterations of the global epigenetic clock.
“This suggests a decelerated epigenetic and biological aging in these two groups of individuals, confirming the results of three other studies performed on Italian, Australian and Israeli long-lived individuals. In addition, our study also demonstrated the possibility of using epigenetic clocks based on a small number of CpG sites to reveal DNAmage and chronological age differences between individuals with different life expectancy.”
DOI: https://doi.org/10.18632/aging.204316
Corresponding Author: Alexandre How-Kit - Email: alexandre.how-kit@fjd-ceph.org
Keywords: epigenetic clock, DNAmage, centenarians, DNA methylation, pyrosequencing, longevity
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About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at https://www.Aging-US.com and connect with us:
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Blog summary of a trending research paper published in Volume 14, Issue 18, entitled, "The association between continuous ambulatory heart rate, heart rate variability, and 24-h rhythms of heart rate with familial longevity and aging." ______________________________________
A normal resting heart rate (HR) for adults should be anywhere between 60 and 100 beats per minute. A low resting heart rate has been associated with better overall health and fitness. Crosswise, a higher resting heart rate appears to have a strong correlation with mortality. Heart rate variability (HRV), the beat-to-beat changes in heart rate, is indicative of the heart’s ability to respond to changes in physical and emotional stress. Low HRV has been shown to be a risk factor for heart disease, while high HRV has been associated with good heart health. Although HR and HRV are frequently studied, these parameters are not often investigated continuously or over long periods of time in healthy, middle-aged individuals.
“Parameters of HR and HRV are often investigated during a short electrocardiogram (ECG) measurement at the study center or in the hospital, but not continuously over a longer period while individuals continue with their daily lives.”
In a new study, researchers Janneke M. Wiersema, Annelies E.P. Kamphuis, Jos H.T. Rohling, Laura Kervezee, Abimbola A. Akintola, Steffy W. Jansen, P. Eline Slagboom, Diana van Heemst, and Evie van der Spoel from Leiden University Medical Center and Catharina Hospital used continuous ambulatory ECG measurements collected over a period of 24 to 90 hours to investigate the relationship between heart rate parameters and familial longevity and chronological age. On August 16, 2022, their research paper was published in Aging’s Volume 14, Issue 18, and entitled, “The association between continuous ambulatory heart rate, heart rate variability, and 24-h rhythms of heart rate with familial longevity and aging.”
Full blog - https://aging-us.org/2022/10/does-a-link-exist-between-longevity-aging-and-heart-rate-parameters/
DOI - https://doi.org/10.18632/aging.204219
Corresponding author - Evie van der Spoel - e.van_der_spoel@lumc.nl
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Keywords - aging, longevity, continuous ambulatory measurements, heart rate, heart rate variability
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at https://www.Aging-US.com and connect with us:
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In the fifth episode of the Longevity & Aging Series, Dr. Amit Sharma, Group Lead from SENS Research Foundation, Mountain View, CA, discusses a research paper he co-authored that was published in Volume 14, Issue 5, of Aging (Aging-US), entitled, “Enhanced co-culture and enrichment of human natural killer cells for the selective clearance of senescent cells.”
DOI - https://doi.org/10.18632/aging.203931
Corresponding Author - Amit Sharma - amit.sharma@sens.org
Video - https://www.youtube.com/watch?v=WQR8_gm2gUI
Abstract
In the context of aging and age-associated diseases, Natural Killer (NK) cells have been revealed as a key cell type responsible for the immune clearance of senescent cells. Subsequently, NK cell-based therapies have emerged as promising alternatives to drug-based therapeutic interventions for the prevention and treatment of age-related disease and debility. Given the promise of NK cell-mediated immunotherapies as a safe and effective treatment strategy, we outline an improved method by which primary NK cells can be efficiently enriched from human peripheral blood across multiple donors (ages 20-42 years old), with a practical protocol that reliably enhances both CD56dim and CD56bright NK cells by 15-fold and 3-fold, respectively. Importantly, we show that our co-culture protocol can be used as an easily adaptable tool to assess highly efficient and selective killing of senescent cells by primary NK cells enriched via our method using longer co-culture durations and a low target to effector ratio, which may be more physiological than has been achieved in previous literature.
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Longevity & Aging Series
Aging (Aging-US) and FOXO Technologies have teamed up for a special collaboration on aging research with a monthly video series: Longevity & Aging Series. This series invites Aging researchers to speak with host Dr. Brian Chen, an adjunct faculty member at the University of California San Diego and Chief Science Officer of FOXO Technologies.
Learn more - https://www.aging-us.com/longevity
Keywords - aging, senescence, natural killer cells, NKCC, immune surveillance
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at https://www.Aging-US.com and connect with us:
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Blog summary of a research paper published in Aging’s Volume 14, Issue 18, entitled, “Humoral immunoresponse elicited against an adenoviral-based SARS-CoV-2 coronavirus vaccine in elderly patients.” _________________________________________
Around the world, more than 180 COVID-19 vaccines are currently in production or development. Some COVID-19 vaccines have been less effective in the elderly—a population that is already highly vulnerable to severe viral infection. Humoral immunity, or antibody-mediated immunity, is an important weapon against COVID-19. Immune responses in the elderly are often hindered by aging, an unfortunate process known as age-related immunosenescence. Vaccines that can successfully elicit a robust humoral immune response in the elderly are critical for achieving COVID-19 immunity and interrupting disease transmission in this population.
“The development of an effective vaccine against SARS-CoV-2 targeted for an elder population is a challenge [17]. Furthermore, there is limited data describing the behavior of COVID-19 vaccines when administered to the elderly.”
Sputnik V The two most widely available vaccines in the United States are both mRNA vaccines, the Pfizer-BioNTech and Moderna vaccines. Of course, there are other vaccines that are more commonly available in other countries, such as Gam-COVID-Vac, or Sputnik V. Sputnik V is an adenoviral-based SARS-CoV-2 vaccine.
“Gam-COVID-Vac (Sputnik V), uses a heterologous recombinant adenovirus 26 (Ad26) and adenovirus 5 (Ad5) as vectors that deliver the genetic sequence of the SARS-CoV-2 Spike protein, has been administered to tens of millions of volunteers worldwide, and has a good tolerability profile [14, 15].”
Adenoviral-based vaccines use a weakened form of a common cold virus (adenovirus) to deliver the genetic instructions for making the SARS-CoV-2 spike protein. When these instructions are delivered to human cells, they cause the cells to produce the spike protein. The body then produces antibodies against the spike protein, which provides immunity against SARS-CoV-2. In early 2021, Sputnik V was the only vaccine available to the elderly in Argentina. The ability of this particular vaccine to elicit humoral immunity in this elderly population had yet to be fully investigated.
Full blog - https://aging-us.org/2022/10/adenoviral-covid-19-vaccine-elicits-robust-immunity-in-elderly-cohort/
DOI - https://doi.org/10.18632/aging.204299
Corresponding authors - Silvia Inés Cazorla - scazorla@cerela.org.ar, Diego Ploper - diegoploper@conicet.gov.ar
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About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at https://www.Aging-US.com and connect with us:
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A new research paper was published on the cover of Aging (listed as “Aging (Albany NY)” by Medline/PubMed and “Aging-US” by Web of Science) Volume 14, Issue 18, entitled, “Psychological factors substantially contribute to biological aging: evidence from the aging rate in Chinese older adults.”
Aging clocks are statistical models that enable measurements of biological age, as opposed to chronological age. While the latter is determined by one’s date of birth, the former depends on the intensity of aging processes and can be affected by genetics, life choices, and the environment. Most commonly, such aging clocks are regressors, trained to predict a person’s chronological age based on a vector of input parameters, such as clinical blood test results, gene expression levels, or DNA methylation intensities.
In a new study, researchers Fedor Galkin, Kirill Kochetov, Diana Koldasbayeva, Manuel Faria, Helene H. Fung, Amber X. Chen, and Alex Zhavoronkov from Deep Longevity, Stanford University, The Chinese University of Hong Kong, Insilico Medicine, and the Buck Institute for Research on Aging developed a deep learning aging clock using blood test data from the China Health and Retirement Longitudinal Study (CHARLS), which has a mean absolute error of 5.68 years.
“Using data from the Chinese CHARLS database, we have demonstrated that organismal aging is not only determined by physical factors but also, to a certain degree, affected by mental state and social status.”
The clock detects accelerated aging in people with heart, liver, and lung conditions. The researchers demonstrated that psychological factors, such as feeling unhappy or being lonely, add up to 1.65 years to one’s biological age, and the aggregate effect exceeds the effects of biological sex, living area, marital status, and smoking status. They concluded that the psychological component should not be ignored in aging studies due to its significant impact on biological age. The study findings further support the necessity of companionship and a psychologically pleasant environment for healthy longevity.
“We interpreted biological age as a proxy for the general state of health and show that positive feelings (happiness, hope, safety) have a significant impact on the former.”
DOI: https://doi.org/10.18632/aging.204264
Corresponding Author: Fedor Galkin – Email: fedor@deeplongevity.com
Keywords: psychological aging, lifespan psychology, aging clocks, longevity
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About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at https://www.Aging-US.com and connect with us:
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Blog summary of a trending research paper published by Aging (Aging-US), entitled, "Fetal programming: in utero exposure to acrylamide leads to intergenerational disrupted ovarian function and accelerated ovarian aging." ________________________________________
The food, beverages and products that women are exposed to before and during pregnancy can have lifelong consequences for babies in the womb. This concept is known as fetal programming. Introducing endocrine-disrupting chemicals (EDCs; toxins) during critical moments of fetal development can significantly impact the child’s health, development and fertility. These negative impacts may even compound in future generations.
“However, our understanding of the negative effects of chemicals on health in women is less than those in men [24].”
ACRYLAMIDE Frying, roasting or baking starchy food at high temperatures produces a Maillard reaction. A problematic result of this reaction is the formation of a chemical compound called acrylamide (ACR). Acrylamide can be found in many common foods, including french fries, chips, bread, crackers, coffee, and so on. Exposure to this chemical during pregnancy has been linked to reduced development and reproductive function.
“Based on the formation of ACR in food during high temperatures and its presence in water and cosmetics [25, 26], this potential EDC may constitute a major problem for human health and could notably affect female fertility by influencing the ovary structure and function.”
While the effects of ACR in-utero have been documented, researchers Nouf Aldawood, Maroua Jalouli, Abdulkarem Alrezaki, Saber Nahdi, Abdullah Alamri, Mohamed Alanazi, Salim Manoharadas, Saleh Alwasel, and Abdel Halim Harrath from King Saud University wondered how exposure to acrylamide impacts health, development and fertility after a second generation. In a new study, the team investigated exposure to this toxin and its effects on ovarian function over the course of two generations of rats. On September 6, 2022, their research paper was published in Aging’s Volume 14, Issue 17, and entitled, “Fetal programming: in utero exposure to acrylamide leads to intergenerational disrupted ovarian function and accelerated ovarian aging.”
Full blog - https://aging-us.org/2022/09/unborn-children-exposed-to-common-chemical-leads-to-fertility-defects/
DOI - https://doi.org/10.18632/aging.204269
Corresponding author - Abdel Halim Harrath - hharrath@ksu.edu.sa
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Keywords - aging, acrylamide, transgeneration, apoptosis, female fertility, ovary aging
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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A new research paper was published in Aging (listed as “Aging (Albany NY)” by MEDLINE/PubMed and “Aging-US” by Web of Science) Volume 14, Issue 17, entitled, “Probiotics treatment for Parkinson disease: a systematic review and meta-analysis of clinical trials.”
People with Parkinson’s disease (PwP) exhibit gut dysbiosis and considerable gastrointestinal (GI) symptoms. Probiotics, beneficial strains of microorganisms, and supplements optimize the intestinal environment and alleviate GI symptoms among elderly people.
In a new study, researchers Chien-Tai Hong, Jia-Hung Chen and Tsai-Wei Huang from Taipei Medical University conducted a systematic review and meta-analysis of clinical trials to investigate the effects of probiotics on people with Parkinson’s disease. PubMed, Embase and Cochrane Library databases were used. Six randomized controlled trials (RCTs) and two open-label studies were included. Most of the probiotic regimens were based on Lactobacillus and Bifidobacterium. Six studies investigated the benefit of probiotics for GI symptoms, especially for PwP with functional constipation, and two RCTs assessed probiotics’ effect on systematic metabolism and inflammation. Major outcomes were the effects of probiotics on GI symptoms, including bowel movement and stool characteristics.
“In the meta-analysis, probiotic treatment significantly increased the frequency of bowel movements among PwP (mean difference [MD]: 1.06 /week, 95% confidence interval [CI]: 0.61 to 1.51, p < 0.001, I2 = 40%). Additionally, probiotic treatment significantly normalized stool consistency (standard MD: 0.61, 95% CI = 0.31 to 0.91, p < 0.001, I2 = 0%).”
Although the probiotic compositions varied, the researchers found that probiotic treatment significantly attenuated constipation for people with Parkinson’s disease and exhibited possible systematic effects on inflammation and metabolism. Given the tolerability of probiotics, the present meta-analysis may provide more consolidated evidence of the benefit of probiotics on constipation in people with Parkinson’s disease and a possible new therapeutic approach for disease modification.
“This review and meta-analysis determined that probiotic treatments, mainly Lactobacilli and Bifidobacterium–based regimens, effectively alleviated constipation. Adverse effects are generally tolerable. However, considering the gut microbiota is highly associated with a person’s environment and diet, studies from other continents are required to establish the benefit of probiotics on constipation. Moreover, probiotic treatment is likely to affect the systemic inflammation and metabolism of PwP, but further studies are warranted to investigate the possibility of the disease modification effect on PD.”
DOI: https://doi.org/10.18632/aging.204266
Corresponding Author: Tsai-Wei Huang – Email: tsaiwei@tmu.edu.tw
About Aging-US:
Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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A new research paper was published in Aging (listed as "Aging (Albany NY)" by Medline/PubMed and "Aging-US" by Web of Science) Volume 14, Issue 17, entitled, “Aging, prevalence and risk factors of MRI-visible enlarged perivascular spaces.”
Cerebral small vessel disease (CSVD) increases with age and is associated with stroke and cognitive decline. Enlarged Perivascular Spaces (ePVS) is an emerging marker of CSVD, but its prevalence over the life span remains unclear.
In a new study, researchers Frances Rodriguez Lara, Ashlea Lynn Scruton, Adlin Pinheiro, Serkalem Demissie, Pedram Parva, Andreas Charidimou, Michael Francis, Jayandra J. Himali, Charles DeCarli, Alexa Beiser, Sudha Seshadri, and Jose R. Romero from Boston University School of Medicine, Boston University School of Public Health, NHLBI’s Framingham Heart Study, Veterans Affairs Boston Health System, University of Texas Health Sciences Center, and University of California at Davis characterized the age and sex-specific prevalence of ePVS and its relation to age-specific risk factors in a large community-based sample.
“In this report we aim to describe 1) the age and sex specific prevalence of ePVS in a large sample of asymptomatic, community dwelling individuals, and contrast ePVS prevalence with the prevalence of vascular risk factors in the same age groups, and 2) study the association of vascular risk factors with burden of ePVS by brain region. This knowledge will help support the increasing number of studies of ePVS as a biomarker of aging and age related adverse neurological outcomes.”
Full Press Release - https://aging-us.net/2022/09/22/aging-aging-prevalence-and-risk-factors-of-mri-visible-enlarged-perivascular-spaces/
DOI: https://doi.org/10.18632/aging.204181
Corresponding Author: Jose R. Romero - Email: joromero@bu.edu
Keywords: neurological markers, aging, disease marker, perivascular spaces
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About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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Listen to a blog summary about a trending research paper published by Aging (Aging-US as the cover of Volume 14, Issue 17, entitled, "Extracellular microRNA and cognitive function in a prospective cohort of older men: The Veterans Affairs Normative Aging Study.” __________________________________________
Can factors in our bloodstream tell us about our cognitive abilities or predict cognitive decline later in life? Among individuals with dementias, including Alzheimer’s disease (AD), studies have identified extracellular microRNAs (miRNAs) as potential biomarkers of cognitive impairment. In cognitively normal individuals, however, this association has not yet been fully investigated.
“Understanding the functions of miRNAs in the earliest stages of cognitive decline will expand our knowledge on the biology of prodromal AD and the roles of circulating miRNAs in neurodegenerative diseases and could result in identification of therapeutic targets to guide drug development [17].”
In a new research paper, published on the cover of Volume 14, Issue 17, of Aging (listed as “Aging (Albany NY)” by Medline/PubMed and “Aging-US” by Web of Science), researchers Nicole Comfort, Haotian Wu, Peter De Hoff, Aishwarya Vuppala, Pantel S. Vokonas, Avron Spiro, Marc Weisskopf, Brent A. Coull, Louise C. Laurent, Andrea A. Baccarelli, and Joel Schwartz from Columbia University Mailman School of Public Health, University of California San Diego, VA Boston Healthcare System, Boston University School of Medicine, and Harvard TH Chan School of Public Health investigated expression levels of extracellular miRNAs circulating in blood plasma taken from cognitively normal men and the association between these miRNAs and cognitive function. Their secondary goal was to investigate the genes and biological pathways associated with miRNAs linked to cognitive function or decline. The research paper was published on September 6, 2022, and entitled, “Extracellular microRNA and cognitive function in a prospective cohort of older men: The Veterans Affairs Normative Aging Study.”
Full blog - https://aging-us.org/2022/09/can-micrornas-in-the-bloodstream-signal-cognitive-decline/
DOI - https://doi.org/10.18632/aging.204268
Corresponding author - Nicole Comfort - nicole.comfort@columbia.edu
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Press release - https://aging-us.com/news_room/Extracellular-microRNA-and-cognitive-function-in-a-prospective-cohort-of-older-men
Keywords - aging, plasma, extracellular RNA, RNA-seq, microRNA, cognitive decline, cognitive impairment
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at https://www.Aging-US.com and connect with us:
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Dr. May Beydoun from the Laboratory of Epidemiology and Population Sciences, NIA/NIH/IRP, in Baltimore, MD, discusses a research paper she co-authored that was published by Aging (Aging-US) as the cover for Volume 14, Issue 13, entitled, “Epigenetic clocks and their association with trajectories in perceived discrimination and depressive symptoms among US middle-aged and older adults.”
DOI - https://doi.org/10.18632/aging.204150
Corresponding author - May A. Beydoun - baydounm@mail.nih.gov
Video version - https://www.youtube.com/watch?v=gkiDhjTL0YY
Abstract
Background: Perceived discrimination may be associated with accelerated aging later in life, with depressive symptoms acting as potential mediator.
Methods: A nationally representative sample of older adults was used [Health and Retirement Study 2010–2016, Age: 50–100 y in 2016, N = 2,806, 55.6% female, 82.3% Non-Hispanic White (NHW)] to evaluate associations of perceived discrimination measures [Experience of discrimination or EOD; and Reasons for Perceived discrimination or RPD) and depressive symptoms (DEP)] with 13 DNAm-based measures of epigenetic aging. Group-based trajectory and four-way mediation analyses were used.
Results: Overall, and mostly among female and NHW participants, greater RPD in 2010–2012 had a significant adverse total effect on epigenetic aging [2016: DNAm GrimAge, DunedinPoAm38 (MPOA), Levine (PhenoAge) and Horvath 2], with 20–50% of this effect being explained by a pure indirect effect through DEP in 2014–2016. Among females, sustained elevated DEP (2010–2016) was associated with greater LIN DNAm age (β ± SE: +1.506 ± 0.559, p = 0.009, reduced model), patterns observed for elevated DEP (high vs. low) for GrimAge and MPOA DNAm markers. Overall and in White adults, the relationship of the Levine clock with perceived discrimination in general (both EOD and RPD) was mediated through elevated DEP.
Conclusions: Sustained elevations in DEP and RPD were associated with select biological aging measures, consistently among women and White adults, with DEP acting as mediator in several RPD-EPICLOCK associations.
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Press release - https://www.aging-us.com/news_room/epigenetic-clocks-and-their-association-with-perceived-discrimination-and-depressive-symptoms
Keywords - aging, DNA methylation, epigenetic clocks, biological age, perceived discrimination, depressive symptoms
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at https://www.Aging-US.com and connect with us:
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A new research paper was published on the cover of Aging (Aging-US) Volume 14, Issue 17, entitled, “Extracellular microRNA and cognitive function in a prospective cohort of older men: The Veterans Affairs Normative Aging Study.”
Aging-related cognitive decline is an early symptom of Alzheimer’s disease and other dementias, and on its own can have substantial consequences on an individual’s ability to perform important everyday functions. Despite increasing interest in the potential roles of extracellular microRNAs (miRNAs) in central nervous system (CNS) pathologies, there has been little research on extracellular miRNAs in early stages of cognitive decline.
In a new study, researchers Nicole Comfort, Haotian Wu, Peter De Hoff, Aishwarya Vuppala, Pantel S. Vokonas, Avron Spiro, Marc Weisskopf, Brent A. Coull, Louise C. Laurent, Andrea A. Baccarelli, and Joel Schwartz from Columbia University Mailman School of Public Health, University of California San Diego, VA Boston Healthcare System, Boston University School of Medicine, and Harvard TH Chan School of Public Health leveraged the longitudinal Normative Aging Study (NAS) cohort to investigate associations between plasma miRNAs and cognitive function among cognitively normal men.
“In a cohort of older men from Massachusetts, we investigated associations between plasma miRNAs and global cognition and rate of global cognitive decline measured by the MMSE.”
Full press release - https://aging-us.net/2022/09/15/aging-extracellular-microrna-and-cognitive-function-in-a-prospective-cohort-of-older-men-the-veterans-affairs-normative-aging-study/
DOI: https://doi.org/10.18632/aging.204268
Corresponding Author: Nicole Comfort – nicole.comfort@columbia.edu
Keywords: plasma, extracellular RNA, RNA-seq, microRNA, cognitive decline, cognitive impairment
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About Aging-US:
Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at www.Aging-US.com and connect with us:
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Listen to a blog summary of a trending review published by Aging (Aging-US), entitled, "New hallmarks of ageing: a 2022 Copenhagen ageing meeting summary." ______________________________________
Humans battle a number of biological processes with age that lead to the gradual deterioration of cells and tissues. Frailty, disability, disease, and death are all costly fates of aging. Researchers who study aging aim to change this fate, however, the mechanisms of aging are still all but fully understood.
In 2013, López-Otín and colleagues attempted to identify these biological processes and proposed the original nine hallmarks of aging: genomic instability, telomere attrition, epigenetic alterations, mitochondrial dysfunction, loss of proteostasis, deregulated nutrient-sensing, cellular senescence, stem cell exhaustion, and altered intercellular communication. These hallmarks of aging have helped to provide a framework for thought about the causes and consequences of aging, as well as potential targets for therapeutic interventions. Now, nine years later, the hallmarks of aging have been updated in light of recent discoveries.
“In the nearly past 10 years, our in-depth exploration on ageing research has enabled us to formulate new hallmarks of ageing which are compromised autophagy, microbiome disturbance, altered mechanical properties, splicing dysregulation, and inflammation, among other emerging ones.”
This update was presented on March 22, 2022, at the “New Hallmarks of Ageing” research symposium in Copenhagen, Denmark. On August 29, 2022, a review paper summarizing the symposium was published in Aging (Aging-US), entitled, “New hallmarks of ageing: a 2022 Copenhagen ageing meeting summary.”
Full blog - https://aging-us.org/2022/09/the-2022-new-hallmarks-of-ageing-research-symposium/
DOI - https://doi.org/10.18632/aging.204248
Corresponding authors - Tinna Stevnsner - tvs@mbg.au.dk, Lene Juel Rasmussen - lenera@sund.ku.dk, Evandro F. Fang - e.f.fang@medisin.uio.no
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Keywords - aging, hallmarks of ageing, neurodegeneration, healthspan, longevity, autophagy
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at https://www.Aging-US.com and connect with us:
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In the fourth episode of the Longevity & Aging Series, Dr. Carly Bobak from Dartmouth College, Dr. Cristian Coarfa from Baylor College of Medicine, and Dr. Andrew DiNardo from Baylor College of Medicine, discuss a research paper they co-authored that was published in Volume 14, Issue 5, of Aging (Aging-US), entitled, “Increased DNA methylation, cellular senescence and premature epigenetic aging in guinea pigs and humans with tuberculosis.”
DOI - https://doi.org/10.18632/aging.203936
Corresponding Authors - Carly A. Bobak - carlybobak@dartmouth.edu, Cristian Coarfa - coarfa@bcm.edu, and Andrew R. DiNardo - andrew.dinardo@bcm.edu
Abstract
Background: Tuberculosis (TB) is the archetypical chronic infection, with patients having months of symptoms before diagnosis. In the two years after successful therapy, survivors of TB have a three-fold increased risk of death.
Methods: Guinea pigs were infected with Mycobacterium tuberculosis (Mtb) for 45 days, followed by RRBS DNA methylation analysis. In humans, network analysis of differentially expressed genes across three TB cohorts were visualized at the pathway-level. Serum levels of inflammation were measured by ELISA. Horvath (DNA methylation) and RNA-seq biological clocks were used to investigate shifts in chronological age among humans with TB.
Results: Guinea pigs with TB demonstrated DNA hypermethylation and showed system-level similarity to humans with TB (p-value = 0.002). The transcriptome in TB in multiple cohorts was enriched for DNA methylation and cellular senescence. Senescence associated proteins CXCL9, CXCL10, and TNF were elevated in TB patients compared to healthy controls. Humans with TB demonstrate 12.7 years (95% CI: 7.5, 21.9) and 14.38 years (95% CI: 10.23–18.53) of cellular aging as measured by epigenetic and gene expression based cellular clocks, respectively.
Conclusions: In both guinea pigs and humans, TB perturbs epigenetic processes, promoting premature cellular aging and inflammation, a plausible means to explain the long-term detrimental health outcomes after TB.
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Longevity & Aging Series
Aging (Aging-US) and FOXO Technologies have teamed up for a special collaboration on aging research with a monthly video series: Longevity & Aging Series. This series invites Aging researchers to speak with host Dr. Brian Chen, an adjunct faculty member at the University of California San Diego and Chief Science Officer of FOXO Technologies.
Learn more - https://www.aging-us.com/longevity
Keywords - aging, tuberculosis, multi-cohort analysis, network analysis, DNA methylation, senescence, Cavia porcellus, DNA hypermethylation, epigenetic aging
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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A new research paper was published in Aging (“Aging (Albany NY)” by Medline/PubMed, “Aging-US” by Web of Science) Volume 14, Issue 16, entitled, “Systemic lipolysis promotes physiological fitness in Drosophila melanogaster.”
A large body of literature shows that lipid metabolism exerts profound regulatory effects on aging and affects stress responses. Interventions such as caloric restriction or fasting robustly promote lipid catabolism and improve aging-related phenotypical markers.
Researchers Linshan Shang, Elizabeth Aughey, Huiseon Kim, Timothy D. Heden, Lu Wang, Charles P. Najt, Nicholas Esch, Sophia Brunko, Juan E. Abrahante, Marissa Macchietto, Mara T. Mashek, Todd Fairbanks, Daniel E. L. Promislow, Thomas P. Neufeld, and Douglas G. Mashek from the University of Minnesota and University of Washington investigated the direct effect of increased lipid catabolism via overexpression of bmm (brummer, FBgn0036449), the major triglyceride hydrolase in Drosophila, on lifespan and physiological fitness.
Comprehensive characterization was carried out using RNA-seq, lipidomics and metabolomics analysis. Global overexpression of bmm strongly promoted numerous markers of physiological fitness, including increased female fecundity, fertility maintenance, preserved locomotion activity, increased mitochondrial biogenesis and oxidative metabolism. Since bmm drives fatty acid oxidation, the data in this study implicated differential partitioning of glucose into the pentose phosphate pathway and purine biosynthesis between males and females. However, the underlying mechanisms through which bmm elicits these sex-specific effects remains to be determined.
“Increased bmm robustly upregulated the heat shock protein 70 (Hsp70) family of proteins, which equipped the flies with higher resistance to heat, cold, and ER [endoplasmic reticulum] stress via improved proteostasis.”
Despite improved physiological fitness, bmm overexpression did not extend lifespan. Taken together, these data show that bmm overexpression has broad beneficial effects on physiological fitness, but not lifespan.
“Collectively, these studies reveal diverse beneficial effects of global elevation of lipolysis on physiological fitness. This work provides additional rationale for pursuing therapeutic approaches, as done previously [39], that enhance lipolysis to mitigate metabolic and aging-related diseases.”
DOI: https://doi.org/10.18632/aging.204251
Corresponding Author: Douglas G. Mashek – Email: dmashek@umn.edu
Keywords: brummer, lipolysis, physiological fitness, stress resistance, proteostasis
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About Aging-US:
Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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A new research paper was published in Aging (“Aging (Albany NY)” by Medline/PubMed, “Aging-US” by Web of Science) on the cover of Volume 14, Issue 16, entitled, “Synergism of BCL-2 family inhibitors facilitates selective elimination of senescent cells.”
Cellular senescence, a complex cellular response to stress characterized by a halt of cell cycle progression, is one factor contributing to aging. Accumulation of senescent cells in tissues with advancing age participates in the pathogenesis of several human age-associated diseases.
Specific senescent secretome, the resistance of senescent cells to apoptotic stimuli, and lack of immune system response contribute to the accumulation of senescent cells and their adverse effects in tissues. Inhibition of antiapoptotic machinery, augmented in senescent cells, by BCL-2 protein family inhibitors represents a promising approach to eliminate senescent cells from tissues.
“In this study, with the goal of decreasing the toxicity and potential onset of resistance to senolytic BCL-2 inhibitor monotherapy, we explored the effects of combined treatment covering both BCL-2 and MCL-1 anti-apoptotic factors in human cells.”
Researchers David Rysanek, Pavla Vasicova, Jayaprakash Narayana Kolla, David Sedlak, Ladislav Andera, Jiri Bartek, and Zdenek Hodny from the Czech Academy of Sciences and the Danish Cancer Society Research Center aimed to explore synergistic and selective senolytic effects of anti-apoptotic BCL-2 family targeting compounds, particularly BH3 mimetics.
“Using human non-transformed cells RPE-1, BJ, and MRC-5 brought to ionizing radiation-, oncogene-, drug-induced and replicative senescence, we found synergy in combining MCL-1 selective inhibitors with other BH3 mimetics.”
In an attempt to uncover the mechanism of such synergy, the team revealed that the surviving subpopulation of cells resistant to individually applied ABT-737/ABT-263, MIK665, ABT-199, and S63845 BCL-2 family inhibitors showed elevated MCL-1 compared to untreated control cells indicating the presence of a subset of cells expressing high MCL-1 levels and, therefore, resistant to BCL-2 inhibitors within the original population of senescent cells.
Overall, the researchers found that combining BCL-2 inhibitors can be beneficial for eliminating senescent cells, thereby enabling use of lower, potentially less toxic, doses of drugs compared to monotherapy, thereby overcoming the resistance of the subpopulation of senescent cells to monotherapy.
DOI: https://doi.org/10.18632/aging.204207
Corresponding Author: Jiri Bartek, Zdenek Hodny – Email: jb@cancer.dk, hodny@img.cas.cz
Keywords: homoharringtonine, cellular senescence, BCL-2, MCL-1, senolytics
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About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at https://www.Aging-US.com and connect with us:
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Listen to a blog summary of a trending research paper published by Aging, entitled, "Regulation of microglial activation in stroke in aged mice: a translational study.“ __________________________________________
A stroke can occur when the blood supply in and around the brain becomes interrupted. A hemorrhagic stroke is when a blood vessel bursts in or near the brain. An ischemic stroke is caused when a blood vessel carrying oxygen and nutrients to the brain is obstructed—usually by a clot. The most common type of stroke is ischemic, which accounts for approximately 87% of all strokes in humans. A major risk factor for an ischemic stroke is aging.
Inflammation (a chronic condition among the elderly) is a key contributing factor to strokes, and microglia are the primary immune cells in the brain. Researchers recently identified a role for the microglial IRF5-IRF4 regulatory axis in mediating responses after stroke. However, whether or not aged microglia also undergo the same regulatory mechanisms after a stroke had previously not been determined.
“Microglial activation plays a central role in initiating and perpetuating the post-stroke inflammation, and acts as a ‘double-edged’ sword to confer both detrimental and beneficial effects [9].”
In a recent study, researchers Conelius Ngwa, Abdullah Al Mamun, Shaohua Qi, Romana Sharmeen, Yan Xu, and Fudong Liu from The University of Texas Health Science Center at Houston investigated aged mice and the role of the microglial IRF5-IRF4 regulatory axis after a stroke. On August 12, 2022, their research paper was published in Aging’s Volume 14, Issue 15, and entitled, “Regulation of microglial activation in stroke in aged mice: a translational study.“
Full blog - https://aging-us.org/2022/08/stroke-outcomes-mediated-by-these-2-mechanisms/
DOI - https://doi.org/10.18632/aging.204216
Corresponding author - Fudong Liu - Fudong.Liu@uth.tmc.edu
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Keywords - aging, inflammation, IRF, inflammation, microglia, stroke
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at https://www.Aging-US.com and connect with us:
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In the third episode of the Longevity & Aging Series, Dr. Steve Horvath, Professor of Human Genetics and Biostatistics at UCLA, and Principal Investigator at Altos Labs, discusses the evolution of aging research and epigenetic clocks with host Brian Chen.
Special Collection on Steve Horvath's Publications in Aging - https://www.aging-us.com/special-collections-archive/steve-horvath
Author contact - Steve Horvath - shorvath@mednet.ucla.edu
Longevity & Aging Series - https://www.aging-us.com/longevity
Transcript - https://aging-us.net/2022/08/23/longevity-aging-series-ep-3-dr-steve-horvath-epigenetic-clocks/
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us:
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Listen to a blog summary of a trending research paper featured as the cover for Volume 14, Issue 15 of Aging (Aging-US), entitled, "Profiles of behavioral, social and psychological well-being in old age and their association with mobility-limitation-free survival." _____________________________
Successful, or healthy, aging may be the result of adherence to several protective factors simultaneously within all three of the well-being domains. Previously, the majority of research on healthy aging has been limited to a single domain per study. In a new study, researchers Marguerita Saadeh, Xiaonan Hu, Serhiy Dekhtyar, Anna-Karin Welmer, Davide L. Vetrano, Weili Xu, Laura Fratiglioni, and Amaia Calderón-Larrañaga (from Karolinska Institutet, Karolinska University Hospital, Stockholm University, Lund University, and Stockholm Gerontology Research Center) believe that the vast heterogeneity in aging phenotypes cannot be explained by one domain of well-being alone. On July 18, 2022, their research paper was published on the cover of Aging’s Volume 14, Issue 15, and entitled, “Profiles of behavioral, social and psychological well-being in old age and their association with mobility-limitation-free survival.”
Full blog - https://aging-us.org/2022/08/3-domains-of-well-being-extend-elderly-mobility-and-longevity/
DOI - https://doi.org/10.18632/aging.204182
Corresponding author - Marguerita Saadeh - marguerita.saadeh@ki.se
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Keywords - aging, mobility, survival, well-being, older adults, successful aging
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at https://www.Aging-US.com and connect with us:
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Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM
Aging (Aging-US) Volume 14, Issue 15: https://www.aging-us.com/issue/v14i15
Research Paper (Cover): “Profiles of behavioral, social and psychological well-being in old age and their association with mobility-limitation-free survival” https://doi.org/10.18632/aging.204182
Editorial: “Sex difference in epigenomic instability during human aging” https://doi.org/10.18632/aging.204199
Editorial: “NAD+ to assess health in aging humans” https://doi.org/10.18632/aging.204220
Editorial: “T cell senescence by N-glycan branching” https://doi.org/10.18632/aging.204239
Research Paper: “mtDNA variability determines spontaneous joint aging damage in a conplastic mouse model” https://doi.org/10.18632/aging.204153
Research Paper: “Senolytic drugs relieve pain by reducing peripheral nociceptive signaling without modifying joint tissue damage in spontaneous osteoarthritis” https://doi.org/10.18632/aging.204204
Research Paper: “Ascorbic acid induces salivary gland function through TET2/acetylcholine receptor signaling in aging SAMP1/Klotho (-/-) mice” https://doi.org/10.18632/aging.204213
Research Paper: “Regulation of microglial activation in stroke in aged mice: a translational study” https://doi.org/10.18632/aging.204216
Research Paper: “PDCD10 promotes the aggressive behaviors of pituitary adenomas by up-regulating CXCR2 and activating downstream AKT/ERK signaling” https://doi.org/10.18632/aging.204206
Research Paper: “Influence of cardiovascular risk burden on pulmonary function trajectory: role of physical and social activities” https://doi.org/10.18632/aging.204201
Research Paper: “miRNA-338-3p inhibits the migration, invasion and proliferation of human lung adenocarcinoma cells by targeting MAP3K2” https://doi.org/10.18632/aging.204198
Research Paper: “Serial neurocognitive changes following transcatheter aortic valve replacement: comparison between low and intermediate-high risk groups” https://doi.org/10.18632/aging.204202
Research Paper: “MAB21L1 promotes survival of lens epithelial cells through control of αB-crystallin and ATR/CHK1/p53 pathway” https://doi.org/10.18632/aging.204203
Research Paper: “Interleukin-17D promotes lung cancer progression by inducing tumor-associated macrophage infiltration via the p38 MAPK signaling pathway” https://doi.org/10.18632/aging.204208
Research Paper: “A signature constructed with mitophagy-related genes to predict the prognosis and therapy response for breast cancer” https://doi.org/10.18632/aging.204209
Research Paper: “Artemisia argyi exhibits anti-aging effects through decreasing the senescence in aging stem cells” https://doi.org/10.18632/aging.204210
Research Paper: “SIAH1-mediated RPS3 ubiquitination contributes to chemosensitivity in epithelial ovarian cancer” https://doi.org/10.18632/aging.204211
Research Paper: “CBXs-related prognostic gene signature correlates with immune microenvironment in gastric cancer” https://doi.org/10.18632/aging.204214
Research Paper: “Targeting circRNA-MAP4K2 for the treatment of diabetes-induced retinal vascular dysfunction” https://doi.org/10.18632/aging.204215
Research Paper: “The comprehensive expression and functional analysis of m6A modification “readers” in hepatocellular carcinoma” https://doi.org/10.18632/aging.204217
Research Paper: “Establishing and validating an ADCP-related prognostic signature in pancreatic ductal adenocarcinoma” https://doi.org/10.18632/aging.204221
Research Paper: “SAAL1, a novel oncogene, is associated with prognosis and immunotherapy in multiple types of cancer” https://doi.org/10.18632/aging.204224
Research Paper: “Comprehensive pan-cancer analysis reveals the prognostic value and immunological role of SPIB” https://doi.org/10.18632/aging.204225
Research Paper: “Clinical outcomes and potential therapies prediction of subgroups based on a ferroptosis-related long non-coding RNA signature for gastric cancer” https://doi.org/10.18632/aging.204227
Visit our website at https://www.Aging-US.com.
Listen to a blog summary of an editorial published in Volume 14, Issue 14 of Aging (Aging-US), entitled, "Restoring rhythm to prevent age-related fractures.” ________________________________
The circadian rhythm is a daily cycle (24 hours) of biological activity that is driven by an internal biological clock. A regular circadian rhythm is important for maintaining numerous facets of human life. Aging-related changes to this delicate rhythm have demonstrated negative consequences in many aspects of health, including bone health.
“Among the many risk factors for osteoporosis, a new kid on the block is disruption of the biological clock.”
On July 19, 2022, an editorial paper was published in Aging‘s Volume 14, Issue 14, entitled, “Restoring rhythm to prevent age-related fractures.” In this editorial, Annelies E. Smit, Maaike Schilperoort and Elizabeth M. Winter from Leiden University Medical Center discuss the treatment of osteoporosis by way of restoring the circadian rhythm. The researchers review the use of both medical and lifestyle interventions that aim to restore the circadian rhythm to minimize the risk of aging-related osteoporotic fractures.
Full blog - https://aging-us.org/2022/08/osteoporosis-linked-to-age-related-changes-in-circadian-rhythm/
DOI - https://doi.org/10.18632/aging.204192 (PDF Download)
Corresponding author - Elizabeth M. Winter - e.m.winter@lumc.nl
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Keywords - aging, circadian rhythm, fractures, osteoporosis, glucocorticoids, chronotherapy
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at https://www.Aging-US.com and connect with us:
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A new research paper was published in Aging (Aging-US) Volume 14, Issue 14, entitled, “Common electrocardiogram measures are not associated with telomere length.”
Aging is accompanied by telomere shortening. Increased telomere shortening is considered a marker of premature aging. Cardiac aging results in the development of cardiac pathologies.
Electrocardiogram (ECG) measures reflect cardiac excitation, conduction, and repolarization. ECG measures also prolong with aging and are associated with cardiac pathologies including atrial fibrillation. As premature prolongation of ECG measures is observed, researchers (Aenne S. von Falkenhausen, Rebecca Freudling, Melanie Waldenberger, Christian Gieger, Annette Peters, Martina Müller-Nurasyid, Stefan Kääb, and Moritz F. Sinner), from Ludwig-Maximilians-University Munich, Partner Site Munich Heart Alliance, German Research Center for Environmental Health, and Johannes Gutenberg University, hypothesized that such prolongation may be associated with telomere length.
“We studied the large, community-based KORA F4 Study. Of 3,080 participants enrolled between 2006 and 2007 with detailed information on demographic, anthropometric, clinical, and ECG characteristics, 2,575 presented with available data on leukocyte telomere length.”
Telomere length was determined by real-time quantitative PCR and expressed relative to a single copy gene. The researchers fitted multivariable adjusted linear regression models to associate the ECG measures RR-interval, PR-interval, QRS-duration, and heart rate corrected QTc with telomere length.
In this cohort, the mean age was 54.9±12.9 years and 46.6% were men. Increased age was associated with shorter telomere length (p<0.01), and men had shorter telomere length than women (p<0.05). In unadjusted models, heart rate (p=0.023), PR-interval (p<0.01), and QTc-interval (p<0.01) were significantly associated with shorter telomere length. However, no significant associations remained after accounting for age, sex, and covariates.
The researchers found that ECG measures are age-dependent, but not associated with shortened telomere length as a marker of biological aging. Further research is warranted to clarify if shortened telomeres are associated with clinical cardiac pathologies including atrial fibrillation.
“In conclusion, ECG measures are clearly age-dependent. However, in a large, well-characterized, and sufficiently powered cohort we were not able to substantiate the hypothesis that telomere length as a marker of biological age is a relevant contributor to this age-dependent prolongation of ECG measures.”
DOI: https://doi.org/10.18632/aging.204149
Corresponding Author: Moritz F. Sinner – Email: moritz.sinner@med.uni-muenchen.de
Keywords: electrocardiogram, telomere length, cardiac aging
About Aging-US:
Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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In the second installment of the Longevity & Aging Series, Dr. Steve Horvath, a world-renowned researcher, geneticist, biostatistician, Professor of Human Genetics and Biostatistics at the University of California, and Principal Investigator at Altos Labs, revisits 29 papers he co-authored that were published by Aging (Aging-US) and featured as a special collection of his research.
Special Collection - https://www.aging-us.com/special-collections-archive/steve-horvath
Author contact - Steve Horvath - shorvath@mednet.ucla.edu
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at https://www.Aging-US.com or connect with us:
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Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com
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A new research paper was published in Aging (abbreviated as "Aging (Albany NY)" by Medline/PubMed and as "Aging-US" by Web of Science) on the cover of Volume 14, Issue 14, entitled, “Aging the brain: multi-region methylation principal component based clock in the context of Alzheimer’s disease.”
Alzheimer’s disease (AD) risk increases exponentially with age and is associated with multiple molecular hallmarks of aging, one of which is epigenetic alterations. Epigenetic age predictors based on 5’ cytosine methylation (DNAm), or epigenetic clocks, have previously suggested that epigenetic age acceleration may occur in AD brain tissue.
“Epigenetic clocks are promising tools for the quantification of biological aging, yet we hypothesize that investigation of brain aging in AD will be assisted by the development of brain-specific epigenetic clocks.”
In this new study, researchers Kyra L. Thrush, David A. Bennett, Christopher Gaiteri, Steve Horvath, Christopher H. van Dyck, Albert T. Higgins-Chen, and Morgan E. Levine, from Yale University, Rush University Medical Center, University of California Los Angeles, VA Connecticut Healthcare System, and Altos Labs, hypothesized that a brain age methylation-based predictor could be developed with meaningful disease associations and broad multi-brain-region utility.
“To test this, we used DNAm capture to generate a PC-based epigenetic predictor of brain aging which we show to: (1) strongly reflect AD neuropathology and cognitive decline, and (2) track age across multiple brain regions.”
The team generated a novel age predictor, termed PCBrainAge, that was trained solely in cortical samples. This predictor utilizes a combination of principal components analysis and regularized regression, which reduces technical noise and greatly improves test-retest reliability.
“To characterize the scope of PCBrainAge’s utility, we generated DNAm data from multiple brain regions in a sample from the Religious Orders Study and Rush Memory and Aging Project.”
PCBrainAge captures meaningful heterogeneity of aging: Its acceleration demonstrates stronger associations with clinical AD dementia, pathologic AD, and APOE ε4 carrier status compared to extant epigenetic age predictors. It further does so across multiple cortical and subcortical regions.
“Overall, PCBrainAge’s increased reliability and specificity makes it a particularly promising tool for investigating heterogeneity in brain aging, as well as epigenetic alterations underlying AD risk and resilience.”
DOI: https://doi.org/10.18632/aging.204196
Corresponding Author: Albert T. Higgins-Chen - Email: a.higginschen@yale.edu
Keywords: epigenetic clocks, unsupervised machine learning, brain, Alzheimer's disease, age acceleration
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About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at https://www.Aging-US.com and connect with us:
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Dr. Cristina Aguayo-Mazzucato from Beta Cell Aging Lab, Joslin Diabetes Center, Harvard Medical School, discusses an editorial she co-authored that was published by Aging (Aging-US) in Volume 14, Issue 11, entitled, “Biological age in diabetes and precision medicine.”
DOI - https://doi.org/10.18632/aging.204123 (PDF download)
Corresponding author - Cristina Aguayo-Mazzucato - cristina.aguayo-mazzucato@joslin.harvard.edu
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Keywords - biological age, diabetes mellitus, chronological age, DNA methylation, clinical biomarkers
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us:
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A new research paper was published in Aging (Aging-US / Albany NY)’s Volume 14, Issue 13, entitled, “Age-related neuroendocrine, cognitive, and behavioral co-morbidities are promoted by HIV-1 Tat expression in male mice.”
In the United States, approximately 1.2 million people are living with human immunodeficiency virus type-1 (HIV-1), with men accounting for the majority of cases (~75%). About half of HIV-infected individuals are 50 years of age and older. People living with HIV contend with an accelerated onset of age-related diseases and disorders; however, the pathophysiology underlying accelerated aging is poorly understood.
While the mechanisms(s) are unknown, the HIV-1 trans-activator of transcription (Tat) protein disrupts neuroendocrine function in mice partly by dysregulating mitochondria and neurosteroidogenesis.
Researchers Alaa N. Qrareya, Fakhri Mahdi, Marc J. Kaufman, Nicole M. Ashpole, and Jason J. Paris, from the University of Mississippi and Harvard Medical School’s McLean Hospital, investigated the combined effects of aging and HIV-1 Tat expression on the development of neuroHIV-like sequelae in young adult (6–8 months) and middle-aged (11–13 months) male mice to determine whether Tat precipitates age-related dysfunction.
“We hypothesized that conditional Tat expression in middle-aged male transgenic mice [Tat(+)] would promote age-related comorbidities compared to age-matched controls [Tat(−)]. We expected Tat to alter steroid hormone milieu consistent with behavioral deficits.”
Middle-aged Tat(+) mice had lower circulating testosterone and progesterone than age-matched controls and greater circulating corticosterone and central allopregnanolone than other groups. Young Tat(+) mice had greater circulating progesterone and estradiol-to-testosterone ratios. Older age or Tat exposure increased anxiety-like behavior (open field; elevated plus-maze), increased cognitive errors (radial arm water maze), and reduced grip strength. Young Tat(+), or middle-aged Tat(−), males had higher mechanical nociceptive thresholds than age-matched counterparts. Steroid levels correlated with behaviors. Thus, Tat may contribute to HIV-accelerated aging.
“In conclusion, our data suggest that older age and Tat expression exert independent and interactive effects to worsen neuroendocrine, affective, cognitive, and neuromuscular comorbidities. Novel steroid replacement therapies may be useful adjunctive therapeutics to cART in the aging HIV+ population.”
DOI: https://doi.org/10.18632/aging.204166
Corresponding Author: Jason J. Paris - Email: parisj@olemiss.edu
Keywords: aging, hypothalamic-pituitary-adrenal axis, hypothalamic-pituitary-gonadal axis, secondary hypogonadism, trans-activating transcriptor
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About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at https://www.Aging-US.com and connect with us:
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Listen to a press release about the cover paper of Volume 14, Issue 13, entitled, "Epigenetic clocks and their association with trajectories in perceived discrimination and depressive symptoms among US middle-aged and older adults.” ______________________________
A new research paper was published in Aging (Aging-US / Albany NY) on the cover of Volume 14, Issue 13, entitled, “Epigenetic clocks and their association with trajectories in perceived discrimination and depressive symptoms among US middle-aged and older adults.”
“Perceived discrimination may be associated with accelerated aging later in life, with depressive symptoms acting as potential mediator.”
In this recently published study, researchers May A. Beydoun, Hind A. Beydoun, Nicole Noren Hooten, Ana I. Maldonado, Jordan Weiss, Michele K. Evans, and Alan B. Zonderman from the National Institute on Aging’s Intramural Research Program, Fort Belvoir Community Hospital, University of Maryland, and University of California Berkeley examined a nationally representative sample of 2,806 older U.S. adults. The team evaluated associations of perceived discrimination measures with 13 DNA methylation (DNAm)-based measures of epigenetic aging. They used group-based trajectory and four-way mediation analyses.
“Here we examined retrospective data from the HRS [Health and Retirement Study 2010–2016] cohort study of U.S. adults aged 50–100 years and investigated measures of perceived discrimination and depressive symptoms in relation to 13 different DNAm-based epigenetic clocks (EPICLOCK) age-estimators.”
Read the full press release - https://www.aging-us.com/news_room/epigenetic-clocks-and-their-association-with-perceived-discrimination-and-depressive-symptoms
DOI - https://doi.org/10.18632/aging.204150
Corresponding Author: May A. Beydoun – Email: baydounm@mail.nih.gov
Keywords: DNA methylation, epigenetic clocks, biological age, perceived discrimination, depressive symptoms
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About Aging-US:
Launched in 2009, Aging (Aging-US / Albany NY) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at www.Aging-US.com and connect with us:
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Aging Journal Office 6666 E. Quaker Str., Suite 1B Orchard Park, NY 14127 Phone: 1-800-922-0957, option 1
Aging is indexed by Web of Science: Science Citation Index Expanded (abbreviated as Aging‑US). As of June 29, 2022, Web of Science (Clarivate Analytics) released their 2021 JCR Impact Factor List. Aging is pleased to report that our 2021 impact factor is 5.955. This number has increased from last year’s 5.682.
Aging is listed in the Web of Science: Science Citation Index Expanded in two categories: Cell Biology and Geriatrics & Gerontology. According to the Journal Citation Indicator (JCI), Aging is ranked in the Q1 quartile in both categories.
Since 2009, Aging has published research papers in all fields of aging research including, but not limited to, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development, and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan.
This journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, and prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.
To learn more about Aging, publication standards, and past or current issues, visit www.aging-us.com.
About Aging-US: Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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Aging (Aging-US) Journal Office 6666 E. Quaker Str., Suite 1B Orchard Park, NY 14127 Phone: 1-800-922-0957, option 1
A new research paper was published in Aging (Aging-US) on the cover of Volume 14, Issue 12, entitled, “Time makes histone H3 modifications drift in mouse liver.”
Aging is known to involve epigenetic histone modifications, which are associated with transcriptional changes, occurring throughout the entire lifespan of an individual.
“So far, no study discloses any drift of histone marks in mammals which is time-dependent or influenced by pro-longevity caloric restriction treatment.”
To detect the epigenetic drift of time passing, researchers—from Istituto di Ricovero e Cura a Carattere Scientifico, University of Urbino ‘Carlo Bo’, University of Milan, and University of Padua—determined the genome-wide distributions of mono- and tri-methylated lysine 4 and acetylated and tri-methylated lysine 27 of histone H3 in the livers of healthy 3, 6 and 12 months old C57BL/6 mice.
“In this study, we used chromatin immunoprecipitation sequencing technology to acquire 108 high-resolution profiles of H3K4me3, H3K4me1, H3K27me3 and H3K27ac from the livers of mice aged between 3 months and 12 months and fed 30% caloric restriction diet (CR) or standard diet (SD).”
The comparison of different age profiles of histone H3 marks revealed global redistribution of histone H3 modifications with time, in particular in intergenic regions and near transcription start sites, as well as altered correlation between the profiles of different histone modifications. Moreover, feeding mice with caloric restriction diet, a treatment known to retard aging, reduced the extent of changes occurring during the first year of life in these genomic regions.
“In conclusion, while our data do not establish that the observed changes in H3 modification are causally involved in aging, they indicate age, buffered by caloric restriction, releases the histone H3 marking process of transcriptional suppression in gene desert regions of mouse liver genome most of which remain to be functionally understood.”
DOI: https://doi.org/10.18632/aging.204107
Corresponding Author: Marco Giorgio - marco.giorgio@unipd.it
Keywords: epigenetics, aging, histones, ChIP-seq, diet
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About Aging-US:
Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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Dr. Liang-Kung Chen from the National Yang-Ming Chiao-Tung University, Taipei, Taiwan details a research paper he co-authored that was published by Aging (Aging-US) in Volume 14, Issue 3, entitled, “Predicting neuropsychiatric symptoms of persons with dementia in a day care center using a facial expression recognition system.”
DOI - https://doi.org/10.18632/aging.203869
Corresponding author - Liang-Kung Chen - lkchen2@vghtpe.gov.tw
Video - https://www.youtube.com/watch?v=wO7PulizlR0
Video transcript - https://aging-us.net/2022/06/28/behind-the-study-facial-expression-recognition-predicts-neuropsychiatric-symptoms-of-dementia/
Abstract
Background: Behavioral and psychological symptoms of dementia (BPSD) affect 90% of persons with dementia (PwD), resulting in various adverse outcomes and aggravating care burdens among their caretakers. This study aimed to explore the potential of artificial intelligence-based facial expression recognition systems (FERS) in predicting BPSDs among PwD.
Methods: A hybrid of human labeling and a preconstructed deep learning model was used to differentiate basic facial expressions of individuals to predict the results of Neuropsychiatric Inventory (NPI) assessments by stepwise linear regression (LR), random forest (RF) with importance ranking, and ensemble method (EM) of equal importance, while the accuracy was determined by mean absolute error (MAE) and root-mean-square error (RMSE) methods.
Results: Twenty-three PwD from an adult day care center were enrolled with ≥ 11,500 FERS data series and 38 comparative NPI scores. The overall accuracy was 86% on facial expression recognition. Negative facial expressions and variance in emotional switches were important features of BPSDs. A strong positive correlation was identified in each model (EM: r = 0.834, LR: r = 0.821, RF: r = 0.798 by the patientwise method; EM: r = 0.891, LR: r = 0.870, RF: r = 0.886 by the MinimPy method), and EM exhibited the lowest MAE and RMSE.
Conclusions: FERS successfully predicted the BPSD of PwD by negative emotions and the variance in emotional switches. This finding enables early detection and management of BPSDs, thus improving the quality of dementia care.
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Keywords - aging, artificial intelligence, behavioral and psychological symptoms of dementia, dementia, facial expression recognition system, machine learning
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us:
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Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com
Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM
Click here for the transcript of this interview: https://aging-us.net/2022/06/22/longevity-aging-series-ep-1-drs-alex-zhavoronkov-and-frank-pun/
Aging (Aging-US) and FOXO Technologies have teamed up to present a special collaboration on aging research with a new monthly video series: the Longevity & Aging Series. This series of video interviews invites Aging researchers to speak with researcher and host Dr. Brian Chen. Dr. Chen is an adjunct faculty member at the Herbert Wertheim School of Public Health and Human Longevity Science at the University of California San Diego. He is also the Chief Science Officer of FOXO Technologies.
In the first episode of the Longevity & Aging Series, Drs. Alex Zhavoronkov and Frank Pun discuss, in detail, their recently published research paper, “Hallmarks of aging-based dual-purpose disease and age-associated targets predicted using PandaOmics AI-powered discovery engine.”
DOI - https://doi.org/10.18632/aging.203960
Corresponding author - Alex Zhavoronkov - alex@insilico.com
Press release - https://aging-us.net/2022/06/22/aging-aging-us-and-foxo-present-the-longevity-aging-series/
Video of first episode - https://www.youtube.com/watch?v=Td8tK5SX0kA
Abstract
Aging biology is a promising and burgeoning research area that can yield dual-purpose pathways and protein targets that may impact multiple diseases, while retarding or possibly even reversing age-associated processes. One widely used approach to classify a multiplicity of mechanisms driving the aging process is the hallmarks of aging. In addition to the classic nine hallmarks of aging, processes such as extracellular matrix stiffness, chronic inflammation and activation of retrotransposons are also often considered, given their strong association with aging. In this study, we used a variety of target identification and prioritization techniques offered by the AI-powered PandaOmics platform, to propose a list of promising novel aging-associated targets that may be used for drug discovery. We also propose a list of more classical targets that may be used for drug repurposing within each hallmark of aging. Most of the top targets generated by this comprehensive analysis play a role in inflammation and extracellular matrix stiffness, highlighting the relevance of these processes as therapeutic targets in aging and age-related diseases. Overall, our study reveals both high confidence and novel targets associated with multiple hallmarks of aging and demonstrates application of the PandaOmics platform to target discovery across multiple disease areas.
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Keywords - aging, artificial intelligence, deep learning, drug discovery, multi-omics, target identification
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com and connect with us:
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Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com
Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM
Aging (Aging-US) and FOXO Technologies have teamed up to present a special collaboration on aging research with a new monthly video series: the Longevity & Aging Series. This series of video interviews invites Aging researchers to speak with researcher and host Dr. Brian Chen. Dr. Chen is an adjunct faculty member at the Herbert Wertheim School of Public Health and Human Longevity Science at the University of California San Diego. He is also the Chief Science Officer of FOXO Technologies.
The Longevity & Aging Series offers a platform for Aging authors to discuss their aging research in a long-form video format. Once a month, Dr. Chen will invite distinguished authors to present their research studies and results published in Aging (Aging-US). Upcoming author interviews include Drs. Alex Zhavoronkov, Frank Pun, Steve Horvath, Andrew DiNardo, Cristian Coarfa, Carly Bobak, and Amit Sharma.
The goal of this collaboration between Aging (Aging-US) and FOXO Technologies is to foster the rapid dissemination of research, encourage thought leadership and jumpstart new breakthrough studies in the field of aging.
The series will be available to watch on our YouTube and LabTube channels, and will also be available for listeners on Spotify, SoundCloud or wherever high-quality podcasts are downloaded. In addition, Longevity & Aging Series discussions will be posted on Aging-US.com, Aging-US.net and ImpactJournals.com, and promoted across our family of social media channels.
Watch the first episode of the Longevity & Aging Series, featuring Drs. Alex Zhavoronkov and Frank Pun as they discuss their recently published research paper, entitled, “Hallmarks of aging-based dual-purpose disease and age-associated targets predicted using PandaOmics AI-powered discovery engine.”
“This is an exciting partnership between FOXO and Aging,” Dr. Chen said. “Remarkable breakthroughs are emerging every day in aging and healthy longevity. I hope this series helps to promote all the exciting work that is being done to a broader audience.”
AVAILABLE NOW: Episode One with Drs. Alex Zhavoronkov and Frank Pun: https://www.youtube.com/watch?v=Td8tK5SX0kA
About Aging-US:
Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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Aging (Aging-US) is proud to sponsor this year’s NAD + Metabolism and Signaling Conference (#NBCSRC22). This science research conference will take place from June 26 to June 30, 2022, in Steamboat Springs, Colorado, United States.
A coenzyme called nicotinamide adenine dinucleotide, also known as NAD+, can be found ubiquitously in nature (and within every cell in the human body). This molecule plays a critically important role in hundreds of processes related to energy production, metabolism, immunity, cognition, and even cancer. As humans age, researchers have observed a steady decline in the natural production of NAD+.
Organized biannually by the Foundation of American Societies for Experimental Biology (FASEB), the goal of the NAD + Metabolism and Signaling Conference is intended to bring scientists and researchers together from different fields and disciplines to explore the latest findings in NAD+ metabolism and signaling as they relate to human health, disease and medicine. This five-day conference will cover eight major topics across eight sessions, a “Meet the Expert” session, a career development workshop, and two social activities.
Full press release - https://aging-us.net/2022/06/21/aging-aging-us-sponsors-2022-nad-metabolism-and-signaling-conference/
About Aging-US:
Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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For media inquiries, please contact media@impactjournals.com.
BUFFALO, NY- June 16, 2022 – A new editorial paper was published in Aging (Aging-US) Volume 14, Issue 11, entitled, “WRNing for the right DNA repair pathway choice.”
Premature aging diseases, also called ‘progeroid syndrome’, display signs and features of normal aging in early life, ultimately leading to premature death. Although progeroid syndromes do not perfectly mimic chronological aging, they can be excellent model systems to study characteristics of normal aging.
Werner syndrome (WS) is one of the rare autosomal recessive progeroid syndromes, characterized by accelerated aging. WRN is suggested to play a central role in maintaining genome stability and rapidly recruits to the DNA damage sites to take part in DNA repair, including base excision DNA repair (BER), classical/alternative non-homologous end joining (NHEJ), homologous recombination (HR), and replication re-start after DNA damage.
WRN makes critical DNA-repair pathway choices between classical and alternative NHEJs. In addition to its key role in NHEJ, WRN has been suggested to also participate in HR. However, how it regulates the pathway choice between NHEJ and HR was still unclear.
Full press release - https://aging-us.net/2022/06/16/aging-us-wrning-for-the-right-dna-repair-pathway-choice/
DOI: https://doi.org/10.18632/aging.204120
Corresponding Author: Vilhelm A. Bohr - vbohr@nih.gov
Keywords: DNA repair, RecQ helicase, helicase, DNA double strand repair pathways
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About Aging-US:
Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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BUFFALO, NY- June 15, 2022 – A new research paper was published in Aging (Aging-US) on the cover of Volume 14, Issue 11, entitled, “Histone deacetylase 4 reverses cellular senescence via DDIT4 in dermal fibroblasts.”
Researchers—from Seoul National University, Seoul National University College of Medicine, Seoul National University Graduate School, and Daegu Gyeongbuk Institute of Science and Technology (DGIST)—previously demonstrated that histone deacetylase 4 (HDAC4) is consistently downregulated in aged and ultraviolet (UV)-irradiated human skin. However, there is little research on how HDAC4 causes skin aging.
“To elucidate the potential role of HDAC4 in the regulation of cellular senescence and skin aging, we established oxidative stress- and UV-induced cellular senescence models using primary human dermal fibroblasts (HDFs).”
After overexpression or knockdown of HDAC4 in primary HDFs, RNA sequencing identified candidate molecular targets of HDAC4.
“Integrative analyses of our current and public mRNA expression profiles identified DNA damage-inducible transcript 4 (DDIT4) as a critical senescence-associated factor regulated by HDAC4.”
Full press release - https://aging-us.net/2022/06/15/aging-us-ddit4-identified-as-candidate-target-of-hdac4-associated-skin-aging/
DOI: https://doi.org/10.18632/aging.204118
Corresponding Authors: Daehee Hwang - daehee@snu.ac.kr, Dong Hun Lee - ivymed27@snu.ac.kr, Jin Ho Chung - jhchung@snu.ac.kr
Keywords: cellular senescence, DNA damage-inducible transcript 4, histone deacetylase 4, oxidative stress, ultraviolet light
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About Aging-US:
Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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Dennis Mangan from MTOR LLC in Bakersfield, California details his theory article published by Aging (Aging-US), entitled, “Iron: an underrated factor in aging.”
DOI - https://doi.org/10.18632/aging.203612
Corresponding author - Dennis Mangan - pdmangan@outlook.com
Abstract
Iron is an essential element for virtually all living organisms, but its reactivity also makes it potentially harmful. Iron accumulates with aging, and is associated with many age-related diseases; it also shortens the lifespans of several model organisms. Blocking iron absorption through drugs or natural products extends lifespan. Many life-extending interventions, such as rapamycin, calorie restriction, and old plasma dilution can be explained by the effects they have on iron absorption, excretion, and metabolism. Control of body iron stores so that they remain in a low normal range may be an important, lifespan- and healthspan-extending intervention.
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Press release - https://www.aging-us.com/news_room/iron-an-underrated-factor-in-aging
Blog post - https://www.impactjournals.com/journals/blog/aging/trending-with-impact-is-iron-a-driver-of-aging/
Keywords - iron, aging, oxidative stress, calorie restriction, plasma dilution
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us:
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Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com
Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM
Listen to a blog summary of a trending research paper published by Aging (Aging-US) on May 16, 2022, entitled, " Effect of Humanin G (HNG) on inflammation in age-related macular degeneration (AMD)." _______________________
One of the leading causes of vision loss among aging populations in the United States, and worldwide, is age-related macular degeneration (AMD). The progression of this disease is known to be driven by inflammatory processes. However, the exact inflammation-associated proteins and the mechanisms that drive them have not yet been fully elucidated.
“Inflammation plays a crucial role in the etiology and pathogenesis of AMD (Age-related Macular Degeneration).”
In a new study in Aging (Aging-US), researchers from the University of California Irvine and the University of Southern California investigated a potential therapeutic intervention to reduce chronic inflammation in AMD and delay or prevent retinal degeneration. On May 16, 2022, this trending research paper was published on the cover of Aging’s Volume 14, Issue 10, and entitled, “Effect of Humanin G (HNG) on inflammation in age-related macular degeneration (AMD).”
Full blog - https://aging-us.org/2022/06/trending-with-impact-humanin-g-treatment-in-amd-reduces-inflammation/
DOI - https://doi.org/10.18632/aging.204074
Corresponding authors - Cristina Kenney - mkenney@hs.uci.edu
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Press release - https://www.aging-us.com/news_room/novel-discovery-in-age-related-macular-degeneration
Keywords - aging, Humanin G, HNG, AMD, inflammation, age-related macular degeneration
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com and connect with us:
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A new research paper was published in Aging (Aging-US) on the cover of Volume 14, Issue 10, entitled, “Effect of Humanin G (HNG) on inflammation in age-related macular degeneration (AMD).”
Inflammatory processes drive the progression of age-related macular degeneration (AMD) disease—a leading cause of vision loss in the United States.
In this new Aging study, researchers from the University of California Irvine and University of Southern California compared the protein levels of inflammation markers in normal and AMD retinal pigment epithelial (RPE) transmitochondrial cybrid cells and investigated the effects of treatment with exogenous Humanin G.
Humanin G (HNG) is a mitochondrial derived peptide that is cytoprotective in AMD and can protect against mitochondrial and cellular stress induced by damaged AMD mitochondria.
“The goal of this study was to test our hypothesis that inflammation-associated marker protein levels are increased in AMD and treatment with HNG leads to reduction in their protein levels.”
Humanin G protein levels were measured in the plasma of AMD patients and normal subjects using ELISA assay. Humanin G was added to AMD and normal (control) cybrids derived from clinically characterized AMD patients and normal (control) subjects. Cell lysates were extracted from untreated and HNG-treated AMD and normal cybrids, and the Luminex XMAP multiplex assay was used to measure the levels of inflammatory proteins.
The researchers found that there were differential levels of inflammation proteins between normal and AMD plasma samples. Compared to control plasma samples, AMD plasma showed higher protein levels of inflammation markers. However, plasma levels of endogenous Humanin protein were 36.58% lower in AMD patients compared to that in age-matched normal subjects. After treatment with Humanin G, the researchers observed a marked reduction in protein levels of inflammation markers that were elevated in AMD RPE transmitochondrial cybrid cells.
“In conclusion, we present novel findings that: A) show reduced Humanin protein levels in AMD plasma vs. normal plasma; B) suggest the role of inflammatory markers in AMD pathogenesis, and C) highlight the positive effects of Humanin G in reducing inflammation in AMD.”
To the teams’ knowledge, this is the first study to report notably reduced Humanin protein levels in AMD patients, thereby corroborating the pivotal role of Humanin in maintaining tissue homeostasis and normal functioning in the eye.
“Our discovery is novel and may contribute to the development of therapeutics/ tools for reducing inflammation to alleviate AMD disease pathology.”
DOI: https://doi.org/10.18632/aging.204074
Correspondence to: Cristina Kenney - Email: mkenney@hs.uci.edu
Keywords: Humanin G, HNG, AMD, inflammation, age-related macular degeneration
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About Aging-US:
Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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Listen to a blog summary of a trending editorial published in Volume 14, Issue 9 of Aging (Aging-US), entitled, "Cognitive training and neuromodulation for Alzheimer treatment." ______________________________________
Many neurodegenerative disorders among elderly populations share common characteristics. In dementias, for example, neurons and glial cells undergo a progressive loss of structure or function in the brain and spinal cord. Alzheimer’s disease (AD) is the most common form of dementia and the main cause of cognitive impairment. Studies have confirmed that cognitive treatments, such as cognitive stimulation, training and rehabilitation, can improve brain function by increasing brain plasticity.
Recently, researcher Fabrizio Vecchio, from IRCCS San Raffaele Roma‘s Brain Connectivity Laboratory, discussed innovative treatment options for Alzheimer’s disease. On April 27, 2022, Dr. Vecchio published his new editorial paper in Volume 14, Issue 9, of Aging (Aging-US), entitled, “Cognitive training and neuromodulation for Alzheimer treatment.”
“Neuromodulation techniques are having a growing consensus as a therapeutic approach of incipient and mild to moderate dementia because of their capability to be modulated both in space, i.e. in different cortical and subcortical areas of the brain, and time.”
Full blog -https://aging-us.org/2022/05/trending-with-impact-neuromodulation-in-alzheimers-disease-treatment/
DOI - https://doi.org/10.18632/aging.204044
Corresponding author - Fabrizio Vecchio - fabrizio.vecchio@uniecampus.it
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Keywords - aging, EEG, Small World, cognitive training, rTMS, Alzheimer
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com and connect with us:
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BUFFALO, NY- May 24, 2022 – Aging (Aging-US) is sponsoring the Systems Aging Gordon Research Conference, “Systemic Processes, Omics Approaches and Biomarkers in Aging,” from May 29 to June 3, 2022, at the Grand Summit Hotel at Sunday River in Newry, Maine, USA.
This year, the Chair and Vice Chair of the conference are Aging Editorial Board members Vadim N. Gladyshev, Professor of Medicine at Harvard Medical School and Director of Redox Medicine at Brigham and Women’s Hospital, and Steve Horvath, Professor of Human Genetics and Biostatistics at the University of California, Los Angeles. Dr. Gladyshev is known for his characterization of the human selenoproteome. He was also elected as a member of the U. S. National Academy of Sciences in 2021. Dr. Horvath is a world-renowned researcher, geneticist and biostatistician. Recently, Aging devoted a research collection to Dr. Horvath’s profound contributions in epigenetics and DNA methylation research. Read Aging’s Special Collection on Steve Horvath Publications: https://www.aging-us.com/special-collections-archive/steve-horvath.
Both Drs. Gladyshev and Horvath will be speaking and leading discussions at this meeting. In addition, a number of prestigious researchers from renowned institutions will be presenting at this conference. Presenters who are also members of Aging’s Editorial Board include Cynthia Kenyon, Manuel Serrano, Alex Zhavoronkov, and Vera Gorbunova.
Over the course of the six-day Systems Aging Gordon Research Conference, presentations will cover many topics, including delaying aging, aging clocks, clinical biomarkers, advances in systemic rejuvenation, comparative and multi-omics approaches, applications of machine learning and artificial intelligence, the current understanding of the molecular basis of aging, and longevity interventions in model organisms. The organizers of the conference hope this meeting will facilitate deep discussions and the free exchange of ideas between not only established researchers but also junior scientists.
“The 2022 Systems Aging GRC will set the stage for subsequent meetings and future development of this field, with the idea to ultimately help delay and reverse aging and age-related pathology.” (Source: 2022 Systems Aging GRC)
About Aging-US:
Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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In 2000 and 2011, Drs. Douglas Hanahan and Robert Weinberg authored two papers which stand as the original hallmarks of cancer. Since then, the hallmarks of cancer have been used as a critical framework to develop effective new cancer theranostics. In 2013, López-Otín et al. used the hallmarks of cancer in an effort to construct hallmarks of aging. However, in 2021, Drs. David Gems and João Pedro de Magalhães authored a paper critiquing the hallmarks of aging as a paradigm and urging researchers to move beyond the hallmarks to better understand the process of aging.
On May 9, 2022, Dr. Mikhail Blagosklonny published an original review paper in Aging (Aging-US) Volume 14, Issue 9, entitled, “Hallmarks of cancer and hallmarks of aging.” Dr. Blagosklonny expands on Gems and de Magalhães’ sentiment and writes that “canonic hallmarks of aging are superficial imitations of the hallmarks of cancer.” He takes their work to the next level by offering his own original concept that rearranges the hallmarks of cancer and the hallmarks of aging based on the hierarchical principle and the hyperfunction theory of aging.
“According to hyperfunction theory, aging is a continuation of developmental and reproductive programs that were not turned off upon their completion.”
Full blog - https://aging-us.org/2022/05/an-original-review-on-the-hallmarks-of-cancer-and-aging/
DOI - https://doi.org/10.18632/aging.204082
Corresponding author - Mikhail V. Blagosklonny - Blagosklonny@oncotarget.com, Blagosklonny@rapalogs.com
Press release - https://aging-us.com/news_room/hallmarks-of-cancer-and-hallmarks-of-aging-reviewed
Keywords - aging, oncology, carcinogenesis, geroscience, mTOR, rapamycin, hyperfunction theory
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com and connect with us:
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BUFFALO, NY- May 18, 2022 – Dr. Mikhail Blagosklonny published his new review paper in Aging (Aging-US) Volume 14, Issue 9, entitled, “Hallmarks of cancer and hallmarks of aging.”
In this review, Dr. Blagosklonny expands on Gems and de Magalhães’ notion that canonic hallmarks of aging are superficial imitations of the hallmarks of cancer. He takes their work a step further and proposes the hallmarks of cancer and aging based on a hierarchical principle and the hyperfunction theory.
“Here I present the hallmarks of cancer, depicted as a circle by Hanahan and Weinberg [1], not as the circle but hierarchically, from molecular levels to the organism (Figure 1).”
Next, Dr. Blagosklonny depicts the hallmarks of aging suggested by López-Otín et al. based on the hierarchical principle.
“This representation renders hallmarks tangible but reveals three shortcomings (Figure 2).”
The first shortcoming that Dr. Blagosklonny notes is the lack of hallmarks on the organismal level. The second is that the relationship between hallmarks on different levels is unclear. The third is that the inclusion of genetic instability as a hallmark is based on the theory that aging is caused by the accumulation of molecular damage.
“The molecular damage theory was refuted by key experiments, as discussed in detail [44–51].”
Dr. Blagosklonny then uses the hyperfunction theory to arrange the hierarchical hallmarks of aging.
“Let us depict hallmarks of aging, according to the hyperfunction theory of aging (Figure 3).”
Dr. Blagosklonny continues by discussing the key to understanding aging and aging as a selective force for cancer. He concludes this review by discussing the common hallmarks of cancer, aging and cell senescence.
“In organismal aging, cancer and cellular senescence, the same key signaling pathways, such as mTOR, are involved. This is why the same drugs, such as rapamycin, can suppress all of them.”
DOI: https://doi.org/10.18632/aging.204082
Correspondence to: Mikhail V. Blagosklonny
Email: Blagosklonny@oncotarget.com, Blagosklonny@rapalogs.com
Keywords: oncology, carcinogenesis, geroscience, mTOR, rapamycin, hyperfunction theory
Follow Dr. Blagosklonny on Twitter: https://twitter.com/Blagosklonny
About Aging-US:
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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A new research paper was published on the cover of Aging (Aging-US) Volume 14, Issue 9, entitled, “Single-cell transcriptomics reveals age-resistant maintenance of cell identities, stem cell compartments and differentiation trajectories in long-lived naked mole-rats skin.”
Researchers who authored this research paper are affiliated with the Université Paris Cité, Sorbonne Université, Fondation pour la Recherche en Physiologie, Queen Mary University of London, Hôpital Tenon, Université de Namur ASBL, Ecole Nationale Vétérinaire d’Alfort, and Hôpital Cochin.
“In the present study, we performed extensive in situ analysis and single-cell RNA-sequencing comparing young and older animals.”
Skin acts as an essential barrier and protects organisms from external threats, preventing fluid loss, stabilizing body temperature and relaying sensory information to the brain.
Maintaining skin homeostasis is essential, as alterations in skin functions can cause various deleterious conditions ranging from fluid loss to more severe diseases, such as infections or UV-induced cancers.
Naked mole-rats (NMR) are subterranean rodents characterized by an unusual longevity coupled with an unexplained resistance to aging.
At variance with other species, naked mole-rats exhibited a striking stability of skin compartments and cell types, which remained stable over time without aging-associated changes.
“Thus, we hypothesize that the maintenance of cellular compartments in the older NMR, especially the stem cell pool through high Igfbp3 expression, coupled with an increase skin immunity, could explain their skin slower rate of aging.”
The researchers used single-cell RNA-sequencing (scRNA-seq) to obtain an unbiased molecular RNA profile of the naked mole-rats’ epidermal cell populations. They found that epidermal gene expression did not change with aging. Three classical cellular states defined a unique keratinocyte differentiation trajectory that were not altered after pseudo-temporal reconstruction.
NMR skin healing closure was similar in young and older animals and, remarkably, the number of stem cells was constant throughout aging. The researchers found that NMR epidermal cells displayed two main populations, immune cells (one cluster) and keratinocytes, subdivided into 10 clusters.
“Performing a deeper analysis within each cluster individually, we found 2 genes overexpressed in basal stem cells of older animals and 5 genes overexpressed in immune cells of older animals.”
“Altogether, these results indicate that NMR skin is characterized by peculiar genetic and cellular features, different from those previously demonstrated for mice and humans. The remarkable stability of the aging NMR skin transcriptome likely reflects unaltered homeostasis and resilience.”
DOI: https://doi.org/10.18632/aging.204054
Correspondence to: Romain H. Fontaine
Email: romain.fontaine@inserm.fr
Keywords: naked mole-rat, skin stem cells, wound healing, aging
About Aging-US:
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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Listen to a blog summary of Dr. Blagosklonny's latest research perspective published in Oncoscience, entitled, “Altos Labs and the quest for immortality: but can we live longer right now?” ___________________________
After the January 2022 launch of Altos Labs, a new anti-aging biotechnology company, Mikhail (Misha) Blagosklonny, M.D., Ph.D., joined this exciting public conversation with a recommendation. Dr. Blagosklonny is a prominent scientist in the fields of cancer and aging research. He is well-known for his experimental research articles and theoretical papers on the hyperfunction theory of aging and the pursuit of longevity with rapamycin. On April 22, 2022, his latest research perspective was published in Oncoscience, and entitled, “Altos Labs and the quest for immortality: but can we live longer right now?”
Full blog - https://aging-us.org/2022/05/dr-blagosklonnys-rapamycin-based-recommendation-for-altos-labs/
DOI - https://doi.org/10.18632/oncoscience.552
Corresponding author - Mikhail V. Blagosklonny - Blagosklonny@oncotarget.com, Blagosklonny@rapalogs.com
Keywords - aging, longevity, lifespan, geroscience, rapalogs, gerostatics
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com and connect with us:
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BUFFALO, NY- May 11, 2022 – A new research perspective was published in Oncoscience journal by Mikhail Blagosklonny, M.D., Ph.D., entitled, “Altos Labs and the quest for immortality: but can we live longer right now?”
“Here I discuss how combining rapamycin with other modalities may let us live long enough to benefit from future discoveries in cellular reprogramming and what needs to be done at Altos Labs to make this happen.”
Altos Labs—a new anti-aging biotechnology company funded by multiple billionaire investors, including Jeff Bezos and Yuri Milner—has reported a focus on reprogramming cells in order to reverse the trajectory of diseases, and thus, reverse aging.
In his research perspective, Dr. Blagosklonny writes that potential life-extension with rapamycin may allow us to win time while awaiting future discoveries that will reverse aging.
“Rapamycin treatment is rapidly becoming a mainstream anti-aging intervention.”
However, Dr. Blagosklonny also writes that rapamycin alone is unlikely to extend lifespan sufficiently to benefit from Altos Labs’ future discoveries in our lifetime.
“If Altos Labs would allocate a small percentage of its funding to develop rapamycin based drug combinations, then additional decades of life extension may be available 3–5 years from now.”
“The number of potential combinations with rapamycin is enormous.”
Read Dr. Blagosklonny’s research perspective: https://www.oncoscience.us/article/552/text/
Correspondence to: Mikhail V. Blagosklonny
Email: Blagosklonny@oncotarget.com, Blagosklonny@rapalogs.com
Keywords: aging, longevity, lifespan, geroscience, rapalogs, gerostatics
Follow Dr. Blagosklonny on Twitter: https://twitter.com/Blagosklonny
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Listen to a blog summary of a research paper selected as the cover for Volume 14, Issue 8, entitled, "Wild type and gain of function mutant TP53 can regulate the sensitivity of pancreatic cancer cells to chemotherapeutic drugs, EGFR/Ras/Raf/MEK, and PI3K/mTORC1/GSK-3 pathway inhibitors, nutraceuticals and alter metabolic properties." __________________________
Patients over the age of 50 years old who have been diagnosed with pancreatic cancer have a poorer rate of survival compared to younger patients. This means that pancreatic cancer is a disease associated with aging. The most common type of pancreatic cancer is pancreatic ductal adenocarcinoma (PDAC) and it is frequently diagnosed in its later stages. PDAC is often refractive to chemotherapies and develops resistance to inhibitors and other drugs. Therefore, there is a critical need for researchers to discover novel strategies to overcome drug resistance in PDAC cells.
One potential strategy is to focus on a key gene known for its involvement in many cell processes, including drug resistance and metabolism: TP53. The TP53 gene is often mutated or deleted in cancer cells, which can lead to drug resistance and cancer metastasis. In PDACS, this tumor suppressor gene has been shown to be mutated in 50–75% of patients.
“Many genes have been implicated in PDAC including KRAS, TP53, CDKN2A, SMAD4 and PDGFβR [3, 8, 9, 18–22].”
In a new study, researchers—from Brody School of Medicine at East Carolina University, Università di Bologna, University of Parma, and University of Wroclaw—further elucidated TP53’s role in drug resistance in PDAC cells. On April 27, 2022, their research paper was published in Aging (Aging-US) on the cover of Volume 14, Issue 8, and entitled, “Wild type and gain of function mutant TP53 can regulate the sensitivity of pancreatic cancer cells to chemotherapeutic drugs, EGFR/Ras/Raf/MEK, and PI3K/mTORC1/GSK-3 pathway inhibitors, nutraceuticals and alter metabolic properties.”
Full blog - https://aging-us.org/2022/05/tp53-restoration-sensitizes-pancreatic-cancer-to-multiple-drugs/
DOI - https://doi.org/10.18632/aging.204038
Corresponding author - James A. McCubrey - mccubreyj@ecu.edu
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Keywords - aging, TP53, targeted therapy, PDAC, metabolic properties, chemotherapeutic drugs
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us:
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Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com
Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM
Listen to a blog summary of a trending research paper published by Aging (Aging-US) in Volume 14, Issue 7, entitled, “The tobacco phosphatidylethanolamine-binding protein NtFT4 increases the lifespan of Drosophila melanogaster by interacting with the proteostasis network.” ___________________________
Full blog - https://aging-us.org/2022/04/trending-with-impact-tobacco-pebp-increases-lifespan-in-fruit-flies/
DOI - https://doi.org/10.18632/aging.204005
Corresponding author - Philip Känel - philip.kaenel@ime.fraunhofer.de
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Keywords - aging, proteostasis, heat shock proteins, chaperone, locomotor activity
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com and connect with us:
SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/
Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com
Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM
Listen to a blog summary of a trending research paper selected as the cover for Volume 14, Issue 7 of Aging (Aging-US), entitled, "Downregulation of IGFBP5 contributes to replicative senescence via ERK2 activation in mouse embryonic fibroblasts." ___________________________________
In 1961, Leonard Hayflick and Paul Moorhead proposed a theory later named the Hayflick Limit. They discovered that a normal human cell can divide between 50 and 70 times before it can no longer proliferate and eventually dies. Researchers have since continued to explore this phenomenon and, today, this aging process is known as cellular (replicative) senescence.
“There are currently several experimental models of cellular senescence. Hayflick and Moorhead observed that primary human fibroblasts in culture exhibit a limited proliferative capacity [6]. This growth arrest during passages is called replicative senescence.”
This permanent cessation of the cell cycle is universally found in biology due to known and unknown causes, including the shortening of telomeres. While telomere shortening plays an important role, it is not the only event responsible for inducing cellular senescence. Thus, researchers have spent decades under the microscope experimenting with cellular models of replicative senescence.
In a new study released on April 4, 2022, researchers from Sapporo Medical University in Sapporo, Japan, investigated mechanisms of replicative senescence in vitro. Their research paper was published on the cover of Aging (Aging-US) Volume 14, Issue 7, and entitled, “Downregulation of IGFBP5 contributes to replicative senescence via ERK2 activation in mouse embryonic fibroblasts.”
Full blog - https://aging-us.org/2022/04/trending-with-impact-underlying-mechanisms-of-replicative-senescence/
DOI - https://doi.org/10.18632/aging.203999
Corresponding author - Atsushi Kuno - kuno@sapmed.ac.jp
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Keywords - aging, IGFBP5, replicative senescence, mouse embryonic fibroblasts, ERK2, ERK1
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com and connect with us:
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Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com
Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM
Dr. Frank Pun, Associate Director (Project & Operations) and Application Science Lead at Insilico Medicine in Hong Kong, describes his experience publishing a research paper that he co-authored, entitled, “Hallmarks of aging-based dual-purpose disease and age-associated targets predicted using PandaOmics AI-powered discovery engine” with Aging (Aging-US).
DOI - https://doi.org/10.18632/aging.203960
Corresponding author - Alex Zhavoronkov - alex@insilico.com
Abstract Aging biology is a promising and burgeoning research area that can yield dual-purpose pathways and protein targets that may impact multiple diseases, while retarding or possibly even reversing age-associated processes. One widely used approach to classify a multiplicity of mechanisms driving the aging process is the hallmarks of aging. In addition to the classic nine hallmarks of aging, processes such as extracellular matrix stiffness, chronic inflammation and activation of retrotransposons are also often considered, given their strong association with aging. In this study, we used a variety of target identification and prioritization techniques offered by the AI-powered PandaOmics platform, to propose a list of promising novel aging-associated targets that may be used for drug discovery. We also propose a list of more classical targets that may be used for drug repurposing within each hallmark of aging. Most of the top targets generated by this comprehensive analysis play a role in inflammation and extracellular matrix stiffness, highlighting the relevance of these processes as therapeutic targets in aging and age-related diseases. Overall, our study reveals both high confidence and novel targets associated with multiple hallmarks of aging and demonstrates application of the PandaOmics platform to target discovery across multiple disease areas.
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Keywords - aging, artificial intelligence, deep learning, drug discovery, multi-omics, target identification
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us:
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Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com
Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM
Listen to a blog summary of this priority research paper published in Volume 13, Issue 11, entitled, "GRSF1 deficiency in skeletal muscle reduces endurance in aged mice." ________________________________
Skeletal muscle is responsible for regulating physical movement and comprises between 30 and 40% of the human body’s mass. The loss of skeletal muscle has major impacts on overall health and quality of life—leading to frailty and a decreased ability to perform activities of daily living. The most common cause of muscle loss is aging, and a prevalent pattern of aging-associated muscular decline is known as sarcopenia.
“With advancing age, the progressive loss of skeletal muscle mass and function, known as sarcopenia, leads to reduced muscle strength and diminishes individual mobility, quality of life, and lifespan [12].”
In a research paper published in Aging (Aging-US) Volume 13, Issue 11, researchers from National Institutes of Health’s National Institute on Aging and Chungnam National University investigated a protein that may play a role in aging-related muscle loss. Their paper was published on June 2, 2021, and entitled, “GRSF1 deficiency in skeletal muscle reduces endurance in aged mice.”
Full blog - https://aging-us.org/2022/04/protein-linked-to-aging-related-muscle-loss/
DOI - https://doi.org/10.18632/aging.203151
Corresponding authors - Chang-Yi Cui - cuic@grc.nia.nih.gov, and Myriam Gorospe - myriam-gorospe@nih.gov
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Keywords - aging, skeletal muscle aging, GRSF1, RNA-binding protein, mouse aging
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com and connect with us:
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Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com
Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM
Blog summary of a trending research paper published by Aging (Aging-US) in Volume 14, Issue 6, entitled, “Ovarian reserve parameters and IVF outcomes in 510 women with poor ovarian response (POR) treated with intraovarian injection of autologous platelet rich plasma (PRP).” ______________________________
In a day and age when women and men are beginning families later in the life cycle, women of advanced age (or with some health conditions) often have trouble becoming pregnant. Today, in vitro fertilization (IVF) is a widely-used form of assisted reproductive technology. This manual process of fertilization is achieved first by combining an egg and a sperm outside of the uterus and then helping the fertilized egg become implanted in the uterus.
The world’s first IVF baby was born in Lancashire, England, in 1978. Since then, this technique has solved reproductive issues for millions of women and men around the world. While this procedure has helped build many families, there is a subset of reproductively challenged women who exhibit resistance to IVF. Researchers have observed accelerated ovarian aging in women who demonstrate a poor ovarian response (POR) to IVF.
“These women are labeled ‘poor ovarian response’ (POR) or ‘poor responders’ due to a combination of low parameters of ovarian reserve and previous low oocyte yield after ovarian stimulation.”
In previous small-scale cohort and in vitro studies, exposure to platelet-rich plasma (PRP) has demonstrated improvements in ovarian tissue repair, regeneration and follicular development. In a new study, published in Aging (Aging-US) on March 22, 2022, researchers— from Acibadem Maslak Hospital, Acibadem University, IVI RMA New Jersey, Thomas Jefferson University, and Yale School of Medicine—sought to validate these small-scale results by assessing the effects of intra-ovarian injection of autologous PRP in a cohort of 510 women with POR. Their trending research paper can be found in Volume 14, Issue 6, entitled, “Ovarian reserve parameters and IVF outcomes in 510 women with poor ovarian response (POR) treated with intraovarian injection of autologous platelet rich plasma (PRP).”
Full blog - https://aging-us.org/2022/04/trending-with-impact-plasma-injection-improves-poor-response-to-ivf/
DOI - https://doi.org/10.18632/aging.203972
Corresponding author - Emre Seli - emre.seli@yale.edu
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Keywords - poor ovarian response, platelet rich plasma, in vitro fertilization
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com and connect with us:
SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/
Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com
Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM
Listen to a blog summary of a research paper chosen as the cover for Volume 14, Issue 6 of Aging (Aging-US), entitled, "Hallmarks of aging-based dual-purpose disease and age-associated targets predicted using PandaOmics AI-powered discovery engine." _________________________________
What if drugs designed to treat conditions such as diabetes, osteoporosis and rheumatoid arthritis could at the same time provide patients with anti-aging benefits? On March 29, 2022, researchers—from Insilico Medicine, University of Chicago, George Mason University, University of Liverpool, and Buck Institute for Research on Aging—released a new study on the cover of Aging (Aging-US) Volume 14, Issue 6, about Insilico’s next-generation artificial intelligence (AI)-powered discovery software, called the PandaOmics platform. Their trending research paper is entitled, “Hallmarks of aging-based dual-purpose disease and age-associated targets predicted using PandaOmics AI-powered discovery engine.”
Full blog - https://aging-us.org/2022/03/pandaomics-identifies-duel-targets-of-aging-and-age-related-diseases/
DOI - https://doi.org/10.18632/aging.203960
Corresponding author - Alex Zhavoronkov - alex@insilico.com
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Keywords - aging, artificial intelligence, deep learning, drug discovery, multi-omics, target identification
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us:
SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/
Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com
Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM
Listen to a blog summary of the announcement for a special collection of Steve Horvath research papers published by Aging (Aging-US). ____________________
Epigenetics is the study of gene expression and the changes that occur which do not involve alterations in the DNA sequence. These changes can occur as a result of environmental influences, including exposure to chemicals, diet and stress. Epigenetic modifications can be passed down through generations and play an important role in disease development. An exciting area of epigenetics research is its role in the aging process. Studies have shown that epigenetic modifications can affect aging and the onset of age-related diseases. Recently, researchers also discovered that epigenetic modifications may be used to measure biological age and aging rate.
Steve Horvath, Ph.D., ScD is a world-renowned researcher, geneticist, biostatistician, and Professor of Human Genetics and Biostatistics at the University of California, Los Angeles. His research areas of study include aging, cancer, cardiovascular disease, HIV, Huntington’s disease, and neurodegenerative diseases. Today, he is well-known for his contributions in epigenetics research. In 2013, Dr. Horvath developed the first multi-tissue DNA methylation-based epigenetic biomarker of aging, known as the Horvath aging clock. Dr. Horvath earned numerous awards for his groundbreaking research, including the Allen Distinguished Investigator award, the Open Philanthropy Project award and the Schober Award. In 2018, 2019, 2020, and 2021, the Clarivate Web of Science Group named him as one of the world’s most influential scientific researchers.
Full blog - https://aging-us.net/2022/03/special-collection-of-steve-horvath-publications-in-aging/
Steve Horvath Special Collection - https://www.aging-us.com/special-collections-archive/steve-horvath
Contact information - Steve Horvath - shorvath@mednet.ucla.edu
Keywords - aging, aging research, epigenetics, epigenetic clock, longevity, healthspan, lifespan, lifestyle, research, research papers
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com and connect with us:
SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/
Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com
Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM
Dr. Brian Chen, adjunct faculty at the Herbert Wertheim School of Public Health and Human Longevity Science at UC San Diego and the Chief Science Officer of FOXO Technologies, describes his experience publishing numerous papers with Aging (Aging-US).
Aging (Aging-US) papers co-authored by Dr. Chen:
Predicting physiological aging rates from a range of quantitative traits using machine learning: https://doi.org/10.18632/aging.203660
An epigenetic biomarker of aging for lifespan and healthspan: https://doi.org/10.18632/aging.101414
Leukocyte telomere length, T cell composition and DNA methylation age: https://doi.org/10.18632/aging.101293
Epigenetic clock analysis of diet, exercise, education, and lifestyle factors: https://doi.org/10.18632/aging.101168
DNA methylation-based measures of biological age: meta-analysis predicting time to death: https://doi.org/10.18632/aging.101020
Contact information - Brian Chen - bchen@foxotechnologies.com
Keywords - aging, aging clock, mortality, machine learning, epigenetic clock, DNA methylation, biomarker, healthspan, diet, lifestyle, lifespan, epigenetics, all-cause mortality
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us:
SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/
Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com
Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM
Listen to a blog summary of a trending editorial published in Volume 14, Issue 5 of Aging (Aging-US), entitled, “Sex matters in Alzheimer’s disease?“ ____________________________
As the worldwide elderly population continues to expand, the symptoms of dementia, including Alzheimer’s disease (AD), are simultaneously increasing around the globe. Researchers are driven to investigate new ways to detect and treat AD in earlier stages—before symptoms become more difficult or impossible to overturn. An important piece of data to consider is that dementia is more prevalent among women than among men; dementia affects 8.1 % of women and 5.4% of men. Many AD studies have not used gender/sex as a variable to cross-examine their research findings. This information may be a key factor that leads to developing more efficacious strategies for AD detection and treatment in all patients, and especially in women.
“In the long run, the underrepresentation of female biology in biomedical research will hamper the development of effective drugs with negative consequences on women’s health.”
In a recent editorial paper published on March 12, 2022, by Aging (Aging-US) in Volume 14, Issue 5, researchers from the National University of Singapore discussed the importance of understanding sex differences in Alzheimer’s disease. Their trending editorial paper, entitled, “Sex matters in Alzheimer’s disease?“, was based on results from their previous study published in 2021.
Full blog - https://aging-us.org/2022/03/trending-with-impact-how-biological-sex-impacts-alzheimers-disease/
DOI - https://doi.org/10.18632/aging.203950
Corresponding author - Sreedharan Sajikumar - phssks@nus.edu.sg
Keywords - Alzheimer's disease, LTP, behavioural tagging, sexual dimorphism, transcriptome profiling
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com and connect with us:
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Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com
Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM
Listen to a blog summary of a trending research paper selected as the cover for Volume 14, Issue 5 of Aging (Aging-US), entitled, "Depletion of transmembrane mucin 4 (Muc4) alters intestinal homeostasis in a genetically engineered mouse model of colorectal cancer." __________
With age, humans undergo bodily changes which include a decline in organ and tissue function. The average age men and women are diagnosed with colorectal cancer (CRC) is 68 and 72 years old, respectively. Healthy intestinal epithelial cells are usually lined with a sufficient layer of mucus; important components in this mucus layer, called mucins, help to maintain physiological homeostasis. While transmembrane mucin 4 (Muc4) has been found to be overexpressed in pancreatic, ovarian and breast cancers, Muc4 expression is decreased in patients with CRC. The functional role and implications of Muc4 in CRC’s intestinal pathology have not yet been adequately investigated.
Researchers—from the University of Nebraska Medical Center, Baylor College of Medicine, University of California San Diego, and VA San Diego Healthcare System—sought to better understand the role of Muc4 in CRC by developing genetically engineered mouse (GEM) models. Their priority research paper was published as the cover of Aging-US Volume 14, Issue 5, and entitled, “Depletion of transmembrane mucin 4 (Muc4) alters intestinal homeostasis in a genetically engineered mouse model of colorectal cancer.“
“Therefore, to understand the functional significance of MUC4 in intestinal homeostasis and CRC progression, we developed a GEM model by crossing mice carrying a conditional mutation of Apc [adenomatous polyposis coli] gene with colon-specific caudal type homeobox transcription factor 2 (Cdx2)-Cre fused with estrogen receptor.”
Full blog post - https://aging-us.org/2022/03/trending-with-impact-muc4-role-in-intestinal-balance-and-cancer/
DOI - https://doi.org/10.18632/aging.203935
Corresponding author - Surinder K. Batra - sbatra@unmc.edu
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Keywords - aging, mucin, MUC4, intestinal homeostasis, colorectal cancer
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us:
SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/
Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com
Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM
Dennis Mangan from MTOR LLC in Bakersfield, California describes his experience publishing his theory article, “Iron: an underrated factor in aging,” in Volume 13, Issue 19 of Aging (Aging-US).
DOI - https://doi.org/10.18632/aging.203612
Corresponding author - Dennis Mangan - pdmangan@outlook.com
Abstract
Iron is an essential element for virtually all living organisms, but its reactivity also makes it potentially harmful. Iron accumulates with aging, and is associated with many age-related diseases; it also shortens the lifespans of several model organisms. Blocking iron absorption through drugs or natural products extends lifespan. Many life-extending interventions, such as rapamycin, calorie restriction, and old plasma dilution can be explained by the effects they have on iron absorption, excretion, and metabolism. Control of body iron stores so that they remain in a low normal range may be an important, lifespan- and healthspan-extending intervention.
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Press release - https://www.aging-us.com/news_room/iron-an-underrated-factor-in-aging
Blog post - https://www.impactjournals.com/journals/blog/aging/trending-with-impact-is-iron-a-driver-of-aging/
Mangan interview with Dr. Mikhail Blagosklonny - https://www.youtube.com/watch?v=e-if3zjYSfY
Keywords - iron, aging, oxidative stress, calorie restriction, plasma dilution
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us:
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Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com
Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM
Listen to a blog summary of a trending research paper published by Aging (Aging-US) on February 16, 2022, entitled, “Elevated levels of serum CDCP1 in individuals recovering from severe COVID-19 disease.” _____
Among people who have been fortunate to recover from COVID-19, at least 40% had or have long-term lingering effects from this disease. Sometimes appearing months after recovering, these “long covid” effects can include (not limited to) fatigue, trouble sleeping, difficulty concentrating, joint or muscle pain, and respiratory issues, such as shortness of breath and chest pain. Researchers are still unsure as to whether or not lasting COVID-19 effects in the lungs are associated with the severity of disease at the time of infection.
“Thus, prospective studies related to outcomes following recovery from COVID-19 might improve our understanding of this disease, its sequelae, and possible interventions to improve this situation.”
Researchers—from Hospital Universitario San Pedro, Centro de Investigación Biomédica de La Rioja, Universidad de Córdoba, Hospital Universitario Reina Sofía, Hospital Costal de Sol, HCU Lozano Blesa, Hospital Universitario Marqués de Valdecilla, Unidad de Enfermedades Infecciosas, Hospital Universitario de Burgos, Vitro Laboratory, Instituto de Investigación-IdiPaz, and Universidad Rey Juan Carlos—conducted a new study aimed at identifying biomarkers of severe disease in patients after hospitalization for COVID-19. Their research paper was published by Aging (Aging-US) on February 16, 2022, and entitled, “Elevated levels of serum CDCP1 in individuals recovering from severe COVID-19 disease.”
Full blog - https://aging-us.org/2022/03/trending-with-impact-do-biomarkers-of-long-covid-exist/
DOI - https://doi.org/10.18632/aging.203898
Corresponding Author - Jose-Ramon Blanco - jrblancoramos@gmail.com; https://orcid.org/0000-0002-4268-0150
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Keywords - biomarkers, CDCP1, recovery, COVID-19
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com and connect with us:
SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/
Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com
Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM
Dr. Andrei Gudkov of the Roswell Park Cancer Institute in Buffalo, NY discusses the research paper he co-authored that was published by Aging (Aging-US) in Volume 9, Issue 8, entitled, "p16(Ink4a) and senescence-associated β-galactosidase can be induced in macrophages as part of a reversible response to physiological stimuli."
DOI - https://doi.org/10.18632/aging.101268
Correspondence to - Olga Chernova - ochernova@tartiscorp.com and Andrei Gudkov - andrei.gudkov@roswellpark.org
Abstract: Constitutive p16Ink4a expression, along with senescence-associated β-galactosidase (SAβG), are commonly accepted biomarkers of senescent cells (SCs). Recent reports attributed improvement of the healthspan of aged mice following p16Ink4a-positive cell killing to the eradication of accumulated SCs. However, detection of p16Ink4a/SAβG-positive macrophages in the adipose tissue of old mice and in the peritoneal cavity of young animals following injection of alginate-encapsulated SCs has raised concerns about the exclusivity of these markers for SCs. Here we report that expression of p16Ink4a and SAβG in macrophages is acquired as part of a physiological response to immune stimuli rather than through senescence, consistent with reports that p16Ink4a plays a role in macrophage polarization and response. Unlike SCs, p16Ink4a/SAβG-positive macrophages can be induced in p53-null mice. Macrophages, but not mesenchymal SCs, lose both markers in response to M1- [LPS, IFN-α, Poly(I:C)] and increase their expression in response to M2-inducing stimuli (IL-4, IL-13). Moreover, interferon-inducing agent Poly(I:C) dramatically reduced p16Ink4a expression in vivo in our alginate bead model and in the adipose tissue of aged mice. These observations suggest that the antiaging effects following eradication of p16Ink4a-positive cells may not be solely attributed to SCs but also to non-senescent p16Ink4a/SAβG-positive macrophages.
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Keywords - aging, macrophage, senescent cell, p16(Ink4a), beta-galactosidase
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com and connect with us:
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Listen to a blog summary of the research paper selected as the cover for Volume 14, Issue 4 of Aging (Aging-US):
Aging seems nearly synonymous with brewing cognitive decline, but does it have to be? There are interventions that may help preserve cognitive function with age, however, the first order of business is identifying early biological aging markers that present before symptoms begin emerging. Mid-life biomarkers that can indicate accelerated aging and predict age-related cognitive decline (including Alzheimer’s disease and dementia) may provide humans with enough time to course-correct and improve our quality of life in old age.
The latest to endeavor in search of these early aging markers are researchers from Northwestern University Feinberg School of Medicine, University of Texas Health Science Center at San Antonio, University of Pennsylvania, Boston University School of Medicine, National Institute on Aging from the National Institutes of Health, University of Minnesota, Columbia University Mailman School of Public Health, Kaiser Permanente Division of Research, University of Texas at Austin, University of California San Francisco, and the San Francisco Veterans Affairs Medical Center. Their new research study was published in Aging (Aging-US) as the cover paper in Volume 14, Issue 4, on February 27, 2022. The paper is entitled, “Mid-life epigenetic age, neuroimaging brain age, and cognitive function: coronary artery risk development in young adults (CARDIA) study.”
Full blog - https://aging-us.org/2022/03/trending-with-impact-cognitive-decline-predicted-from-middle-age/
Paper DOI - https://doi.org/10.18632/aging.203918
Corresponding Authors - Yinan Zheng - y-zheng@northwestern.edu, Kristine Yaffe - Kristine.Yaffe@ucsf.edu, and Lifang Hou - l-hou@northwestern.edu
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Keywords - cognitive function, epigenetic age, brain age, DNA methylation, magnetic resonance imaging
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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Listen to a blog summary of a research paper published by Aging (Aging-US)in Volume 11, Issue 17, entitled, "Conclusions from a behavioral aging study on male and female F2 hybrid mice on age-related behavior, buoyancy in water-based tests, and an ethical method to assess lifespan."
________________________
Mice are frequently used as research models in aging studies. In 2019, researchers from the University of Gothenburg, R&D AstraZeneca, Harvard Medical School, and Karolinska Institutet identified logistical and ethical issues with the standard system of handling murine models in aging studies. Historically, researchers have favored using male mouse models instead of females, especially in pharmaceutical drug discovery and testing. However, half of the human population is female, and thus, females are half of the recipients of pharmaceuticals on the market. There is a need to fill this gap in research by emphasizing the assessment of both male and female subjects in research studies. The second logistical problem is the use of inbred mice. Inbred mice in the laboratory tend to have strain-specific behaviors that can skew study results. Therefore, there is a need to replace inbred mice with hybrid mice, especially in behavioral aging studies.
Lastly, the researchers addressed lifespan assessment in mice. Due to ethical concerns, many institutions do not allow researchers to study lifespan in mice. These concerns arose from researchers allowing mice to pass away naturally, even if some mice are terminally ill and suffering. In a research paper published by Aging (Aging-US) in 2019, the researchers came up with a novel method of ethically assessing lifespan. They also employed male and female F2 hybrid mice in a behavioral aging study. Their paper was entitled, “Conclusions from a behavioral aging study on male and female F2 hybrid mice on age-related behavior, buoyancy in water-based tests, and an ethical method to assess lifespan.”
Full blog - https://aging-us.org/2022/03/behavioral-aging-study-and-ethical-lifespan-assessment-of-hybrid-mice/
Paper DOI - https://doi.org/10.18632/aging.102242
Corresponding Author - Malin Hernebring - malin.hernebring@gu.se
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Press release - https://www.aging-us.com/news_room/conclusions-from-a-behavioral-aging-study-on-male-and-female-f2-hybrid-mice-on-age-related-behavior-buoyancy-in-water-based-tests-and-an-ethical-method-to-assess-lifespan
Keywords - F2 hybrid mice, aging, sex comparison, exploratory activity, water-based behavioral tests
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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Dr. Cameron Hill from the Randall Centre for Cell and Molecular Biophysics, Kings College London, and Dr. Paul Morgan from the University of Birmingham, United Kingdom, discuss the topic of an editorial that was co-authored by Dr. Hill - along with Dr. Jason Tallis from Coventry University Centre for Sport, School of Life Sciences, Coventry, West Midlands, United Kingdom - and published by Aging (Aging-US) in Volume 11, Issue 8, entitled, “Is obesity a risk factor for skeletal muscle ageing?”
DOI - https://doi.org/10.18632/aging.101941 (PDF download)
Full text - https://www.aging-us.com/article/101941
Corresponding Author - Cameron Hill - cameron.hill@kcl.ac.uk
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Keywords - isolated muscles, obesity, sarcopenic obesity, power, force, muscle quality
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com and connect with us:
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In aging research, recent evidence has encouraged more focus on investigating socioeconomic status (SES) and its role in human health trajectories. Previous studies have used DNA methylation measures and epigenetic clocks to demonstrate a consistent association between low SES and epigenetic age acceleration (EAA). Moreover, researchers have identified a need to further investigate the relationship between SES characteristics and aging.
“Little is known whether current occupational characteristics or job-related stress – crucial SES characteristics – are associated with EAA.”
Recently, researchers—from Imperial College London, University of Sassari, University of Eastern Finland, Karolinska Institutet, University of Oulu, and the Italian Institute for Genomic Medicine—conducted a research study in an effort to help elucidate potential mechanisms by which work characteristics and job stressors may be impacting health and accelerating aging. Their trending research paper was published by Aging (Aging-US) on February 2, 2022, and entitled, “Work-related stress and well-being in association with epigenetic age acceleration: A Northern Finland Birth Cohort 1966 Study.”
Full blog - https://aging-us.org/2022/02/trending-with-impact-can-job-stress-cause-epigenetic-aging/
DOI - https://doi.org/10.18632/aging.203872
Corresponding author - Anna Freni-Sterrantino - a.freni-sterrantino@imperial.ac.uk
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Keywords - epigenetic age, job strain, effort-reward imbalance, work-related well-being, DNA methylation
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com and connect with us:
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Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com
Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM
Drs. Malin Hernebring, Julia Adelöf, Jaime Ross discuss their 2019 study published by Aging (Aging-US) in Volume 11, Issue 17, entitled, “Conclusions from a behavioral aging study on male and female F2 hybrid mice on age-related behavior, buoyancy in water-based tests, and an ethical method to assess lifespan.”
DOI - https://doi.org/10.18632/aging.102242
Correspondence to - Malin Hernebring - malin.hernebring@gu.se
Abstract Due to strain-specific behavioral idiosyncrasies, inbred mouse strains are suboptimal research models for behavioral aging studies. The aim of this study is to determine age-related behavioral changes of F2 hybrid C57BL/6NxBALB/c male and female mice. Lifespan was followed (nmales=48, nfemales=51) and cohorts of mature adult (7 months), middle-aged (15 months), and old mice (22 months of age; n=7-12 per group) were assessed regarding open-field activity, exploration, passive avoidance learning/memory, and depressive-like behavior. We found that both males and females demonstrated decreased exploratory behavior with age, while memory and depressive-like behavior were maintained. Females exhibited enhanced depressive-like behavior compared to males; however, a correlation between fat mass and swimming activity in the test directly accounted for 30-46% of this behavioral sex difference. In addition, we suggest a method to qualitatively estimate natural lifespan from survival analyses in which animals with signs of pain or severe disease are euthanized. This is, to our knowledge, the first behavioral study to consider both sex and aging in hybrid mice. We here define decreased exploratory behavior as a conserved hallmark of aging independent of sex, highlight the effect of buoyancy in water tests, and provide a method to assay lifespan with reduced animal suffering.
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Press release - https://www.aging-us.com/news_room/conclusions-from-a-behavioral-aging-study-on-male-and-female-f2-hybrid-mice-on-age-related-behavior-buoyancy-in-water-based-tests-and-an-ethical-method-to-assess-lifespan
Keywords: F2 hybrid mice, aging, sex comparison, exploratory activity, water-based behavioral tests
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com and connect with us:
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Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com
Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM
Radiation therapy is a highly-effective inducer of cancer cell death. With this being said, radiation has also previously been shown to cause premature senescence in the lung parenchyma. Senescence in cancer cells was previously only thought of as a mechanism capable of suppressing tumor cell proliferation by halting the cell cycle. However, a growing body of evidence shows that senescent cells may play a pro-tumorigenic role in cancer.
In the tumor microenvironment, the accumulation of senescent cells can become tumorigenic due to a lack of normal tissue stem cells and due to the expression of the senescence-associated secretory phenotype (SASP). SASP expression is when senescent cells secrete high levels of inflammatory cytokines, immune modulators, growth factors, and proteases. In addition to reinforcing senescence, SASP can create a biological environment that is immuno-suppressed and tumor-permissive. Radiation-induced senescence has previously been shown to have negative impacts on cancer patients.
“Cells that have undergone premature senescence due to stress, such as irradiation, are resistant to apoptotic cell death and effectively escape immune surveillance, resulting in their accumulation in tissue over time.”
Recently, researchers from the National Cancer Institute investigated the irradiated lung and the impact of radiation-induced senescent parenchymal cells on tumor growth. They also explored three senotherapeutics, rapamycin, INK-128 and ABT-737, for their potential to mitigate radiation-induced senescence. On February 12, 2022, the team’s priority research paper was published on the cover of Aging (Aging-US) Volume 14, Issue 3, and entitled, “Senescence-associated tumor growth is promoted by 12-Lipoxygenase.”
Full blog - https://www.impactjournals.com/journals/blog/aging/trending-with-impact-radiation-senescence-and-senotherapeutics/
DOI - https://doi.org/10.18632/aging.203890
Corresponding author - Deborah E. Citrin - citrind@mail.nih.gov
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Keywords - aging, senescence, radiation, senolytic, metastasis, Alox12
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us:
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The 8th Annual Aging Research and Drug Discovery (ARDD21) meeting was held in Copenhagen, Denmark, from August 30 to September 3, 2021. This meeting was attended by over 130 people on-site, with an additional 1800 people engaged online. The focus of this meeting was the current landscape of aging research and various ways it can be applied to drug discovery. Topics included: age-dependent control of cellular maintenance processes, longevity pathways, artificial intelligence-based drug screening, cellular stress and aging, the benefits of dietary restriction, stem cell rejuvenation, senolytics as an aging therapeutic, diverse models of aging, aging clocks and biomarkers of aging, new ideas in preclinical and clinical aging research, the longevity industry landscape, and a Longevity Medicine Workshop.
In total, there were 75 presentations given at ARDD21 by prominent and dedicated aging researchers. The meeting was thoroughly summarized in a paper published in Aging (Aging-US) Volume 14, Issue 2, entitled, “Meeting Report: Aging Research and Drug Discovery.”
Full blog - https://www.impactjournals.com/journals/blog/aging/trending-with-impact-ardd21-meeting-report-highlights/
DOI - https://doi.org/10.18632/aging.203859
Corresponding authors - Daniela Bakula - bakula@sund.ku.dk, Alex Zhavoronkov - alex@insilico.com, and Morten Scheibye-Knudsen - mscheibye@sund.ku.dk
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Keywords - aging, drug discovery, conference, AI, longevity
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com and connect with us:
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Aging Editorial Board member and Founder and CEO of Insilico Medicine, Dr. Alex Zhavoronkov, discusses his 2020 COVID-19 research perspective published by Aging (Aging-US), entitled, "Geroprotective and senoremediative strategies to reduce the comorbidity, infection rates, severity, and lethality in gerophilic and gerolavic infections."
DOI - https://doi.org/10.18632/aging.102988
Corresponding author - Alex Zhavoronkov - alex@insilico.com
Abstract: The recently identified SARS-CoV-2 betacoronavirus responsible for the COVID-19 pandemic has uncovered the age-associated vulnerability in the burden of disease and put aging research in the spotlight. The limited data available indicates that COVID-19 should be referred to as a gerolavic (from Greek, géros “old man” and epilavís, “harmful”) infection because the infection rates, severity, and lethality are substantially higher in the population aged 60 and older. This is primarily due to comorbidity but may be partially due to immunosenescence, decreased immune function in the elderly, and general loss of function, fitness, and increased frailty associated with aging. Immunosenescence is a major factor affecting vaccination response, as well as the severity and lethality of infectious diseases. While vaccination reduces infection rates, and therapeutic interventions reduce the severity and lethality of infections, these interventions have limitations. Previous studies showed that postulated geroprotectors, such as sirolimus (rapamycin) and its close derivative rapalog everolimus (RAD001), decreased infection rates in a small sample of elderly patients. This article presents a review of the limited literature available on geroprotective and senoremediative interventions that may be investigated to decrease the disease burden of gerolavic infections. This article also highlights a need for rigorous clinical validation of deep aging clocks as surrogate markers of biological age. These could be used to assess the need for, and efficacy of, geroprotective and senoremediative interventions and provide better protection for elderly populations from gerolavic infections. This article does not represent medical advice and the medications described are not yet licensed or recommended as immune system boosters, as they have not undergone clinical evaluation for this purpose.
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Press release - https://www.aging-us.com/news_room/scientist-proposes-clinical-trials-w-low-dose-rapamycin-to-protect-elderly-from-covid-19
Keywords - COVID-19, SARS-CoV-2, coronavirus, sirolimus, rapalog
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com and connect with us:
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Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com
Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM
Cellular senescence appears to be a phenomenon fundamentally ingrained within the aging process and linked to age-related diseases. Characterized broadly by permanent cessation of the cell cycle, cellular senescence may not be as permanent as once thought.
Researchers from Incheon National University and Korea University conducted a new study exploring analogs of oxazoloquinoline and their potential to alleviate cellular senescence. Their trending research paper was published as the cover of Aging (Aging-US) Volume 14, Issue 2, and entitled, “Targeting regulation of ATP synthase 5 alpha/beta dimerization alleviates senescence.”
Full blog - https://www.impactjournals.com/journals/blog/aging/trending-with-impact-therapeutic-strategy-improves-cell-senescence/
DOI - https://doi.org/10.18632/aging.203858
Correspondence to - Youngjoo Byun - yjbyun1@korea.ac.kr and Joon Tae Park - joontae.park@inu.ac.kr
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Keywords - aging, senescence amelioration, KB1541, ATPase synthase 5, OXPHOS
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com and connect with us:
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Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com
Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM
After water, tea is the most popular beverage in the world. While many people enjoy tea for the flavor, aroma and caffeine boost, research suggests that there may be another reason to regularly drink this beverage: its effects on the brain. In 2019, researchers from Wuyi University, University of Essex, University of Cambridge, and the National University of Singapore conducted the first study exploring the effects of tea on system-level brain networks. Their paper was published in Aging (Aging-US) Volume 11, Issue 11, and entitled, “Habitual tea drinking modulates brain efficiency: evidence from brain connectivity evaluation.”
“In this study, we comprehensively explored brain connectivity with both global and regional metrics derived from structural and functional imaging to unveil putative differential connectivity organizations between tea drinking group and non-tea drinking group.”
Full blog - https://www.impactjournals.com/journals/blog/aging/how-habitual-tea-drinking-impacts-brain-structure/
DOI - https://doi.org/10.18632/aging.102023
Correspondence to - Junhua Li - junhua.li@essex.ac.uk and Lei Feng - pcmfl@nus.edu.sg
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Press release - https://www.aging-us.com/news_room/habitual-tea-drinking-modulates-brain-efficiency-evidence-from-brain-connectivity-evaluation
Keywords - tea drinking, brain efficiency, fMRI, DTI, default mode network, hemispheric asymmetry, aging
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com and connect with us:
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Dr. Ariella Oppenheim from the Department of Hematology, Hebrew University Faculty of Medicine, Jerusalem, Israel, details an editorial she co-authored that was published by Aging (Aging-US) in Volume 9, Issue 5, entitled, “The puzzling interplay between p53 and Sp1.”
DOI - https://doi.org/10.18632/aging.101238 (PDF download)
Full text - https://www.aging-us.com/article/101238
Correspondence to - Ariella Oppenheim - ariellao@mail.huji.ac.il
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Keywords - cancer, p53, Sp1, transcription factors, apoptosis, proliferation
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com and connect with us:
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Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com
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Listen to the list of the 10 most-viewed papers on Aging-US.com of 2021.
10 - “Iron: an underrated factor in aging” DOI - https://doi.org/10.18632/aging.203612
9 - “Reversal of cognitive decline: A novel therapeutic program” https://doi.org/10.18632/aging.100690
8 - “Shorter telomere lengths in patients with severe COVID-19 disease” https://doi.org/10.18632/aging.202463
7 - “Hyperbaric oxygen therapy alleviates vascular dysfunction and amyloid burden in an Alzheimer’s disease mouse model and in elderly patients” https://doi.org/10.18632/aging.203485
6 - “Fighting the storm: could novel anti-TNFα and anti-IL-6 C. sativa cultivars tame cytokine storm in COVID-19?” https://doi.org/10.18632/aging.202500
5 - “Examining sleep deficiency and disturbance and their risk for incident dementia and all-cause mortality in older adults across 5 years in the United States” https://doi.org/10.18632/aging.202591
4 - “Rejuvant®, a potential life-extending compound formulation with alpha-ketoglutarate and vitamins, conferred an average 8 year reduction in biological aging, after an average of 7 months of use, in the TruAge DNA methylation test” https://doi.org/10.18632/aging.203736
3 - “Aging and rejuvenation - a modular epigenome model” https://doi.org/10.18632/aging.202712
2 - “Potential reversal of epigenetic age using a diet and lifestyle intervention: a pilot randomized clinical trial” https://doi.org/10.18632/aging.202913
1 - “Hyperbaric oxygen therapy increases telomere length and decreases immunosenescence in isolated blood cells: a prospective trial” https://doi.org/10.18632/aging.202188
Keywords - aging, science, research, longevity, lifespan, healthspan, openaccess, researchpapers, journalpublication
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us:
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Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM
Is muscle wasting a fate humans can avoid, or will the problem of aging-related muscle loss only be resolved when the mystery of aging is solved? Researchers—from Vrije Universiteit Amsterdam, University of Amsterdam, Sorbonne Université, Amsterdam University Medical Center VUmc, Université Catholique de Louvain, KU Leuven, and Institut NeuroMyoGène—conducted a study aimed at elucidating whether muscle stem cells are inherently impaired by the aging process in their ability to sense and respond to mechanical cues. Their priority research paper was published on the cover of Aging (Aging-US) Volume 14, Issue 1, and entitled, “Reduced growth rate of aged muscle stem cells is associated with impaired mechanosensitivity.”
MUSCLE STEM CELLS Muscle stem cells (MuSCs) are stem cells located within skeletal muscle tissues. MuSCs function to repair damaged myofibers and give rise to new skeletal muscle cells. These self-renewing stem cells are involved in muscle growth, repair and regeneration. As we age, MuSCs decline in number and lose their potential to regenerate damaged myofibers, leading to sarcopenia. The researchers in this study hypothesized that the responsiveness of aged MuSCs is impared by the aging process both physically and mechanically.
“We postulated that aged MuSCs are intrinsically impaired in their responsiveness to omnipresent mechanical cues through alterations in MuSC morphology, mechanical properties, and number of integrins, culminating in impaired proliferative capacity.”
Full blog - https://www.impactjournals.com/journals/blog/trending-with-impact/trending-with-impact-are-our-muscles-intrinsically-impaired-by-aging/
DOI - https://doi.org/10.18632/aging.203830
Correspondence to - Richard T. Jaspers - r.t.jaspers@vu.nl
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Keywords - aging, mechanosensitivity, muscle stem cell, proliferation, YAP signaling
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us:
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Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com
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A variety of eye disorders can occur as humans age, including age-related macular degeneration, cataracts, presbyopia, glaucoma, dry eyes, and temporal arteritis. These conditions can contribute to vision impairment and even vision loss. Unfortunately, the full gambit of common age-related eye lens changes which contribute to these disorders is not yet fully defined. However, while mice and primates are different species, their eye lenses share common characteristics. This means that studies in murine models regarding age-related eye lens changes may provide a baseline for aging studies on human eye lenses in the future.
“Little is known about the morphological, mechanical, refractive and cellular changes that occur with advanced age in the lens. Mice offer an opportunity to investigate changes in lens morphometrics, stiffness, transparency and refractive properties with age in a relatively shortened period of time.”
To further define common age-related changes in eye lenses, researchers—from The Scripps Research Institute, University of Delaware, Morehouse School of Medicine, Nottingham Trent University, Japan Synchrotron Radiation Research Institute, and Boston University School of Medicine—conducted an extensive study of eye lenses among mice between one and 30 months of age. Their paper was published by Aging (Aging-US) in 2019, and entitled, “Age-related changes in eye lens biomechanics, morphology, refractive index and transparency.”
Full bog - https://www.impactjournals.com/journals/blog/trending-with-impact/common-age-related-changes-in-eye-lenses/
Special collection on eye disease - https://www.aging-us.com/special-collections-archive/eye-disease
Press release - https://www.aging-us.com/news_room/age-related-changes-in-eye-lens-biomechanics
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DOI - https://doi.org/10.18632/aging.102584
Full text - https://www.aging-us.com/article/102584/text
Correspondence to: Velia M. Fowler email: vfowler@udel.edu and Catherine Cheng email: ckcheng@iu.edu
Keywords: fiber cell, strain, epithelial cell, cataract, stiffness
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
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Chronobiology is the study of biological rhythms. The human circadian system is a biological process known to regulate the sleeping and waking cycle (circadian rhythm; CR). Components of the circadian system are known as clock genes. Clock genes generate daily oscillations of gene expression and interact as an intricate network to influence biological processes in organisms, tissues and cells. This system is primarily regulated by Earth’s day and night cycles (light and darkness), though it can be affected by other factors, including nutrition, cellular devices, stress, illness, jet lag, and aging.
“It is well established that aging interferes with the regulation of the circadian system, which, in return, contributes to the manifestation and progression of aging-related diseases (reviewed in [4, 5]).”
Across an organism’s lifespan, changes in circadian rhythm take place. These changes can cause aging-related diseases to become more prevalent. Studies have also shown that age-independent alterations in the circadian system can result in premature aging. This interrelation between aging and CR means that aging may play a role in the circadian system and that the circadian system may play a role in aging. However, researchers have not yet fully illuminated the impact of aging-related circadian system changes on healthy organs and tissues.
“Whether aging-related changes of the circadian system’s regulation follow a conserved pattern across different species and tissues, hence representing a common driving force of aging, is unclear.”
In an effort to identify circadian rhythm regulatory patterns over the course of aging, researchers—from Friedrich Schiller University Jena, FLI Leibniz Institute for Age Research, Jena University Hospital, German Center for Integrative Biodiversity Research, and European Virus Bioinformatics Center—performed inter-species and inter-organ transcriptional analyses. The research paper was published in December of 2021 as the cover of Aging (Aging-US) Volume 12, Issue 24, and entitled, “Age-dependent expression changes of circadian system-related genes reveal a potentially conserved link to aging.”
Full blog - https://www.impactjournals.com/journals/blog/aging/aging-and-circadian-rhythm-does-a-conserved-link-exist/
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DOI - https://doi.org/10.18632/aging.203788
Full Text - https://www.aging-us.com/article/203788/text
Correspondence to: Emanuel Barth email: emanuel.barth@uni-jena.de
Keywords: aging, circadian clock system, circadian rhythm, inter-species comparison, longevity, RNA-Seq
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
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Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
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Aging-US published "DNA methylation-based measures of biological age: meta-analysis predicting time to death" in 2016, which reported that estimates of biological age based on DNA methylation patterns, often referred to as "epigenetic age", "DNAm age", have been shown to be robust biomarkers of age in humans.
These authors previously demonstrated that independent of chronological age, epigenetic age assessed in blood predicted all-cause mortality in four human cohorts. Here, they expanded their original observation to 13 different cohorts for a total sample size of 13,089 individuals, including three racial/ethnic groups. In addition, they examined whether incorporating information on blood cell composition into the epigenetic age metrics improves their predictive power for mortality.
All considered measures of epigenetic age acceleration were predictive of mortality, independent of chronological age, even after adjusting for additional risk factors.
The authors said, "DNA methylation-based biomarkers, often referred to as ‘epigenetic age’ or ‘epigenetic clock’, are robust estimators of chronological age of an individual."
Full Press Release - https://www.aging-us.com/news_room/dna-methylation-based-measures-of-biological-age
Full Text - https://www.aging-us.com/article/101020/text/
Correspondence to: Steve Horvath email: shorvath@mednet.ucla.edu
Keywords: all-cause mortality, lifespan, epigenetics, epigenetic clock, DNA+methylation, mortality
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
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Aging-US published "Epigenetic age of the pre-frontal cortex is associated with neuritic plaques, amyloid load, and Alzheimer’s disease related cognitive functioning" in 2015, which reported that there is an urgent need to develop molecular biomarkers of brain age in order to advance our understanding of age related neurodegeneration.
Here the authors use n=700 dorsolateral prefrontal cortex samples from Caucasian subjects of the Religious Order Study and the Rush Memory and Aging Project to examine the association between epigenetic age and Alzheimer’s disease related cognitive decline, and AD related neuropathological markers.
The neuropathological markers may mediate the association between epigenetic age and cognitive decline. Genetic complex trait analysis revealed that epigenetic age acceleration is heritable and has significant genetic correlations with diffuse plaques and possibly working memory. Overall, these results suggest that the epigenetic clock may lend itself as a molecular biomarker of brain age.
Dr. Steve Horvath said, "Cognitive aging is on a continuum from normality, to mild cognitive impairment (MCI), to dementia."
Complete Press Release - https://www.aging-us.com/news_room/epigenetic-age-of-the-pre-frontal-cortex
Full Text - https://www.aging-us.com/article/100864/text/
Correspondence to: Steve Horvath email: shorvath@mednet.ucla.edu
Keywords: epigenetics, neuritic plaques, amyloids, cognitive functioning, memory, Alzheimer's disease, epigenetic clock, DNA methylation
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
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In 2017, the 2nd Interventions in Aging Conference on "Understanding Mechanisms & Compressing Morbidity in Aging Humans" was held in Cancun, Mexico. The co-chairs of this conference, and speakers in this Aging (Aging-US) video, are Drs. Dame Linda Partridge DBE, FRS, FRSE, FMedSci, and Brian Kennedy Ph.D.
Dr. Partridge is currently the Weldon Professor of Biometry in the Department of Genetics, Evolution and Environment at the University College London (UCL), Director of UCL's Institute of Healthy Ageing, and the Founding Director of the Max Planck Institute for the Biology of Ageing.
Dr. Kennedy is a Distinguished Professor in the Department of Biochemistry and Physiology at the National University of Singapore (NUS)'s Yong Loo Lin School of Medicine. Dr. Kennedy is also Director of the National University Health System (NUHS) Centre for Healthy Ageing in Singapore, Professor at the Buck Institute for Research on Ageing, Adjunct Professor at the University of Southern California's Leonard Davis School of Gerontology, and Affiliate Faculty in Department of Biochemistry at the University of Washington.
In this video, these two prominent researchers briefly discussed the state of aging research in 2017, and postulated what the future of aging interventions may look like.
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DOI - https://doi.org/10.18632/aging.101221
Full Text - https://www.aging-us.com/article/101221/text#fulltext
Correspondence to: Brian K. Kennedy email: bkennedy@buckinstitute.org and Linda Partridge email: partridge@age.mpg.de
Keywords: healthspan, organismal aging, epigenetics, longevity, cellular mechanisms, metabolism, aging, conference
About Aging (Aging-US)
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM
The researchers recruited healthy older participants to two groups according to their history of tea drinking frequency and investigated both functional and structural networks to reveal the role of tea drinking on brain organization.
The suppression of hemispheric asymmetry in the structural connectivity network was observed as a result of tea drinking.
The authors did not observe any significant effects of tea drinking on the hemispheric asymmetry of the functional connectivity network.
Dr. Junhua Li and Dr. Lei Feng said, "Tea has been a popular beverage since antiquity, with records referring to consumption dating back to the dynasty of Shen Nong (approximately 2700 BC) in China."
Tea is consumed in diverse ways, with brewed tea and products with a tea ingredient extremely prevalent in Asia, especially in China and Japan.
Although individual constituents of tea have been related to the roles of maintaining cognitive abilities and preventing cognitive decline, a study with behavioural and neurophysiological measures showed that there was a degraded effect or no effect when a constituent was administered alone and a significant effect was observed only when constituents were combined.
The superior effect of the constituent combination was also demonstrated in a comparative experiment that suggested that tea itself should be administered instead of tea extracts; a review of tea effects on the prevention of Alzheimers disease, found that the neuroprotective role of herbal tea was apparent in eight out of nine studies.
It is worth noting that the majority of studies thus far have evaluated tea effects from the perspective of neurocognitive and neuropsychological measures, with direct measurement of brain structure or function less-well represented in the extant literature.
These studies focusing on brain regional alterations did not ascertain tea effects on interregional interactions at the level of the entire brain.
The Li/Feng Research team concluded, "In summary, our study comprehensively investigated the effects of tea drinking on brain connectivity at both global and regional scales using multi-modal imaging data and provided the first compelling evidence that tea drinking positively contributes to brain structure making network organization more efficient."
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DOI - https://doi.org/10.18632/aging.102023
Full Text - https://www.aging-us.com/article/102023/text
Correspondence to: Junhua Li email: junhua.li@essex.ac.uk and Lei Feng email: pcmfl@nus.edu.sg
Keywords: tea drinking, brain efficiency, fMRI, DTI, default mode network, hemispheric asymmetry
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
Media Contact 18009220957x105 MEDIA@IMPACTJOURNALS.COM
The researchers recruited healthy older participants to two groups according to their history of tea drinking frequency and investigated both functional and structural networks to reveal the role of tea drinking on brain organization.
The suppression of hemispheric asymmetry in the structural connectivity network was observed as a result of tea drinking.
The authors did not observe any significant effects of tea drinking on the hemispheric asymmetry of the functional connectivity network.
Dr. Junhua Li and Dr. Lei Feng said, "Tea has been a popular beverage since antiquity, with records referring to consumption dating back to the dynasty of Shen Nong (approximately 2700 BC) in China."
Tea is consumed in diverse ways, with brewed tea and products with a tea ingredient extremely prevalent in Asia, especially in China and Japan.
Although individual constituents of tea have been related to the roles of maintaining cognitive abilities and preventing cognitive decline, a study with behavioural and neurophysiological measures showed that there was a degraded effect or no effect when a constituent was administered alone and a significant effect was observed only when constituents were combined.
The superior effect of the constituent combination was also demonstrated in a comparative experiment that suggested that tea itself should be administered instead of tea extracts; a review of tea effects on the prevention of Alzheimers disease, found that the neuroprotective role of herbal tea was apparent in eight out of nine studies.
It is worth noting that the majority of studies thus far have evaluated tea effects from the perspective of neurocognitive and neuropsychological measures, with direct measurement of brain structure or function less-well represented in the extant literature.
These studies focusing on brain regional alterations did not ascertain tea effects on interregional interactions at the level of the entire brain.
The Li/Feng Research team concluded, "In summary, our study comprehensively investigated the effects of tea drinking on brain connectivity at both global and regional scales using multi-modal imaging data and provided the first compelling evidence that tea drinking positively contributes to brain structure making network organization more efficient."
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DOI - https://doi.org/10.18632/aging.102023
Full Text - https://www.aging-us.com/article/102023/text
Correspondence to: Junhua Li email: junhua.li@essex.ac.uk and Lei Feng email: pcmfl@nus.edu.sg
Keywords: tea drinking, brain efficiency, fMRI, DTI, default mode network, hemispheric asymmetry
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
Media Contact 18009220957x105 MEDIA@IMPACTJOURNALS.COM
Men and women universally experience a decrease in sex hormones with age. Given this knowledge, researchers previously conducted a study to assess the correlation between aging, estrogen levels and the release of glycans (carbohydrate-based polymers) among all proteins in the body. Glycans are also important components of immunoglobulin G (IgG). IgGs are serum antibodies which provide immune protection against bodily infections and mediate systemic inflammation. Each IgG molecule usually includes about 3% glycans. However, changes in the composition of glycans attached to IgGs can significantly influence antibody activity. A decrease in galactosylation has been correlated with the onset of disease and aging.
“The decrease in IgG galactosylation was first reported over 35 years ago in patients with rheumatoid arthritis and osteoarthritis [4].”
The researchers found that estrogen regulates glycosylation. However, the data they analyzed did not differentiate IgG glycosylation from the other proteins. The Glycan Age Index (a combination of three IgG glycans that appear to be both biomarkers and effectors of aging) can be used to calculate glycan age. Glycan age is associated with lifestyle and disease-risk biomarkers, and could potentially be used to monitor healthy or unhealthy aging.
“Here arises probably the most exciting aspect of the relationship between aging and IgG glycosylation: the potential of IgG glycans to distinguish between healthy and unhealthy aging, and to monitor the effect of introduced life-style changes on biological age.”
To identify changes in IgG glycans, researchers—from Genos Glycoscience Research Laboratory, University of Colorado Anschutz Medical Campus, Eastern Colorado VA Geriatric Research, University of Zagreb, Brigham and Women’s Hospital, and Boston Children’s Hospital—reanalyzed samples from the previous intervention study using state-of-the-art glycoprofiling technology. The focus of this study was to evaluate the effects of estrogen suppression, followed by estradiol supplementation, on biological age measured by the glycan age. Their paper was published in Aging (Aging-US) Volume 12, Issue 19, in 2020, and entitled, “Effects of estradiol on biological age measured using the glycan age index”.
Full blog - https://www.impactjournals.com/journals/blog/aging/can-hormone-therapy-improve-aging/
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DOI - https://doi.org/10.18632/aging.104060
Full text - https://www.aging-us.com/article/104060/text
Correspondence to: Gordan Lauc email: glauc@pharma.hr
Keywords: biological age, glycan age, estrogen, aging biomarkers, glycosylation
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
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Aging-US published a Special Collection on Eye Disease which included "Activation of C-reactive protein proinflammatory phenotype in the blood retinal barrier in vitro: implications for age-related macular degeneration" which reported that the retinal pigment epithelium (RPE) is considered one of the main targets of age-related macular degeneration (AMD), the leading cause of irreversible vision loss among the ageing population worldwide. Increased levels of circulating pentameric C-reactive protein (pCRP) are associated with higher risk of AMD. Monomeric form of pCRP has been detected in drusen, the hallmark deposits associated with AMD, and we have found that mCRP induces oBRB disruption
Dr. Blanca Molins from The IDIBAPS, Hospital Clínic de Barcelona said, "Age-related macular degeneration (AMD) is the primary cause of irreversible vision loss among the ageing population worldwide."
AMD presents RPE cell abnormalities, disruption of the outer blood-retinal-barrier (oBRB), and degeneration of photoreceptors. Altered immune responses are thought to contribute to the dry AMD phenotype. Loss of parainflammation control contributes to AMD by invoking a chronic, heightened immune response that causes tissue destruction. mCRP has been identified in ocular drusen and other subepithelial deposits, as well as in the choroid, and contributes to oBRB disruption in vitro.
The "non-risk" Factor H (FH) variant can effectively bind to mCRP to dampen its proinflammatory activity. MCRP levels are elevated in individuals with the high-risk CFH genotype [29, 30] - this is because there is no CRP transcription in retinal tissue.
The Molins Research Team concluded in their https://www.aging-us.com/article/103655/">Aging-US Research Output, "our findings further support mCRP direct contribution to progression of AMD, at least at the RPE level. The topological experiments elicit that mCRP is proinflammatory when present on the apical side of the RPE. However, mCRP is likely to only reach the apical side of the RPE in compromised RPE health and where barrier functions are compromised. Thus, a plausible scenario would infer that, in the presence of an already aged/damaged RPE, mCRP reaches the apical side of the RPE to amplify the proinflammatory microenvironment and enhance barrier disruption. With respect to previous findings, this pathologic mechanism will be more prevalent in patients carrying the FH risk polymorphism for AMD, where mCRP proinflammatory effects remain unrestrained."
Full Text - https://www.aging-us.com/article/103655/text
Correspondence to: Blanca Molins email: bmolins@clinic.cat
Keywords: age-related macular degeneration, retinal pigment epithelium, inflammation, C-reactive protein
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl
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Waiting until the end of a subject’s lifespan is quite a leaden method of validating the efficacy of a longevity-based intervention. This method could take researchers generations upon generations to eventually validate an effective intervention—or—this method might not ever yield results seen by the general public. However, researchers may have devised an innovative way to solve this problem.
“If we hope to control the aging process, we need to learn how to measure the rate of aging in shorter time periods.”
Many researchers believe that measuring the rate of human aging can be done faster by using DNA methylation-based aging clocks. Methylation-based clocks are capable of determining human biological aging with impressive accuracy. Hypermethylated and demethylated regions of DNA (CpG islands near specific aging-associated genes) play key roles in turning certain genes on and off throughout the aging process. Therefore, methylation is an important biomarker of aging. While there is a short list of currently available biological aging clocks for researchers to use in studies of anti-aging therapies, the TruAge DNA methylation test is preferable in some cases, due to its accessibility, use of simple saliva samples and cost effectiveness.
“For the first time, these biomarkers of aging give scientists the opportunity to study the effects of anti-aging compounds in real-time and directly in humans.”
In a new study, researchers from TruMe Labs, National University of Singapore and Ponce de Leon Health used the TruAge DNA methylation test to validate Rejuvant®—a patent-pending anti-aging dietary supplement. The trial study yielded unprecedented results and the research paper authored by the team was published as the cover of Aging (Aging-US) Volume 13, Issue 22, entitled: “Rejuvant®, a potential life-extending compound formulation with alpha-ketoglutarate and vitamins, conferred an average 8 year reduction in biological aging, after an average of 7 months of use, in the TruAge DNA methylation test”.
Full blog - https://www.impactjournals.com/journals/blog/aging/trending-with-impact-aging-reduced-by-8-years-with-rejuvant/
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DOI - https://doi.org/10.18632/aging.203736
Full Text - https://www.aging-us.com/article/203736/text
Correspondence to: Brian K. Kennedy email: bkennedy@nus.edu.sg and Yelena V. Budovskaya email: yelena@trumelabs.com
Keywords: aging, DNA methylation, alpha-ketoglutarate (AKG), biologic age, Rejuvant
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
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Aging-US published a Special Collection on Eye Disease which included "miR-106b suppresses pathological retinal angiogenesis" which reported that microRNAs are small non-coding RNAs that post-transcriptionally regulate gene expression.
Here, the authors show that expression of the miR-106b-25 cluster is negatively regulated by the unfolded protein response pathway of protein kinase RNA-like ER kinase in a mouse model of neovascular AMD. They demonstrate that therapeutic delivery of miR-106b to the retina with lentiviral vectors protects against aberrant retinal angiogenesis in two distinct mouse models of pathological retinal neovascularization.
Dr. Przemyslaw Sapieha and Dr. Vincent De Guire said, "Age-related macular degeneration (AMD) is a common [1] and complex [2, 3] disease of aging and the leading cause of irreversible loss of sight in elderly people."
Early forms of AMD are characterized by subretinal lipoproteinaceous deposits, local attrition of photoreceptors and loss of visual sensitivity. Late forms of AMD are defined by geographic atrophy and/or pathologic choroidal neovascularization characterized by vascular sprouting from the choriocapillaris into the neural retina or subretinal space. Sustained reduction in retinal VEGF levels can lead to neurotoxicity and degeneration of RPE-choriocapillaris in mouse models. Importantly, assessment by fundus photography and fundus fluorescein angiography of patients on anti-VEGF therapy showed accelerated development of geographic atrophy. These findings justify the need for continued exploration of novel therapeutic interventions.
Given that several inflammatory and growth factors in addition to VEGF are associated with the pathogenesis of NV AMD, a multi-targeted approach is warranted. The authors previously elucidated a specific miRNA signature in the vitreous and plasma of patients with NV AMD and observed a disease-associated increase in miR-146a and a decrease in miR-106b and miR-152. Interestingly, within this cohort, they found that both vitreous- and plasma-based miR-146a/miR-106b ratios had greater than 90% discriminatory power for classification of patients with NV AMD with an area under the receiver operating characteristic curve of 0,977 in vitreous humour and 0,915 in plasma, suggesting potential for a blood-based diagnostic.
The Sapieha/De Guire Research Team concluded in their Aging-US Research Output that there are efforts to devise therapeutics that simultaneously inhibit several factors involved in retinal vascular disease given the clinical success of compounds such as Aflibercept. miRNAs regulate translation of multiple genes and hence may be considered as multi-target inhibitors. Their potential to mitigate retinal disease will grow as comprehensive landscapes of miRNAs in health and disease are established. Preclinical studies are underway for mimics or inhibition of specific miRNAs.
Full Text - https://www.aging-us.com/article/202404/text
Correspondence to: Przemyslaw Sapieha email: mike.sapieha@umontreal.ca and Vincent De Guire email: vdeguire.hmr@ssss.gouv.qc.ca
Keywords: age related macular degeneration, miR-106b, PERK, choroidal neovascularization, angiogenesis
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
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Aging-US published a Special Collection on Eye Disease which included "ALKBH5-mediated m6A demethylation of FOXM1 mRNA promotes progression of uveal melanoma" which reported that ALKBH5, a key component of the N6-methyladenosine (m6A) methyltransferase complex, was significantly elevated in uveal melanoma cell lines and inhibited tumor growth in vitro and in vivo.
EP300-induced H3K27 acetylation activation activated increased ALkbH5 expression and inhibited UM cell proliferation, migration, invasion and increased apoptosis in vitro. Besides, it may promote UM metastasis by inducing epithelial-to-mesenchymal transition (EMT) via demethylation of FOXM1 mRNA, which increases its expression and stability. It is a potential prognostic biomarker and therapeutic target in UM.
Dr. Jingxiang Zhong and Dr. Lian Liu said, "Uveal melanoma (UM), which originates from melanocytes, is the most common primary intraocular malignancy in adults."
Up to 50% of patients with primary malignant meningitis (UM) will develop metastatic disease.
The most common sites of UM metastasis are the liver (60.5%), lungs (24.4%), skin/soft tissue (10.9%), and bone (8.4%). Unfortunately, the 1-year survival rate of UM patients with metastases is only 15% [5]. There is a pressing need to find useful prognostic biomarkers and therapeutic targets for this disease. Alkhabh5 overexpression of ALKBH5 promotes EMT of UM by upregulating FOXM1 expression via demethylating the m6A modification and further increasing the stability of FOXm1 mRNA.
The Zhong/Liu Research Team concluded in their Aging-US Research Output, "we demonstrate that ALKBH5, which is positively regulated by epigenetic modifications of H3K27 acetylation, promotes tumor progression by inducing tumor EMT and increasing FOXM1 expression via m6A demethylation (Figure 7). Therefore, ALKBH5 is a potential target of UM molecular therapy."
Full Text - https://www.aging-us.com/article/202371/text
Correspondence to: Jingxiang Zhong email: tzjx@jnu.edu.cn and Lian Liu email: lianliu@jnu.edu.cn
Keywords: uveal melanoma, ALKBH5, FOXM1, senescence-associated T cells, m6A demethylation
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
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For Aging’s Volume 11, Issue 18, the Journal devoted the Cover to a research paper by Dr. Alejandro Martin-Montalvo from the Department of Regeneration and Cell Therapy, Andalusian Center for Molecular Biology and Regenerative Medicine-CABIMER, Junta de Andalucia-University of Pablo de Olavide-University of Seville-CSIC, Sevilla, Spain
Herein, the authors show, using wild-type and the Pax8 ablated model of hypothyroidism in mice, that hyperthyroidism and severe hypothyroidism are associated with an overall unhealthy status and shorter lifespan.
Mild hypothyroid Pax8 +/- mice were heavier and displayed insulin resistance, hepatic steatosis and increased prevalence of liver cancer yet had normal lifespan.
Dr. Martin-Montalvo said, "The increasing burden of age-related diseases highlights the importance of uncovering the mechanisms underlying the aging process."
TSH stimulates the production of T4 and T3 in the thyroid gland, which in turn inhibit both TRH and TSH synthesis when THs reach the hypothalamus and hypophysis, respectively.
Greater life expectancy has been associated with reduced circulating levels of T4, T3, and/or high TSH levels in both animal models and humans.
In this line, the Laron, Ames and Snell dwarf mice, which have reduced GH signalling and reduced circulating TH levels, exhibit a consistent exceptional lifespan as well as other metabolic alterations such as enhanced hepatic insulin sensitivity.
Both rodents and humans under calorie restriction, which comprises a variety of nutritional interventions with several beneficial effects including extended longevity, exhibit reduced circulating T3 levels and/or high TSH levels.
Likewise, nonagenarians from families with exceptional long lifespans, as well as their descendants, have been reported to exhibit increased TSH levels and/or decreased circulating T3 levels.
The Martin-Montalvo research team concluded, "In 1908 Dr. Max Rubner proposed the rate of living theory of aging and longevity, postulating that species with a low metabolic rate would have increased life expectancy when compared to species with a higher metabolic rate.
In this line, restricted levels of THs, which control the metabolic rate, have been associated with increased longevity as well as metabolic fitness."
Full Text - https://www.aging-us.com/article/102285/text
Correspondence to: Alejandro Martin-Montalvo; email: alejandro.martinmontalvo@cabimer.es and Benoit Raymond Gauthier; email: benoit.gauthier@cabimer.es
Keywords: lifespan, healthspan, thyroid hormones, hyperthyroidism, hypothyroidism, glucose metabolism
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
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Copyright © 2021 Impact Journals, LLC Impact Journals is a registered trademark of Impact Journals, LLC
Aging-US published a Special Collection on Eye Disease which included "Age-related changes in eye lens biomechanics, morphology, refractive index and transparency" which reported that life-long eye lens function requires an appropriate gradient refractive index, biomechanical integrity and transparency.
The authors conducted an extensive study of wild-type mouse lenses 1-30 months of age to define common age-related changes. Biomechanical testing and morphometrics revealed an increase in lens volume and stiffness with age. Their results suggest similarities between murine and primate lenses and provide a baseline for future lens aging studies.
Dr. Velia M. Fowler and Dr. Catherine Cheng said, "The eye lens is required for fine focusing of light onto the retina to form a clear image, and the function of the lens is intimately tied to its shape, biomechanical properties, transparency and refractive index."
The eye lens is required for fine focusing of light onto the retina to form a clear image. It has long been known that age-related changes in these lens properties lead to two major lens pathologies, cataracts and presbyopia. Presbyopia is caused by a reduction in the lens' ability to change shape during focusing (accommodation), and, by extension, the need for reading glasses. Mice offer an opportunity to investigate changes in lens morphometrics, stiffness, transparency and refractive properties with age in a relatively shortened period of time. Little is known about the morphological, mechanical, refractive and cellular changes that occur with advanced age in the lens. The authors demonstrate that age-related changes in mouse lenses mimic some aspects of aging in human lenses.
The Fowler/Cheng Research Team concluded in their Aging-US Research Output, "the increases in lens size and nucleus size are correlated with increase stiffness with age. The addition of new fiber cells at the lens periphery becomes disordered with age, but this does not appear to impact lens biomechanical properties. Cataracts in aged lenses can be due to cell structural abnormalities, including incomplete suture closure, collapse of the lens epithelial cell layer into the suture gap and loss of epithelial-fiber cell attachments and compaction of the cortical lens fiber cells forming a circumferential light scattering ring. GRIN is present in the lens from 2 weeks of age and continues to increase until about 6 months of age, after which the maximum refractive index remains stable. The increase in the area of highest refractive index at the center of the lens is directly correlated with the increase in lens nucleus size, suggesting nuclear compaction drives the maximum GRIN. Whether there is a common molecular mechanism that drives changes in all the measured parameters remains unknown, but further biochemical and cell morphology studies will be needed to determine how subcellular aging affects the whole tissue. Thus, our study provides a baseline for future studies of lens aging by providing quantitative measurements of key parameters and identifying common age-related changes in the overall tissue and in individual cells"
Full Text - https://www.aging-us.com/article/102584/text
Correspondence to: Velia M. Fowler email: vfowler@udel.edu and Catherine Cheng email: ckcheng@iu.edu
Keywords: fiber cell, strain, epithelial cell, cataract, stiffness
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com
Aging-US published a Special Collection on Eye Disease which included "ALDH2 protects naturally aged mouse retina via inhibiting oxidative stress-related apoptosis and enhancing unfolded protein response in endoplasmic reticulum" which reported that during the process of aging, the retina exhibits chronic oxidative stress damage.
These authors' preliminary experiment showed that acetaldehyde dehydrogenase 2 could alleviate retinal damage caused by OS. Retinal function and structure in vivo and in vitro were examined in aged ALDH2+ overexpression mice and ALDH2 agonist Alda1-treated aged mice.
Levels of ALDH2, endoplasmic reticulum stress, apoptosis and inflammatory cytokines were evaluated. Moreover, aged ALDH2+ overexpression mice and aged Alda1-treated mice exhibited better retinal function and structure. Increased expression of glucose-regulated protein 78 and ERS-related protein phosphorylated eukaryotic initiation factor 2 and decreased expression of apoptosis-related protein, including C/EBP homologous protein, caspase12 and caspase9, and retinal inflammatory cytokines were detected in the retina of aged ALDH2+ overexpression mice and aged Alda1-treated mice.
Dr. Tao Chen and Dr. Wei Ge said, "The aging process is characterized by a decline in systematic tissue function and the onset of serious of age-related disease."
However, it remained elusive that the potential mechanisms accounting for these phenomena and strategies to intervene to improve cell functions. Recently, the imbalance of protein homeostasis was proposed to be responsible for aging and age-related diseases.
Furthermore, eukaryotic translation initiation factor 2, a protein translation component, is the downstream of PERK. When endoplasmic reticulum stress happens, eIF2 is phosphorylated to slow down protein production and reduce the unfolded and misfolded proteins.
Nevertheless, the underlying mechanisms of UPRER related to aged retinal behaviour remain largely unclear, and effective therapies to intervene in aging-related injury to the retina by targeting the UPRER have not been developed. Mitochondrial aldehyde dehydrogenase 2 is essential for the catabolism of exogenous and endogenous toxic aldehydes associated with oxidative stress-induced lipid peroxidation and adducts with DNA, RNA and protein.
The Chen/Ge Research Team concluded in their Aging-US Research Output, "overexpression of ALDH2 and treatment with the ALDH2 agonist Alda1 in aging mice could both result in good retinal function and structural integrity via attenuating oxidative stress and apoptosis, and enhancing UPRER. Therefore, an increasing expression of ALDH2 could serve to preserve retinal function during the normal aging process or the onset of age-related retinal disease."
Full Text - https://www.aging-us.com/article/202325/text
Correspondence to: Tao Chen email: ct1988@fmmu.edu.cn and Wei Ge email: geweidr@fmmu.edu.cn
Keywords: ALDH2, UPRER, retina, aged mice, oxidative stress
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
Media Contact 18009220957x105 MEDIA@IMPACTJOURNALS.COM
Aging-US published a Special Collection on Eye Disease which included "Exosomes derived from BDNF-expressing 293T attenuate ischemic retinal injury in vitro and in vivo" which reported that this study investigated whether exosomes derived from BDNF-expressing 293T cells can be internalized by ischemic retinal cells and exert neuroprotective roles.
The results demonstrated that 293T-Exo significantly attenuated the loss of cell proliferation and cell death in R28 cells in response to oxygen-glucose deprivation treatment. Mechanistic studies revealed that the endocytosis of 293T-Exo by R28 cells displayed dose- and temperature-dependent patterns and may be mediated by the caveolar endocytic pathway via the integrin receptor.
Dr. Genlin Li and Dr. Yanling Wang said, "Retinal ischemia-reperfusion (I/R) emerges in many ocular diseases and is a leading cause of neuronal death and dysfunction, resulting in irreversible visual impairment or blindness."
Growing reports demonstrated that retinal ischemia is a primary contributor to the pathogenesis of multiple diseases, such as retinal vascular occlusions, diabetic retinopathy, central retinal vein occlusion, as well as age-associated macular degeneration. Exosomes are synthesized and released by various cell types and transport active biological molecules to regulate the physiological activities of recipient cells. Thus, exosomes play an essential role in intercellular communication. Therefore, understanding the mechanism of exosome uptake would promote the development of more efficient delivery systems for disease treatment.
Brain-derived neurotrophic factor, a member of the nerve growth factor gene family, is an essential multi-functional factor in various neuronal processes, including learning and memory, dendritic and synaptic plasticity, and axonal growth.
The Li/Wang Research Team concluded in their Aging-US Research Output "the results suggest that 293T-Exo is endocytosed by retinal cells through the caveolar endocytic pathway via the integrin receptor. In addition, 293T-Exo exerts a neuroprotective role in the ischemic retina, both >in vitro and in vivo. The findings from the present study demonstrates a significant therapeutic potential of exosomes and provides an understanding of how to develop exosome-based therapies for retinal ischemia."
Full Text - https://www.aging-us.com/article/202245/text
Correspondence to: Genlin Li email: ligenlin2018@163.com and Yanling Wang email: wangyanling999@vip.sina.com
Keywords: retinal ischemia, exosome, brain-derived neurotrophic factor, endocytosis, apoptosis
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
Media Contact 18009220957x105 MEDIA@IMPACTJOURNALS.COM
Many aging-associated neurodegenerative disorders, including Alzheimer’s disease, involve the aggregation of abnormal tau in nerve cells (neurons). Normally, tau proteins function to stabilize microtubules in the brain. Tauopathy occurs when tau proteins become misfolded and misshapen (which turns tau into toxic tau). They then continue to proliferate and bind to each other, forming tau oligomers. These tau oligomers are more toxic and have a greater potential to spread tau pathology. Before toxic tau snowballs into neurodegenerative disorders, the events that lead up to abnormal tau have remained elusive to researchers.
“While the association between tau levels and energy metabolism is established, it is not clear whether mitochondrial dysfunction is an early pathological feature of high levels of tau or a consequence of its excessive formation of protein aggregates.”
Previous studies have demonstrated an association between tau levels and mitochondrial metabolism, however, determining which one proceeds the other has yet to be fully illuminated. Shedding light on this subject, researchers—from the University of Copenhagen, National and Kapodistrian University of Athens and the National Institutes of Health’s National Institute on Aging—used a Caenorhabditis elegans (C. elegans; roundworm/nematode) model of tau to examine mitochondrial changes over time. Their paper was chosen as the cover of Aging (Aging-US) Volume 13, Issue 21, published in November of 2021 and entitled, “Alteration of mitochondrial homeostasis is an early event in a C. elegans model of human tauopathy”.
Full blog - https://www.impactjournals.com/journals/blog/aging/trending-with-impact-worms-reveal-early-event-in-neurodegeneration/
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DOI - https://doi.org/10.18632/aging.203683
Full Text - https://www.aging-us.com/article/203683/text
Correspondence to: Konstantinos Palikaras email: palikarask@med.uoa.gr, Mansour Akbari email: akbari@sund.ku.dk and Vilhelm A. Bohr email: bohrv@grc.nia.nih.gov
Keywords: aging, Alzheimer’s disease, C. elegans, energy metabolism, mitochondria, tau, tauopathy
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
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Aging-US published a Special Collection on Eye Disease which included "Suppressing endoplasmic reticulum stress-related autophagy attenuates retinal light injury" which reported that in this study, oxidative stress, endoplasmic reticulum stress and autophagy caused by light exposure were evaluated in vitro and in vivo.
Additionally, inhibiting ER stress either by knocking down PERK signals or with GSK2606414 treatment remarkably suppressed prolonged autophagy and protected the cells against light injury. In vivo experiments verified neuroprotection via inhibiting ER stress-related autophagy in light-damaged retinas of mice. In conclusion, the above results suggest that light-induced photo-oxidative stress may trigger subsequent activation of ER stress and prolonged autophagy in photoreceptors and RPE cells.
Suppressing ER stress may abrogate over-activated autophagy and protect the retina against light injury.
Dr. Guang-Yu Li from The Second Hospital of Jilin University said, "Age-related macular degeneration (AMD) is a degenerative retinal disease, which often occurs in the elderly and causes irreversible loss of central vision."
Indeed, excessive and prolonged light exposure may damage the retina and is an environmental factor that can accelerate AMD. With the rapid development of technology, many electronic devices with screens, and ophthalmic equipment with intensive illumination, have become widely used. Therefore, an increasing amount of attention has been focused on issues of light pollution and retinal light damage. Previous studies have shown that excessive intracellular ROS may lead to depletion of the GSH pool and compromise the function of PDI, which disrupts the folding process of proteins in the ER and produces a massive amount of misfolded proteins.
However, the excessive accumulation of misfolded proteins in the ER may trigger an unfolded-protein response, which may enhance protein folding ability, as well as the homeostasis of protein translation and accelerate protein degradation to recover ER function. However, prolonged autophagy may lead to cell death and is specifically termed autophagy-dependent cell death. The role of autophagy in retinal light injury is controversial.
Autophagy might be a double-edged sword among the molecular mechanisms that lead to retinal light damage. Midorikawa et al. reported that moderate autophagy combined with endosomal degradation pathway activity is neuroprotective and attenuates light-dependent retinal degeneration.
The Li Research Team concluded in their Aging-US Research Output "the current study demonstrated that ER stress and autophagy are both involved in light-induced death of photoreceptors and RPE cells. As an upstream step, photo-oxidation may cause an imbalance in the cellular redox status and interrupt the folding process of proteins, further triggering ER stress in photoreceptors and RPEs. Suppressing ER stress via PERK signals may inhibit prolonged autophagy and protect photoreceptors/RPEs against light damage. Inhibiting ER stress-related autophagy is neuroprotective for retinal against light injury, which may be a potential treatment strategy for AMD."
Full Text - https://www.aging-us.com/article/103846/text
Correspondence to: Guang-Yu Li email: l_gy@jlu.edu.cn
Keywords: oxidative stress, ER stress, autophagy, AMD, PERK
Aging-US published a Special Collection on Eye Disease which included "Development and validation of an immune and stromal prognostic signature in uveal melanoma to guide clinical therapy" which reported that the tumor microenvironment is known to play an important role in uveal melanoma.
Reliable prognostic signatures are needed to aid high risk patients and improve prognosis. Immune and stromal scores were calculated by applying the "ESTIMATE" algorithm. The authors found that the median survival time of the low immune/stromal score group is longer than that of the high-score group.
Dr. Liang Hu from The Wenzhou Medical University said, "Uveal melanoma (UM) is the most common type of malignant tumor of the adult eye, and 50% of patients with UM will eventually die as a result."
Tumor microenvironment (TME) plays a pivotal role in cancer progression and therapeutic responses. Prognostic biomarkers related to TME may hold great promise in identifying molecular targets and guiding patient management. Immune and stromal cells are two major types suggested as crucial for the diagnostic and prognostic assessment of tumors. Scores can be calculated using the ESTIMATE algorithm to predict the infiltration of non-tumor cells in UM patients.
The Hu Research Team concluded in their Aging-US Research Output, "our study reveals a comprehensive landscape of the immune and stromal microenvironment in UM, and provides a promising prognostic signature for UM. Patients with the high risk scores could benefit more from anti-PD-1 therapy and chemotherapy. Further investigations are needed to verify the accuracy in estimating prognoses and to test its clinical utility in patient management."
Full Text - https://www.aging-us.com/article/103779/text
Correspondence to: Liang Hu email: liang_hu@live.cn
Keywords: uveal melanoma, immune, stromal, prognosis
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl
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There may be many paths that lead to the cessation of aging, or there may only be one—this mystery has yet to reveal itself. However, there is a wide array of evidenced methods capable of preserving youth by slowing down the aging process, and even mildly reversing it. Some known natural interventions are healthy diets, consistent exercise and avoiding aging-related risk factors, including carcinogens such as alcohol, cigarettes and excess sun exposure. Researchers have also studied less intuitive repetitive behaviors that appear to improve the cognitive decline associated with aging. For example, in a study published in 2015, researchers found that active singing led to cognitive improvements in participants with dementia.
“People engaging in lifelong music-making have been found to have better cognitive outcomes later in life.”
In a research study published in 2020, 30 researchers—from National University of Singapore, Singapore Institute for Clinical Sciences, National University Health System, University of Cambridge, University of London, Singapore Immunology Network, Maurine Tsakok Inc, Voices of Singapore Choral Society, Presbyterian Community Services, NTUC Health Co-operative Limited, Beijing Chui Yang Liu Hospital, Fudan University, Massachusetts General Hospital, Harvard Medical School, Nanyang Technological University, Imperial College London, and Genome Institute of Singapore—conducted the world’s first study designed to compare the impact of choral singing versus health education on cognitive function and aging in a randomized controlled trial (RCT). Their trending research paper was published by Aging (Aging-US) and entitled, “Effects of choral singing versus health education on cognitive decline and aging: a randomized controlled trial”.
“In this RCT, we hypothesized that choral singing would improve cognitive health and/or reduce cognitive decline in elderly with high risk of dementia.”
Full blog - https://www.impactjournals.com/journals/blog/aging/trending-with-impact-can-singing-improve-aging/
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DOI - https://doi.org/10.18632/aging.202374
Full Text - https://www.aging-us.com/article/202374/text
Correspondence to: Lei Feng email: pcmfl@nus.edu.sg
Keywords: choral singing, health education, cognitive decline, biological markers, randomized controlled trial
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
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The researchers recruited healthy older participants to two groups according to their history of tea drinking frequency and investigated both functional and structural networks to reveal the role of tea drinking on brain organization.
The suppression of hemispheric asymmetry in the structural connectivity network was observed as a result of tea drinking.
The authors did not observe any significant effects of tea drinking on the hemispheric asymmetry of the functional connectivity network.
Dr. Junhua Li and Dr. Lei Feng said, "Tea has been a popular beverage since antiquity, with records referring to consumption dating back to the dynasty of Shen Nong (approximately 2700 BC) in China."
Tea is consumed in diverse ways, with brewed tea and products with a tea ingredient extremely prevalent in Asia, especially in China and Japan.
Although individual constituents of tea have been related to the roles of maintaining cognitive abilities and preventing cognitive decline, a study with behavioural and neurophysiological measures showed that there was a degraded effect or no effect when a constituent was administered alone and a significant effect was observed only when constituents were combined.
The superior effect of the constituent combination was also demonstrated in a comparative experiment that suggested that tea itself should be administered instead of tea extracts; a review of tea effects on the prevention of Alzheimers disease, found that the neuroprotective role of herbal tea was apparent in eight out of nine studies.
It is worth noting that the majority of studies thus far have evaluated tea effects from the perspective of neurocognitive and neuropsychological measures, with direct measurement of brain structure or function less-well represented in the extant literature.
These studies focusing on brain regional alterations did not ascertain tea effects on interregional interactions at the level of the entire brain.
The Li/Feng Research team concluded, "In summary, our study comprehensively investigated the effects of tea drinking on brain connectivity at both global and regional scales using multi-modal imaging data and provided the first compelling evidence that tea drinking positively contributes to brain structure making network organization more efficient."
Full Text - https://www.aging-us.com/article/102023/text
Correspondence to: Junhua Li email: junhua.li@essex.ac.uk and Lei Feng email: pcmfl@nus.edu.sg
Keywords: tea drinking, brain efficiency, fMRI, DTI, default mode network, hemispheric asymmetry
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl
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Aging-US published a Special Collection on Eye Disease which included "Activation of C-reactive protein proinflammatory phenotype in the blood retinal barrier in vitro: implications for age-related macular degeneration" which reported that the retinal pigment epithelium (RPE) is considered one of the main targets of age-related macular degeneration (AMD), the leading cause of irreversible vision loss among the ageing population worldwide. Increased levels of circulating pentameric C-reactive protein (pCRP) are associated with higher risk of AMD. Monomeric form of pCRP has been detected in drusen, the hallmark deposits associated with AMD, and we have found that mCRP induces oBRB disruption
Dr. Blanca Molins from The IDIBAPS, Hospital Clínic de Barcelona said, "Age-related macular degeneration (AMD) is the primary cause of irreversible vision loss among the ageing population worldwide."
AMD presents RPE cell abnormalities, disruption of the outer blood-retinal-barrier (oBRB), and degeneration of photoreceptors. Altered immune responses are thought to contribute to the dry AMD phenotype. Loss of parainflammation control contributes to AMD by invoking a chronic, heightened immune response that causes tissue destruction. mCRP has been identified in ocular drusen and other subepithelial deposits, as well as in the choroid, and contributes to oBRB disruption in vitro.
The "non-risk" Factor H (FH) variant can effectively bind to mCRP to dampen its proinflammatory activity. MCRP levels are elevated in individuals with the high-risk CFH genotype [29, 30] - this is because there is no CRP transcription in retinal tissue.
The Molins Research Team concluded in their https://www.aging-us.com/article/103655/ Aging-US Research Output, "our findings further support mCRP direct contribution to progression of AMD, at least at the RPE level. The topological experiments elicit that mCRP is proinflammatory when present on the apical side of the RPE. However, mCRP is likely to only reach the apical side of the RPE in compromised RPE health and where barrier functions are compromised. Thus, a plausible scenario would infer that, in the presence of an already aged/damaged RPE, mCRP reaches the apical side of the RPE to amplify the proinflammatory microenvironment and enhance barrier disruption. With respect to previous findings, this pathologic mechanism will be more prevalent in patients carrying the FH risk polymorphism for AMD, where mCRP proinflammatory effects remain unrestrained."
Full Text - https://www.aging-us.com/article/103655/text
Correspondence to: Blanca Molins email: bmolins@clinic.cat
Keywords: age-related macular degeneration, retinal pigment epithelium, inflammation, C-reactive protein
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
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Aging-US published a Special Collection on Eye Disease which included "Loss of macroH2A1 decreases mitochondrial metabolism and reduces the aggressiveness of uveal melanoma cells" which reported that uveal melanoma (UM) is the most common primary intraocular tumour in adults.
Most accurate prognostic factor of UM is classification by gene expression profiling. These authors recently showed a strong prognostic role of the expression levels of histone variant macroH2A1 in UM patients. Mitochondrial function was assayed through qPCR and HPLC analyses. Correlation between mitochondrial gene expression and cancer aggressiveness was studied using a bioinformatics approach.
Dr. Giovanni Li Volti and Dr. Manlio Vinciguerra said, "Uveal melanoma (UM) is the most common primary intraocular tumour in adults."
Metastasis is a frequent occurrence in uveal and cutaneous melanomas with a 5 years survival of 15%. By far the most common site of UM metastasis is the liver, reported in 87% of cases.
Epigenetic mechanisms controlling gene expression have long been known to have a role in cancer development. In UM these include DNA methylation at CpG islands leading to decrease expression of p16/INK4a tumour suppressor protein.
The Volti/Vinciguerra Research Team concluded in their Aging-US Research Output, "we suggest that strategies aiming at decreasing the expression of histone variant macroH2A1 [32], might effectively hamper the aggressiveness of UM cells, by inhibiting their mitochondrial phosphorylation. This could be a novel promising therapeutic strategy against UM [51]."
Full Text - https://www.aging-us.com/article/103241/text
Correspondence to: Giovanni Li Volti email: livolti@unict.it and Manlio Vinciguerra email: manlio.vinciguerra@fnusa.cz
Keywords: macroH2A1, histones, uveal melanoma, metabolism, epigenetics
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl
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Aging-US published a Special Collection on Eye Disease which included "Role of Citicoline in an in vitro AMD model" which reported that citicoline is the exogenous form of the nootropic, Cytidine 5'-diphosphate-choline that exerts its neuroprotective effects in the brain as well as in the eye.
Citicoline alleviates apoptotic effects as evidenced by diminished AnnexinV/PI and Caspase-3/7 staining, downregulation of apoptosis genes, enhanced cell viability, and reduced oxidative stress in AMD RPE cybrid cells. However, further studies are required to establish the merit of citrusoline as a cytoprotective molecule in AMD and to decipher the molecular underpinnings of its mechanism of action.
Dr. M. Cristina Kenney from The University of California Irvine said, "Citicoline is the international nonproprietary name given to the exogenous pharmacological form of Cytidine 5'-diphosphate-choline (CDP-Choline, CDPCho), a naturally occurring endogenous nucleotide compound that is water-soluble and has a molecular weight of 488.32 g/mol"
Citicoline maintains neuronal membrane integrity, influences neurotransmitter levels, increases norepinephrine and dopamine levels in the central nervous system, restores the activity of membrane sodium/potassium ATPase and mitochondrial ATPase, and enhances brain function.
Owing to these mechanisms, it has been successfully used as a neuroprotective agent to prevent neuronal aging and improve memory and learning in vitro. It has been extensively used in preclinical studies and clinical trials for neurodegenerative diseases including Parkinson's disease and glaucoma.
This in vitro study supports our hypothesis as Citicoline conferred significant protection against apoptotic cell death that was in-part mediated by damaged mtDNA from AMD patients.
The Kenney Research Team concluded in their Aging-US Research Output, "although further studies with Citicoline/ AMD RPE cybrid cells are underway, these results present novel findings that identify Citicoline to be a potential protector that attenuates apoptotic cell death in AMD. Citicoline is available as an over-the-counter dietary supplement in the U.S. and offers the advantage of easy access that shortens considerably the transition from lab bench to clinic."
Full Text - https://www.aging-us.com/article/103164/text
Correspondence to: M. Cristina Kenney email: mkenney@uci.edu
Keywords: Citicoline, age-related macular degeneration (AMD), neuroprotection, RPE, mitochondria
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
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Will you age quickly or slowly? Is it possible to predict how long you will live based on your genetics, lifestyle and other traits? In a new study, a team of researchers—from the National Institutes of Health’s National Institute on Aging, University of California San Diego, University of Michigan, Consiglio Nazionale delle Ricerche, Azienda Sanitaria di Firenze, and ViQi, Inc.—sought to answer these questions by developing a novel framework designed to estimate human physiological age and aging rate. Their trending paper was published by Aging (Aging-US) in October 2021, and entitled, “Predicting physiological aging rates from a range of quantitative traits using machine learning”.
“We present machine learning as a promising framework for measuring physiological age from broad-ranging physiological, cognitive, and molecular traits.”
Full blog - https://www.mishablagosklonny.com/2021/11/05/trending-with-impact-machine-learning-predicts-human-aging/
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DOI - https://doi.org/10.18632/aging.203660
Full Text - https://www.aging-us.com/article/203660/text
Correspondence to: Luigi Ferrucci email: ferruccilu@grc.nia.nih.gov, David Schlessinger email: schlessingerd@grc.nia.nih.gov, Ilya Goldberg email: ilya@viqi.org and Jun Ding email: jun.ding@nih.gov
Keywords: physiological aging rate, quantitative trait, machine learning, aging clock, mortality, personalized medicine
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
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Aging-US published a Special Collection on Eye Disease which included "Systemic administration of the di-apocarotenoid norbixin (BIO201) is neuroprotective, preserves photoreceptor function and inhibits A2E and lipofuscin accumulation in animal models of age-related macular degeneration and Stargardt disease" which reported that atrophic A\age-related macular degeneration and Stargardt disease are major blinding diseases affecting millions of patients worldwide - but no treatment is available.
Acute and chronic retinal degeneration following blue light damage in BALB/c mice and aging of Abca4-/- Rdh8-/- mice, respectively, reproduce features of AMD and STGD. Norbixin injected intraperitoneally in BALB/c mice, maintained scotopic and photopic electroretinogram amplitude and was neuroprotective.
Dr. Serge Camelo from The Sorbonne Université said, "Age-related macular degeneration (AMD) is the commonest cause of severe visual loss and blindness in developed countries among individuals aged 60 and older."
AMD is a major unmet medical need as it is estimated that more than 20 million patients will be affected by 2050 in the US alone. STGD is the most common hereditary macular dystrophy, mostly affecting young patients aged between 6 and 15 years old with a prevalence of 1/8,000-1/10,000.
It has an autosomal recessive mode of inheritance and may lead to registered blindness within the second or third decade of life. It is formed by the reaction of 2 all-trans retinal molecules with phosphatidylethanolamine generating N-retinylidene-PE, as a detoxication mechanism of retinal isomers including all-trans and 11-cis-retinal.
Under normal conditions the ABCA4 protein participates in the elimination of A2-PE from the photoreceptors and inhibition of this clearance increases the accumulation of A2E and all-trans-retinal dimer in the RPE. Recently, it has been shown that ABCA4 is also expressed in RPE cells where it would participate in the recycling of retinaldehyde released during proteolysis of rhodopsin in endolysosomes following phagocytosis of photoreceptor outer segments.
Indeed, it has been shown that as early as in 3-month-old Abca4-/- Rdh8-/- mice, the amplitudes of scotopic A and B waves and flicker ERG are reduced. Abca4-/- Rdh8-/- mice recapitulate most phenotypic retinal alterations observed during STGD and AMD, and represent a chronic model of these diseases.
Acute white-light exposure is known to induce apoptosis of photoreceptors in albino mice retinas.
The Camelo Research Team concluded in their Aging-US Research Output, "our present study demonstrates that systemic administration of norbixin in the acute BLD model of dry AMD is neuroprotective and partially preserves photoreceptor function. In addition, 6 months of oral supplementation with norbixin is effective in Abca4-/-Rdh8-/- mice. We show that chronic norbixin supplementation reduces the concentration of A2E in the eye, that norbixin is neuroprotective, and preserves visual function of Abca4-/-Rdh8-/- mice, modelling retinal degenerative conditions such as STGD and dry AMD. We believe that treatment using norbixin could potentially preserve “night” and “day” visual acuity in humans affected by dry AMD and STGD. It is essential for patient care to develop drugs that are effective on visual function following oral administration rather than by repeated local intraocular injections. These results demonstrated the effectiveness of the norbixin in a chronic and acute model of retinal degeneration and could offer a new therapeutic strategy, alone or in combination with gene therapies, for AMD and/or STGD patients. Thus, norbixin is a good drug candidate to treat patients and may provide a cure for these very debilitating diseases."
Full Text - https://www.aging-us.com/article/103014/text
Correspondence to: Serge Camelo email: serge.camelo@biophytis.com
Keywords: norbixin, retinal function, A2E, AMD, Stargardt disease
Aging-US published "Effects of estradiol on biological age measured using the glycan age index" which reported that glycan age is a recently developed biomarker based on glycans attached to immunoglobulin G.
In large population cohorts, glycan age associates well with lifestyle and disease-risk biomarkers, while some studies suggested that glycan changes precede development of several age-associated diseases. In this study the authors evaluated effects of estrogen on the glycan age. After the recovery period glycan age returned to baseline values in both groups.
These results suggest that IgG glycans and consequently also the glycan age are under strong influence of gonadal hormones and that estradiol therapy can prevent the increase of glycan age that occurs in the perimenopausal period.
Dr. Gordan Lauc from The Genos Glycoscience Research Laboratory as well as The University of Zagreb said, "The existence of inter-individual differences in the pace of biological aging is an intriguing concept that tries to explain why some people stay healthy until very late chronological age, while other people age faster and have a shorter life expectancy."
A number of biomarkers aimed at an objective estimation of biological age have been developed in the past several years, one of them being the glycan age, which is based on analyzing glycans attached to immunoglobulin G. A key feature of a good biomarker of biological age is that the difference between chronological and biological age should correlate with known biomarkers of an unhealthy lifestyle and that increased biological age should predict future disease development.
Glycans attached to IgG change significantly with age and have been suggested as a promising biomarker of biological age. Furthermore, since glycosylation affects interactions between IgG and different Fc receptors and other ligands, changes in glycosylation have direct effects on the function of the immune system, with multiple functional implications.
IgG glycans have been shown to be a reliable biomarker of aging that explains up to 64% of variation in chronological age. However, IgG glycans are not only biomarkers but also functional effectors that participate in the process of aging. This prevented the calculation of glycan age from the available data since glycan age is based on IgG glycans. Aiming to evaluate the effects of ovarian sex hormone suppression followed by estradiol supplementation on biological age measured by the glycan age these authors reanalysed samples from the same intervention study using state of the art glycoprofiling technology.
The Lauc Research Team concluded in their Aging-US Research Output that recently a modest improvement in epigenetic age was reported in a small group of individuals undertaking quite radical pharmacological intervention and glycan age was shown to slightly improve by exercise. However, all these changes were modest compared to the effects of the suppression of gonadal hormones, which more than doubled glycan age in some of the participants.
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DOI - https://doi.org/10.18632/aging.104060
Full Text - https://www.aging-us.com/article/104060/text
Correspondence to: Gordan Lauc email: glauc@pharma.hr
Keywords: biological age, glycan age, estrogen, aging biomarkers, glycosylation
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl
Aging-US published a Special Collection on Eye Disease which included "Immunological analyses reveal an immune subtype of uveal melanoma with a poor prognosis" which reported that uveal melanoma is an aggressive intraocular malignancy that often exhibits low immunogenicity.
Metastatic uveal Melanoma samples frequently exhibit monosomy 3 or BAP1 deficiency. In this study, the authors used bioinformatic methods to investigate the immune infiltration of uveal melanoma samples in public datasets.
The Kaplan-Meier method and log-rank test were used to assess the prognostic value of particular immune cells and genes in samples. These authors used CIBERSORT and ESTIMATE with RNA-seq data from The Cancer Genome Atlas and the GSE22138 microarray dataset to determine the sample-level immune subpopulations.
Dr. Zhaoyang Wang and Dr. Xianqun Fan said, "Immune heterogeneity within the tumor microenvironment has been linked to the drug sensitivity and prognosis of patients with various cancer types."
Profiling of immune signatures might uncover biomarkers for targeted therapy and clinical outcome assessment. Uveal melanoma (UM) is the most common aggressive intraocular malignancy in adults, and originates from the uveal tract.
Monosomy 3 tumors were found to be enriched for genes in immune pathways such as interferon signaling, T cell invasion and cytotoxicity. Mutation of GNA11/GNAQ was not found to significantly alter the immune infiltration and HLA Class I expression in UM patients. Characterizing the immunological features of UM may provide novel immune biomarkers for prognostic assessment and immunotherapy.
Enhancing the cytolytic functions of infiltrating lymphocytes can significantly improve antitumor immunity. However, due to the low levels of cytotoxic cells in the tumor microenvironment, non-responsiveness to immunotherapy remains a clinical challenge.
The Wang/Fan Research Team concluded in their Aging-US Research Output that gene expression profiling of UM patients treated with immune checkpoint blockers has advanced the application of genomic data to tumor immunology.
The authors hope that large sequencing data from UM patients undergoing immune checkpoint blocker treatment will emerge in the future. The immune features reported herein should be considered for integration into prognostic models or explored as predictors of adjuvant immune therapy responsiveness in patients with BAP1-deficient UM.
The Volti/Vinciguerra Research Team concluded in their Aging-US Research Output, "we suggest that strategies aiming at decreasing the expression of histone variant macroH2A1 [32], might effectively hamper the aggressiveness of UM cells, by inhibiting their mitochondrial phosphorylation. This could be a novel promising therapeutic strategy against UM [51]."
Full Text - https://www.aging-us.com/article/102693/text
Correspondence to: Zhaoyang Wang email: zhaokekewzy@hotmail.com and Xianqun Fan email: fanxq@sjtu.edu.cn
Keywords: immune subtype, uveal melanoma, bioinformatics, immune cell fractions, TCGA
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
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Iron is a mineral naturally found in the environment on Earth, within food sources and in all living organisms. A number of biochemical systems require this mineral and, in humans, the lack of iron results in anemia and a deficiency in hemoglobin—the protein responsible for supplying the body with oxygen. Anemia can also be caused by iron dysregulation. This occurs when iron damages the protein it should be safely stored in, such as ferritin, and then reacts in a toxic manner with surrounding cellular structures and organs. While iron is essential, the chemical properties of iron can make it a harmful substance if it is not tightly regulated.
“The very property of iron that makes it useful, its ability to accept or donate electrons, also gives it the ability to damage molecules and organelles via the Fenton reaction, in which iron reacts with hydrogen peroxide, leading to the formation of the highly reactive and toxic free radical, hydroxyl.”
Dennis Mangan (P. D. Mangan) is a clinical biochemist/microbiologist, researcher, author, health and fitness expert, and anti-aging specialist. In October of 2021, he authored a new theory article that positions iron as a potential driver of aging. This trending paper was published in Aging (Aging-US) Volume 13, Issue 19, and entitled, “Iron: an underrated factor in aging.”
Full blog - https://www.impactjournals.com/journals/blog/aging/trending-with-impact-is-iron-a-driver-of-aging/
Press Release - https://www.aging-us.com/news_room/iron-an-underrated-factor-in-aging
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DOI - https://doi.org/10.18632/aging.203612
Full Text - https://www.aging-us.com/article/203612/text
Correspondence to: Dennis Mangan email: pdmangan@outlook.com
Keywords: iron, aging, oxidative stress, calorie restriction, plasma dilution
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
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Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
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Aging-US published a Special Collection on Eye Disease which included "Pineal gland volume is associated with prevalent and incident isolated rapid eye movement sleep behavior disorder" which reported that pineal gland volume may be associated with the risk of isolated rapid eye movement (REM) sleep behavior disorder (RBD).
The authors enrolled 245 cognitively normal elderly individuals without major psychiatric or neurological disorders at the baseline evaluation and 2-year follow-up evaluation. The smaller the baseline pineal glands volume, the more severe the RBD symptoms at baseline. The individuals with isolated rBD showed smaller pineal gland volumes than those without isolated pRBD.
Dr. Ki Woong Kim from The Seoul National University College of Natural Sciences, The Seoul National University Bundang Hospital as well as The Seoul National University College of Medicine said, "Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia characterized by the loss of normal skeletal muscle atonia during REM sleep and dream-enacting behaviors."
RBD can occur in association with (secondary RBD), or without (isolated RBD) a neurodegenerative disorder such as Parkinson's disease or Lewy body disease. A series of clinical trials found that the symptoms of RBD were improved by N-acetyl-5-methoxytryptamine (melatonin).
In RBD patients, dream-enacting behaviors were reduced and REM sleep muscle atonia were restored by the administration of melatonin. Melatonin is a multifunctioning indoleamine produced by the pineal gland, which regulates sleep and circadian rhythm through its production and synthesis. VPG may predict the risk of developing RBD; they investigated the association of VPG with current RBD symptoms cross-sectionally and with the future risk prospectively in cognitively normal individuals without neurological or psychiatric disorders.
The Kim Research Team concluded in their Aging-US Research Output, "the smaller pineal gland was associated with the more current RBD symptoms and the higher future risk of RBD in cognitively normal elderly individuals, and VPP or VPG may be a candidate biomarker of RBD."
Full Text - https://www.aging-us.com/article/102661/text
Correspondence to: Ki Woong Kim email: kwkimmd@snu.ac.kr
Keywords: pineal gland, RBD, MRI, aging, prospective
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
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Aging-US published a Special Collection on Eye Disease which included "Age-related changes in eye lens biomechanics, morphology, refractive index and transparency" which reported that life-long eye lens function requires an appropriate gradient refractive index, biomechanical integrity and transparency.
The authors conducted an extensive study of wild-type mouse lenses 1-30 months of age to define common age-related changes. Biomechanical testing and morphometrics revealed an increase in lens volume and stiffness with age. Their results suggest similarities between murine and primate lenses and provide a baseline for future lens aging studies.
Dr. Velia M. Fowler and Dr. Catherine Cheng said, "The eye lens is required for fine focusing of light onto the retina to form a clear image, and the function of the lens is intimately tied to its shape, biomechanical properties, transparency and refractive index."
The eye lens is required for fine focusing of light onto the retina to form a clear image. It has long been known that age-related changes in these lens properties lead to two major lens pathologies, cataracts and presbyopia. Presbyopia is caused by a reduction in the lens' ability to change shape during focusing (accommodation), and, by extension, the need for reading glasses. Mice offer an opportunity to investigate changes in lens morphometrics, stiffness, transparency and refractive properties with age in a relatively shortened period of time. Little is known about the morphological, mechanical, refractive and cellular changes that occur with advanced age in the lens. The authors demonstrate that age-related changes in mouse lenses mimic some aspects of aging in human lenses.
The Fowler/Cheng Research Team concluded in their Aging-US Research Output, "the increases in lens size and nucleus size are correlated with increase stiffness with age. The addition of new fiber cells at the lens periphery becomes disordered with age, but this does not appear to impact lens biomechanical properties. Cataracts in aged lenses can be due to cell structural abnormalities, including incomplete suture closure, collapse of the lens epithelial cell layer into the suture gap and loss of epithelial-fiber cell attachments and compaction of the cortical lens fiber cells forming a circumferential light scattering ring. GRIN is present in the lens from 2 weeks of age and continues to increase until about 6 months of age, after which the maximum refractive index remains stable. The increase in the area of highest refractive index at the center of the lens is directly correlated with the increase in lens nucleus size, suggesting nuclear compaction drives the maximum GRIN. Whether there is a common molecular mechanism that drives changes in all the measured parameters remains unknown, but further biochemical and cell morphology studies will be needed to determine how subcellular aging affects the whole tissue. Thus, our study provides a baseline for future studies of lens aging by providing quantitative measurements of key parameters and identifying common age-related changes in the overall tissue and in individual cells"
Full Text - https://www.aging-us.com/article/102584/text
Correspondence to: Velia M. Fowler email: vfowler@udel.edu and Catherine Cheng email: ckcheng@iu.edu
Keywords: fiber cell, strain, epithelial cell, cataract, stiffness
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
Boiled or iced with water or milk, blended in smoothies, condensed into shots or even baked into pastries—humans are infatuated with green tea. Today, green tea is one of the most widely consumed beverages in the world. Molecules found in this plant, named catechins, are known to have numerous evidence-based health benefits, including weight loss and age delaying properties. However, the mechanism by which these effects take place have yet to be fully elucidated.
“The popularity of green tea makes it crucial to study its impact on health and aging.”
Researchers from Friedrich Schiller University Jena, Huazhong Agricultural University, ETH Zurich, and the Medical University of Graz investigated green tea catechins and their effects in roundworms, known as Caenorhabditis elegans (C. elegans), and isolated rodent mitochondria. Their trending paper was published in October of 2021 by Aging (Aging-US), and entitled, “Green tea catechins EGCG and ECG enhance the fitness and lifespan of Caenorhabditis elegans by complex I inhibition.”
“We have designed the current study to investigate the impact and to unveil the target of the most abundant green tea catechins, epigallocatechin gallate (EGCG) and epicatechin gallate (ECG).”
Full blog - https://www.impactjournals.com/journals/blog/aging/trending-with-impact-green-tea-enhances-fitness-and-lifespan-in-worms/
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DOI - https://doi.org/10.18632/aging.203597
Full text - https://www.aging-us.com/article/203597/text
Correspondence to: Corina T. Madreiter-Sokolowski email: corina.madreiter@medunigraz.at and Michael Ristow email: michael-ristow@ethz.ch
Keywords: aging, reactive oxygen species, mitochondria, polyphenols, C. elegans
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
Twitter - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ SoundCloud - https://soundcloud.com/aging-us YouTube - https://www.youtube.com/agingus LinkedIn - https://www.linkedin.com/company/aging
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM
Aging-US published a Special Collection on Eye Disease which included "Involvement of adiponectin in age-related increases in tear production in mice" which reported that the infiltration of lymphocytes into the lacrimal glands occurs with age, and age-related increases in tear production have also been observed in mice.
The mechanisms underlying this increase remain unclear, but these authors show that it is not dependent on body weight gain or systemic conditions, such as insulin resistance, using aged mice and high-fat diet-fed mice. Senescence-associated T (SA-T) cells accumulated in the laceral glands of aged mice, particularly females, and they may represent potential targets for treating dry eyes in humans.
Dr. Yosuke Shikama from The National Center for Geriatrics and Gerontology said, "Epidemiological studies have shown that the prevalence of dry eye increases every five years after the age of 50 years, with a higher prevalence being reported in women than in men."
Age and female sex have been identified as the greatest risk factors for dry eye, and this is supported by clinical findings of decreased tear production in women through the 6th decade of life. Metabolic disorders, such as diabetes, affect tear production and are associated with dry eye. Adiponectin is a 30-kDa multimeric protein that is mainly secreted by white adipose tissue, and has insulin-sensitizing and anti-atherogenic properties.
Adiponectin and adipoR2 mRNA expression levels significantly increased in the lacrimal glands of aged mice, but not in those of high-fat diet-fed mice. These results indicate that these molecules are involved in age-related increases in tear production in mice.
The Shikama Research Team concluded in their Aging-US Research Output, "the present results demonstrated the accumulation of SA-T cells in aged mice, which occurred to a greater extent in female than in male mice. Furthermore, increased tear secretion in aged mice appeared to be mediated by PPARγ and adiponectin-mediated signaling. These results may explain the discrepancy in the volume of tears secreted with age between humans and mice."
Full Text - https://www.aging-us.com/article/102322/text
Correspondence to: Yosuke Shikama email: shikama@ncgg.go.jp
Keywords: dry eye, adiponectin, peroxisome proliferator-activated receptor gamma, senescence-associated T cells, aging
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
Media Contact 18009220957x105 MEDIA@IMPACTJOURNALS.COM
Aging-US published a Special Collection on Eye Disease which included "PU-91 drug rescues human age-related macular degeneration RPE cells; implications for AMD therapeutics" which reported that the PU-91 drug upregulates PGC-1α which is a critical regulator of mitochondrial biogenesis.
Since mitochondrial dysfunction is implicated in the pathogenesis of AMD, this study is based on the premise that repurposing of PU 91 might rescue AMD RPE cells from AMD mitochondria-induced damage. The authors report significant improvement in cell survival, mitochondrial health, and antioxidant potential following treatment with PU 91.
Dr. M. Cristina Kenney from The University of California Irvine said, "The incidence of Age-related Macular Degeneration (AMD) is increasing at an alarming rate in elderly population in the United States."
The incidence of Age-related Macular Degeneration (AMD) is increasing at an alarming rate in elderly population in the United States. Most AMD cases occur among Caucasian Americans, followed by Hispanic and other populations. Despite intensive study, a limited number of FDA-approved treatment options are available for treatment of AMD.
National Eye Institute projection, the estimated number of AMD patients is expected to rise to 5.44 million by 2050. PU-91 is a pro-drug that when metabolized is PPARα ligand and which was developed for the treatment of dyslipidemia.
The drug is estimated to have seen >5 million-years of patient exposure and remains an effective agent for certain dyslipidemias. These findings demonstrated that PU-91 preserved AMD mitochondrial function and integrity, and protected AMD RPE cybrids against oxidative stress-induced and mtDNA-induced apoptotic cell death.
The Kenney Research Team concluded in their Aging-US Research Output, "PU-91 rescues AMD RPE cybrids, and potentially could be repurposed as an FDA-approved drug to prevent/treat AMD. Since it improves mitochondrial function and has already been FDA-approved, the candidate therapeutic PU-91 will be an excellent treatmentoption for AMD. Repositioning of PU-91 will be a smoother transition from lab bench to clinic since the pharmacological profiles of PU-91 have been examined already. Furthermore, because of its extensive safety record it could be potentially prosecuted through NDA more rapidly than a drug-like new chemical entity. Bringing a disease modifying therapeutic to market for the most prevalent form of blindness, AMD, has substantial potential benefit for our aging populations world-wide."
Full Text - https://www.aging-us.com/article/102179/text
Correspondence to: M. Cristina Kenney email: mkenney@uci.edu
Keywords: age-related macular degeneration (AMD), RPE, PGC-1α, RPE, mitochondria, FDA-approved drugs
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
Media Contact 18009220957x105 MEDIA@IMPACTJOURNALS.COM
Whether they are sprinters or distance runners, sled dogs are known for their competitive nature and athletic prowess. With age, however, these athletes eventually run out of steam—just as humans inevitably do. Canines of all breeds are effected by aging, including a loss of resilience, accumulation of molecular damage and age-related diseases. These relatively short-lived, large mammals are one of the few to share environments with humans, and even have access to advanced medical care. Many believe the canine aging process resembles human aging the closest compared to any other animal.
A team of scientists—from Cornell University, North Carolina State University, Tauber Bioinformatic Research Center, and Roswell Park Comprehensive Cancer Center—saw the opportunities and advantages of studying canine aging in a controlled environment. Co-founders Andrei Gudkov, PhD, Dr Sci, Katerina Andrianova, PhD, and Daria Fleyshman, PhD, established a non-profit organization called Vaika Inc. In 2018, Vaika allowed these researchers to begin collaborating in a longitudinal study on the mechanisms of aging among 103 retired sled dogs. The researchers authored a trending research perspective about the details of their long-term study. In September 2021, their paper was published on the cover of Aging (Aging-US)’s Volume 13, Issue 18, and entitled, “Development of infrastructure for a systemic multidisciplinary approach to study aging in retired sled dogs.”
Full blog - https://www.impactjournals.com/journals/blog/aging/trending-with-impact-retired-sled-dogs-in-aging-research/
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DOI - https://doi.org/10.18632/aging.203600
Full text - https://www.aging-us.com/article/203600/text
Correspondence to: Andrei V. Gudkov email: andrei.gudkov@roswellpark.org and Ekaterina L. Andrianova email: kandrianova@vaika.org
Keywords: canine, senescence, frailty, longevity, healthspan
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
Twitter - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ SoundCloud - https://soundcloud.com/aging-us YouTube - https://www.youtube.com/agingus LinkedIn - https://www.linkedin.com/company/aging
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM
Aging-US published a Special Collection on Eye Disease which included "Abnormalities of saccadic eye movements in dementia due to Alzheimer’s disease and mild cognitive impairment" which reported that there is increasing evidence that people in the early stages of Alzheimer’s disease have subtle impairments in cognitive inhibition that can be detected by using relatively simple eye-tracking paradigms, but these subtle impairments are often missed by traditional cognitive assessments.
People with mild cognitive impairment are at an increased likelihood of dementia due to AD.
Participants were 68 people with dementia due to AD, 42 had a diagnosis of aMCI, and 47 had a diagnosis of naMCI, and 92 age-matched cognitively healthy controls.
Dr. Thomas D.W. Wilcockson from The Loughborough University as well as The Lancaster University said, "Alzheimer's disease (AD) is a severe neurodegenerative disease of the human brain, for which there is as yet no cure."
When disease modifying therapy becomes available, it will be essential to administer this treatment in the very earliest stages of the disease, before pathological changes in the brain are widespread, rendering the treatment ineffective.
Thus, identifying the presence of AD in the pre-dementia ‘prodromal’ or even ‘preclinical’ phase is essential. Current biomarkers that are able to detect AD in the earliest stages are either invasive or expensive. A critical issue then is whether eye-movement impairments are detectable in people who are in a preclinical stage of AD and therefore at a greater risk of developing clinical dementia.
A strong correlation has been reported between antisaccade error rate with cortical thinning in a mild cognitive impairment group. However, this work did not distinguish between the different types of MCI, thus the low and high-risk of dementia participants were conflated in their study. People with a diagnosis of MCI are at an increased risk of developing dementia compared to cognitively healthy adults with 5-10% of MCI patients progressing to dementia annually.
Traditionally, the clinical syndrome of MCI was considered to be a relatively distinct stage of dementia since the cognitive deficits were not severe enough to impact significantly on the individual’s ability to conduct their activities of daily living.
The Wilcockson Research Team concluded in their Aging-US Research Output that inhibitory error rates in the antisaccade are sensitive to memory impairment, but may even precede it in a patient with dementia. The results obtained from this study demonstrate that eye movements during the AST could be used to automatically classify participants as being at a higher risk of AD. There are potentially a number of practical implications for this observation.
Full Text - https://www.aging-us.com/article/102118/text
Correspondence to: Thomas D.W. Wilcockson email: t.wilcockson@lboro.ac.uk
Keywords: mild cognitive impairment, Alzheimer’s disease, inhibitory control, eye tracking, anti-saccade
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
Media Contact 18009220957x105 MEDIA@IMPACTJOURNALS.COM
Aging-US published a Special Collection on Eye Disease which included "HMGB1 and Caveolin-1 related to RPE cell senescence in age-related macular degeneration" and reported that AMD is a major unmet medical need as it is estimated that more than 20 million patients will be affected by 2050 in the US alone.
STGD is the most common hereditary macular dystrophy, mostly affecting young patients aged between 6 and 15 years old with a prevalence of 1/8,000-1/10,000. It is formed by the reaction of 2 all-trans retinal molecules with phosphatidylethanolamine generating N-retinylidene-PE, as a detoxication mechanism of retinal isomers including all-trans and 11-cis-retinal. Indeed, it has been shown that as early as in 3-month-old Abca4-/- Rdh8-/- mice, the amplitudes of scotopic A and B waves and flicker ERG are reduced.
Dr. Jin Yang and Dr. Xiaorong Li both from The Tianjin Medical University Eye Hospital said, "Age-related macular degeneration (AMD) is the leading cause of vision loss in older adults worldwide."
AMD can be classified into early-stage or late-stage AMD. The latter is characterized by neovascularization, geographic atrophy, or both. Conversely, early-stage AMD is characterized by a limited amount of drusen, which is mainly caused by lipid and protein accumulation and thought to contribute to atrophic changes.
As the disease progresses, neovascular changes or geographic atrophy involving the macular area can be present in patients for years. Therefore, the authors explored the relationship between dry AMD and RPE dysfunction and senescence using proteomic mass spectrometry to examine differential expression in induced pluripotent stem cell-derived RPE cell lines with and without A2E treatment. They have previously demonstrated that the iPSC-derived RPE is phenotypically and functionally similar to the native RPE. In addition, the young status of iPSC-RPE may provide an excellent means for observing changes in protein expression during the process of RPE cell aging.
A2E photo-oxidation products can cause oxidative stress, membrane permeation, telomere dysfunction and accelerated RPE senescence. Although A2E is clearly present in the retina, there are rather different opinions regarding its distribution. Ablonczy et al. showed that levels of A2E decreased from the periphery to the centre region in aging tissue of macaques and humans but A2E was localized mainly in the centre region of young mouse retina.
The Yang/Li Research Team concluded in their Aging-US Research Output, "upregulation of HMGB1 and Caveolin-1 caused RPE cell senescence and suppressed migration and invasion, and β-catenin and Zo-1 accumulation was enhanced by A2E in RPE cells. In particular, the results showed a change in expression of HMGB1 and Caveolin-1, which suggests that they are prime gatekeepers in RPE cell senescence. The above results indicate that stabilizing expression of HMGB1 and Caveolin-1 is a potential therapeutic target to prevent the progression of RPE cell senescence."
Full Text - https://www.aging-us.com/article/102039/text
Correspondence to: Jin Yang email: yangjinchina324@gmail.com and Xiaorong Li email: lixiaorong@tmu.edu.cn
Keywords: A2E, HMGB1, Caveolin-1, RPE cell senescence, AMD
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
Media Contact 18009220957x105 MEDIA@IMPACTJOURNALS.COM
The root cause of Alzheimer’s disease (AD) is still unknown. For the past decades, the dominant paradigm many scientists have based their AD therapeutic solutions on has been the amyloid cascade hypothesis. The amyloid cascade hypothesis proposes that AD begins with the overproduction and accumulation of amyloid-β, followed by a number of other cascading symptoms. However, over 200 drug candidates based on this model have failed to prove clinical benefits in trial phases.
“The unsettlingly consistent failure of clinical trials led to questioning of the amyloid cascade hypothesis, stimulating a search for alternative AD paradigms [10–13].”
Researchers Alexei Kurakin and Dale E. Bredesen, from the University of California Los Angeles and the Buck Institute for Research on Aging, conducted detailed analyses of early-stage AD patient data and concluded their study by offering an alternative AD hypothesis. Their paper, published by Aging (Aging-US) in 2020, was entitled, “Alzheimer’s disease as a systems network disorder: chronic stress/dyshomeostasis, innate immunity, and genetics.”
“In this report, we outline an alternative perspective on AD as a systems network disorder and discuss biochemical and genetic evidence suggesting the central role of chronic tissue injury/dyshomeostasis, innate immune reactivity, and inflammation in the etiopathobiology of Alzheimer’s disease.”
Full blog - https://www.impactjournals.com/journals/blog/aging/trending-with-impact-alzheimers-disease-as-a-systems-network-disorder/
Press release - https://www.aging-us.com/news_room/alzheimers-disease-as-a-systems-network-disorder
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DOI - https://doi.org/10.18632/aging.103883
Full text - https://www.aging-us.com/article/103883/text
Correspondence to: Alexei Kurakin email: akurakin@mednet.ucla.edu and Dale E. Bredesen email: dbredesen@mednet.ucla.edu
Keywords: Alzheimer’s disease, neurodegeneration, complex chronic disorder, network biology, systems biology
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
Twitter - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ SoundCloud - https://soundcloud.com/aging-us YouTube - https://www.youtube.com/agingus LinkedIn - https://www.linkedin.com/company/aging
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
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Aging-US published a Special Collection on Eye Disease which included "Exploration of age-related mitochondrial dysfunction and the anti-aging effects of resveratrol in zebrafish retina" which reported that resveratrol was shown to not only increase mitochondrial quality and function, but also to suppress Akt/mTOR activity in zebrafish retinas.
These results support the notion that mitochondrial dysfunction and increased Akt/mTOR activity are major players in age-related retinal neuropathy in zebrafish, and demonstrate a trend towards mitochondrial fragmentation in the aging retina. Importantly, resveratrol promoted mitochondrial function, up-regulating Ampk/Sirt1/Pgc1, and down-regulated Akt/mTOR pathway activity in zebrafish retinas, suggesting that it may be able to prevent age-related oculopathy.
Dr. Xu Zhang from The Jiangxi Research Institute of Ophthalmology and Visual Science as well as The Jiangxi Provincial Collaborative Innovation Center for Cardiovascular said, "Aging is the biological process characterized by the accumulation of damage in structure and decline in function of cells and tissues over time, ultimately leading to organismal death."
The causes of aging are complex but include abnormal mitochondria, epigenetic alterations, increased reactive oxygen species, increased DNA methylation, and decreased telomere length. Recently, both dysfunctional mitochondria that overproduce ROS and abnormal mitochondrial dynamics have been recognized as crucial contributors to the aging process as well as age-related neuronal diseases and age-related oculopathies such as glaucoma, age-related macular degeneration, and cataracts.
Fusion can help relieve mtDNA damage by diluting mutant mtDNA with non-mutant mtDNA, whereas fission can allow for turnover of mutant mtDNA through mitophagy. On the other hand, mitochondrial fragmentation is associated with apoptosis and cell death rather than mitophagy and must be distinguished from fission.
Resveratrol, a plant natural product found in high levels in peanuts and grape skin, has well-established antioxidant, anti-inflammatory, anti-mutagenic, neuroprotective, and anti-aging effects in many species. Current evidence suggests that the anti-aging effects of resveratrol are related to its ability to modulate mitochondria. Resveratrol has been found to increase mitochondrial fusion/fission as well as promote Pink1 expression and autophagic activity.
The Zhang Research Team concluded in their Aging-US Research Output, "Maintaining mitochondrial health is crucial to prevent age-related neurodegenerative diseases, including oculopathy. We utilized the zebrafish retina as a model for age-related oculopathy and observed decreased mtDNA integrity, dysfunctional mitochondrial fission-fusion dynamics, decreased expression of antioxidant defense enzymes, and increased activity of the Akt/mTOR pathway in the aging retina. Consistent with its anti-aging effects in other species and model systems, resveratrol treatment helped alleviate most of the age-related changes observed in the zebrafish retina, suggesting its potential for the prevention of aging-induced oculopathy in other species including humans. This study indicates that further testing of resveratrol for oculopathy is warranted, and helps establish the zebrafish retina as a viable model of age-related oculopathy for further studies on the molecular mechanisms and for novel drug screening."
Full Text - https://www.aging-us.com/article/101966/text
Correspondence to: Xu Zhang email: xuzhang19@163.com
Keywords: aging zebrafish, retina, mitochondrial dysfunction, mitophagy, mTOR, resveratrol
Aging-US published a Special Collection on Eye Disease which included "Nutraceutical effects of Emblica officinalis in age-related macular degeneration" which reported that EO has been used extensively as a nutraceutical in several diseases since it is known to boost immunity and offers numerous health benefits such as antioxidant, anti-inflammatory, and anti-aging effects.
AMD RPE transmitochondrial cell lines were created by fusion of mitochondria DNA-deficient APRE-19 (Rho0) cells with platelets isolated from AMD patients. EO significantly improved live cell number and mitochondrial membrane potential, reduced apoptosis and oxidative stress, down-regulated VEGF, and up-regulated PGC-1α.
Dr. M. Cristina Kenney from The University of California Irvine said, "Emblicaofficinalis Gaetrn (Phyllanthus emblica), commonly known as Indian gooseberry or Amla, is an edible fruit which is borne on a deciduous tree of the same name."
All parts of the Emblicaofficinalis (EO) tree i.e, fruits, bark, leaves, seeds, flowers, and roots are known to have medicinal properties. EO is native to the tropical and subtropical regions of Southeast Asia including India, China, Malaysia, Bangladesh, Sri Lanka, and Mascarene Island. Phytochemically it is composed of several bioactive compounds such as flavonoids, phenolic compounds, tannins, amino acids, cellulose, gum, and albumin.
It is well-known as an immunity boosting food due to its high Vitamin C content which on an average is ~600 mg/100 g.
The Kenney Research Team concluded in their Aging-US Research Output, "treatment with purified EO extract preserves mitochondrial and cellular health and function in human AMD RPE cybrids, implying that EO mitigates aging-related damage in AMD. Since EO extract is an over-the-counter nutraceutical and is available in both liquid and capsule forms for easy consumption, it might serve as an effective, inexpensive, and non-invasive therapeutic option for treatment of AMD. Further studies are required to fully understand the precise mechanisms that orchestrate the protective events post EO treatment in AMD cells."
Full Text - https://www.aging-us.com/article/101820/text
Correspondence to: M. Cristina Kenney email: mkenney@uci.edu
Keywords: Emblica officinalis, Phyllanthus emblica, Indian gooseberry, Amla, nutraceutical, age-related macular degeneration, AMD
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
Media Contact 18009220957x105 MEDIA@IMPACTJOURNALS.COM
Aging-US published a Special Collection on Eye Disease which included "A comprehensive evaluation of 181 reported CHST6 variants in patients with macular corneal dystrophy" which reported that macular corneal dystrophy is an autosomal recessive disease featured by bilateral progressive stromal clouding and loss of vision, consequently necessitating corneal transplantation.
In this study, the authors integrated all the reported CHST6 variants described in 408 MCD cases, and performed a comprehensive evaluation to better illustrate the causality of these variants. In addition, the results underscored the strong correlation between mutant frequency and residue conservation in the general population, thus providing potential candidate targets for further genetic manipulation.
Dr. Jianjiang Xu from The Fudan University said, "Macular corneal dystrophy (MCD; OMIM 217800) is an autosomal recessive disease featured by bilateral progressive stromal clouding and loss of vision, finally necessitating corneal transplantation."
The CHST6 gene spans approximate 23 kb of the short arm of chromosome 16 and consists of 4 exons and a 1,187 bp open reading frame. The encoded protein CHST6 contains 395 amino acids with a molecular weight of 44 kDa. Variants in CHST6 gene have been recognized as the most critical genetic components in MCD. To date, more than 100 frameshift, nonsense, or missense variants in CHST6 were described in patients with MCD I/IA.
In MCD II patients, large rearrangements and deletions in the upstream of CHST6 were initially reported, followed by subsequent identification of mutations within the coding region of CHST6. However, substantial genetic heterogeneity still exists, and there is no study systematically evaluating CHST6 variants in MCD patients, in particular with regards to genotype-phenotype correlation and informing on the significance of specific variants. In the current study, the authors conducted a comprehensive evaluation of all 181 CHST6 variants described in MCD patients, and then classified the pathogenicity of those variants according to the American College of Medical Genetics and Genomics guidelines.
The Xu Research Team concluded in their Aging-US Research Output, "the current comprehensive evaluation contributed to the most updated in-silico classification of all reported CHST6 variants till now. Although the vast majority of CHST6 variants are likely to be protein damaging, systematic functional investigations are still in urgent need to demonstrate the pathogenicity of these variants."
Full Text - https://www.aging-us.com/article/101807/text
Correspondence to: Jianjiang Xu email: jianjiangxu@126.com
Keywords: CHST6, macular corneal dystrophy, genetic variants
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
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Aging-US published a Special Collection on Eye Disease which included "Effects of senescent secretory phenotype acquisition on human retinal pigment epithelial stem cells" which reported that loss of retinal pigment epithelium (RPE) cells occurs early in AMD, and their transplant has the potential to slow disease progression.
Age-related MSC changes involve loss of function and acquisition of a senescence-associated secretory phenotype (SASP). These changes can contribute to the maintenance of a chronic state of low-grade inflammation in tissues and organs.
Dr. Cesare Mariotti from The Università Politecnica delle Marche said, "Age-related macular degeneration (AMD) is an eye disorder affecting the elderly which can induce an irreversible loss of central visual function."
Age-related macular degeneration (AMD) is one of the most serious and debilitating forms of aging-related eye disease. Smoking, cataract surgery, high BMI and cardiovascular disease are risk factors for AMD, as well as a family history of AMD.
No effective treatment is available for neovascular AMD, while anti-VEGFD is the mainstay of treatment for dry AMD. Neovascular AMD and GA are characterized by RPE dysfunction; formation of large confluent drusen and hyperpigmentation seem to be the initial insult. AMD patients show a different phenotype as well as functional changes such as altered autophagy, mitochondrial dysfunction, and susceptibility to oxidative stress.
A greater understanding of the molecular pathways that are involved in the various stages of AMD would contribute to the development of innovative therapies.
The Mariotti Research Team concluded in their Aging-US Research Output that RPESCs can undergo replicative senescence, which affects their proliferation and differentiation ability. In addition, they acquired the SASP, which probably compounds the inflammatory RPE microenvironment during AMD development and progression. A greater understanding of the role of RPESCs in AMD pathogenesis is needed to find means to control the disease.
Full Text - https://www.aging-us.com/article/101624/text
Correspondence to: Cesare Mariotti email: mariottiocul@gmail.com
Keywords: AMD, RPESCs, age-related diseases, senescence, inflammation
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
Media Contact 18009220957x105 MEDIA@IMPACTJOURNALS.COM
Compounding evidence from experimental, epidemiological and clinical studies indicate that cerebral amyloid plaque formation, vascular dysfunction and reduced cerebral blood flow (CBF) all play important roles in the cognitive decline associated with aging and aging-related diseases. Recently, hyperbaric oxygen therapy (HBOT) was shown to improve cognitive performance in animal models of Alzheimer’s disease (AD) and in human patients. However, previous research has not directly shown how, or if, HBOT mitigates cerebrovascular dysfunction in AD.
“Therefore, we investigated the effects of HBOT on CBF and cognitive decline in the 5XFAD mouse model of AD that presents aggressive accumulation of amyloid load, cerebrovascular abnormalities and cognitive impairment, as well as in elderly individuals suffering from significant memory loss.”
Researchers from Tel Aviv University and Shamir (Assaf Harofeh) Medical Center conducted a new research study in an effort to better understand the underlying mechanisms of HBOT-mediated effects. They authored a trending research paper, published by Aging (Aging-US) in August 2021, entitled, “Hyperbaric oxygen therapy alleviates vascular dysfunction and amyloid burden in an Alzheimer’s disease mouse model and in elderly patients.”
Full blog - https://www.impactjournals.com/journals/blog/aging/trending-with-impact-new-hyperbaric-oxygen-hbot-study-breaks-ground/
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DOI - https://doi.org/10.18632/aging.203485
Full text - https://www.aging-us.com/article/203485/text
Correspondence to: Uri Ashery email: uria@tauex.tau.ac.il
Keywords: Alzheimer's disease, hyperbaric oxygen therapy, vascular dysfunction, cerebral blood flow, amyloid burden, aging
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
Twitter - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ SoundCloud - https://soundcloud.com/aging-us YouTube - https://www.youtube.com/agingus LinkedIn - https://www.linkedin.com/company/aging
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
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Aging-US published a Special Collection on Eye Disease which included "Long-term intake of Lactobacillus paracasei KW3110 prevents age-related chronic inflammation and retinal cell loss in physiologically aged mice" which reported that age-related chronic inflammation is a major risk factor for the incidence and prevalence of age-related diseases, including infectious and neurodegenerative diseases.
These authors previously reported that Lactobacillus paracasei KW3110 activated macrophages and suppressed inflammation in mice and humans. In this study, they investigated whether long-term intake of heat-killed L. paracases altered the gut microbiota in physiologically aged mice.
Compared with age-matched control mice, fecal analyses of gut microbiota revealed that intake of L.paracases KW 3110 mitigated age-related changes of beneficial bacterial composition, including the Bifidobacteriaceae family.
Dr. Mitsuo Maruyama and Dr. Yuji Morita said, "Aging involves a progressive decline of physiological functions in various organs, influenced by several factors, including genetic factors and environmental factors."
As the aged population grows, the therapeutic and preventive approaches to decelerate senescence are of great concern. The decline in immune function has been widely examined, because it results in chronic low grade inflammation. Age-related retinal neurodegenerative diseases, such as age-related macular degeneration, are major causes of blindness in the elderly. Disruption of gut microbiota composition has been also implicated in retinal diseases through a gut-retina axis.
The Maruyama/Morita Research Team concluded in their Aging-US Research Output, "the intake of L. paracasei KW3110 mitigated chronic inflammation in the intestine and retina, and reduced age-related retinal cell death. Further studies are needed to evaluate the effects in age-related senescent changes of the retina."
Full Text - https://www.aging-us.com/article/101583/text
Correspondence to: Mitsuo Maruyama email: michan@ncgg.go.jp and Yuji Morita email: Yuji_Morita@kirin.co.jp
Keywords: KW3110 Lactobacillus paracasei, age-related inflammation, proinflammatory cytokine, retina
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
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Aging-US published a Special Collection on Eye Disease which included "p62 /SQSTM1 coding plasmid prevents age related macular degeneration in a rat model" which reported that P62/SQSTM1, a multi-domain protein that regulates inflammation, apoptosis, and autophagy, has been linked to age-related pathologies.
In retinal pigment epithelium (RPE), p62DNA administration slowed down development of destructive alterations of RPE cells, including loss of regular hexagonal shape, hypertrophy, and multinucleation. In neuroretina, p 62DNA prevented gliosis, retinal thinning, and significantly inhibited microglia/macrophages migration to the outer retina. Taken together, these results suggest that the p62 DNA has a strong retinoprotective effect in AMD.
Dr. Alexander Shneider and Dr. Nataliya Kolosova said, "Age-related macular degeneration (AMD) is the most common cause of irreversible vision loss in industrialized countries."
AMD is a multifactorial disease involving a complex interplay of genetic, environmental, metabolic, and functional factors. There are effective treatments of vascular complications of AMD by anti-VEGF therapeutics.
Retinopathy that develops in OXYS rats even at a young age corresponds (in terms of clinical manifestations and morphological characteristics) to the dry atrophic form of AMD in humans.
The Shneider/Kolosova Research Team concluded in their Aging-US Research Output, "our data suggests that a p62-encoding plasmid might be a novel preventive and/or therapeutic agent for AMD as it maintained retinal thickness and restored RPE morphology."
Full Text - https://www.aging-us.com/article/101537/text
Correspondence to: Alexander Shneider email: ashneider@curelab.com and Nataliya Kolosova email: kolosova@bionet.nsc.ru
Keywords: p62/SQSTM1, age-related macular degeneration, inflammation, gliosis, OXYS rats, aging, retina
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
Media Contact 18009220957x105 MEDIA@IMPACTJOURNALS.COM
Sarcopenia is a common clinical condition that befalls the elderly—defined as a loss of skeletal muscle and muscle strength. Sarcopenic patients share clinical features with physical frailty (a subtype of the condition of frailty). Frailty is a broadly defined condition that typically encompasses multiple domains of aging, including cognitive impairment and decreased mobility and social activity. Sarcopenia and frailty are both deeply affected by aging, however, the underlying metabolic bases they stem from have remained unclear. How molecularly similar are sarcopenia and frailty? Are they spawned from the same cause?
“[…] little is known about the metabolic basis of sarcopenia, either shared with or discrete from frailty.”
In 2021, researchers from Kyoto University and Okinawa Institute of Science and Technology Graduate University collected blood samples from a cohort of elderly participants (from a previous study on frailty), and analyzed the samples in relation to sarcopenia. Their research paper was published as the cover of Aging (Aging-US) Volume 13, Issue 17, and entitled, “Reduced uremic metabolites are prominent feature of sarcopenia, distinct from antioxidative markers for frailty.”
Full blog - https://www.impactjournals.com/journals/blog/aging/trending-with-impact-metabolomics-discerns-sarcopenia-from-frailty/
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DOI - https://doi.org/10.18632/aging.203498
Full text - https://www.aging-us.com/article/203498/text
Correspondence to: Mitsuhiro Yanagida email: myanagid@gmail.com
Keywords: sarcopenia, muscle mass, metabolomics, frailty, uremic metabolites, aging
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
Twitter - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ SoundCloud - https://soundcloud.com/aging-us YouTube - https://www.youtube.com/agingus LinkedIn - https://www.linkedin.com/company/aging
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM
Aging-US published a Special Collection on Eye Disease which included "The expression of C1 inhibitor (C1INH) in macrophages is upregulated by retinal pigment epithelial cells – implication in subretinal immune privilege in the aging eye" which reported that this study aimed to understand how complement expression in macrophages is regulated by retinal pigment epithelium (RPE) RPE can modulate macrophage complement expression at the retina-choroidal interface even under aging or oxidative conditions.
During inflammation, they may promote the alternative pathway of complement activation through down-regulating CFH and CD59a and upregulating C3, CFB and C1INH. When BMDMs were treated with apoptotic RPE, the expression of C1qb, CFH, and CD 59a was reduced but increased in BMDM. TNF-α pre-treated RPE enhanced C1inH and CFB expression.
Dr. Heping Xu from The Queen’s University Belfast as well as The Central South University said, "The neuronal retina is segregated from the systemic immune system by the blood retina barriers (BRB) and is considered as an immune privileged tissue."
The immune suppressive microenvironment of the eye is critical for retinal immune privilege.
Despite the lack of systemic immune surveillance, the retina is well-protected by its own innate immune defence system, including innate immune cells and the complement system. During aging, the expression of complement proteins or fragments is increased in the retina, particularly at the retina-choroid interface. Subretinal macrophages in the healthy adult eyes (6 -12 months old) often have a small soma and long- fine-dendrites (Fig. 1A), whereas the cells in the aging eye (20 – 27 months) have a large cell body that often contains pigmented debris. This suggests that they are active phagocytizing debris released by stressed RPE cells.
The Xu Research Team concluded in their Aging-US Research Output, "we show that RPE cells can modulate macrophage complement expression. Under normal aging conditions, RPE cells may convert macrophages into a phenotype that can suppress complement activation with enhanced phagocytosis. This immune regulatory function of RPE cells on macrophages may be lost under inflammatory conditions. Instead, inflammatory or apoptotic RPE cells promote macrophages to produce complement components necessary for the AP activation. RPE cells together with subretinal macrophages critically control complement activation at the retina-choroid interface in the ageing eye."
Full Text - https://www.aging-us.com/article/101474/text
Correspondence to: Heping Xu email: heping.xu@qub.ac.uk
Keywords: macrophages, retinal pigment epithelial cells, complement, aging, subretinal immune privilege
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
Media Contact 18009220957x105 MEDIA@IMPACTJOURNALS.COM
Aging-US recently published "Alzheimer’s disease as a systems network disorder: chronic stress/dyshomeostasis, innate immunity, and genetics" which reported that ineffective results of clinical trials of over 200 anti-Alzheimer's drug candidates, with a 99.6% attrition rate, suggest that the current paradigm of Alzheimer's disease may be incomplete, necessitating exploration of alternative and complementary frameworks.
Results of this analysis suggest that Alzheimer’s may not be a brain disease but a progressive system-level network disorder, which is driven by chronic network stress and dyshomeostasis.
The latter can be caused by various endogenous and exogenous factors, such as chronic inflammatory conditions, infections, vascular dysfunction, head trauma, environmental toxicity, and immune disorders.
Whether originating in the brain or on the periphery, chronic stress, toxicity, and inflammation are communicated to the central nervous system via humoral and neural routes, preferentially targeting high-centrality regulatory nodes and circuits of the nervous system, and eventually manifesting as a neurodegenerative CNS disease.
In this report, the Aging-US authors outline an alternative perspective on AD as a systems network disorder and discuss biochemical and genetic evidence suggesting the central role of chronic tissue injury/dyshomeostasis, innate immune reactivity, and inflammation in the etiopathobiology of Alzheimer’s disease.
Dr. Alexei Kurakinn and Dr. Dale E. Bredesen said, "Alzheimer’s disease has become a global epidemic, rapidly advancing in the last decade to become the 5th leading cause of death globally and the 3rd leading cause of death in high-income countries."
In brief, a multimodal clinical profile of a patient is used by a human expert to generate a representative set of terms that characterize the disease configuration of the patient.
The generated set serves as a query to search research literature and databases for information blocks with highest densities of query terms. Selected and rank-ordered blocks of information are analyzed by an expert to identify a parsimonious set of concepts that interconnect cliques of search terms. The identified concepts are then used as new or additional query terms in the next iteration to identify higher level connectors, until all search terms become assimilated within a parsimoniously interconnected network.
Analysis of the generated disease network by a human expert allows for formulation of de novo hypotheses.
Although searches are non-exhaustive and hypothesis generation is inevitably biased by idiosyncratic expertise and choices of human expert, the relative worth of a generated hypothesis is measured in terms of its practical utility by testing hypothesis’ predictions empirically and/or in silico.
The implications of the proposed systemic nature of Alzheimer’s disease for treatment and prevention of cognitive decline are briefly discussed.
The Kurakinn/Bredesen Research Team concluded in their Aging-US Research Paper that the promising results of an integrative, systemic, precision medicine approach to treating Alzheimer’s disease suggests that evaluating and addressing the individual organism as a whole rather than focusing exclusively on an apparently failing part may represent a promising strategy to approach other complex chronic multifactorial disorders, which warrants further exploration and development.
Full Text - https://doi.org/10.18632/aging.103883
Correspondence to: Alexei Kurakin email: akurakin@mednet.ucla.edu and Dale E. Bredesen email: dbredesen@mednet.ucla.edu
Keywords: Alzheimer’s disease, neurodegeneration, complex chronic disorder, network biology, systems biology
Aging-US recently published "Alzheimer’s disease as a systems network disorder: chronic stress/dyshomeostasis, innate immunity, and genetics" which reported that ineffective results of clinical trials of over 200 anti-Alzheimer's drug candidates, with a 99.6% attrition rate, suggest that the current paradigm of Alzheimer's disease may be incomplete, necessitating exploration of alternative and complementary frameworks.
Results of this analysis suggest that Alzheimer’s may not be a brain disease but a progressive system-level network disorder, which is driven by chronic network stress and dyshomeostasis.
The latter can be caused by various endogenous and exogenous factors, such as chronic inflammatory conditions, infections, vascular dysfunction, head trauma, environmental toxicity, and immune disorders.
Whether originating in the brain or on the periphery, chronic stress, toxicity, and inflammation are communicated to the central nervous system via humoral and neural routes, preferentially targeting high-centrality regulatory nodes and circuits of the nervous system, and eventually manifesting as a neurodegenerative CNS disease.
In this report, the Aging-US authors outline an alternative perspective on AD as a systems network disorder and discuss biochemical and genetic evidence suggesting the central role of chronic tissue injury/dyshomeostasis, innate immune reactivity, and inflammation in the etiopathobiology of Alzheimer’s disease.
Dr. Alexei Kurakinn and Dr. Dale E. Bredesen said, "Alzheimer’s disease has become a global epidemic, rapidly advancing in the last decade to become the 5th leading cause of death globally and the 3rd leading cause of death in high-income countries."
In brief, a multimodal clinical profile of a patient is used by a human expert to generate a representative set of terms that characterize the disease configuration of the patient.
The generated set serves as a query to search research literature and databases for information blocks with highest densities of query terms. Selected and rank-ordered blocks of information are analyzed by an expert to identify a parsimonious set of concepts that interconnect cliques of search terms. The identified concepts are then used as new or additional query terms in the next iteration to identify higher level connectors, until all search terms become assimilated within a parsimoniously interconnected network.
Analysis of the generated disease network by a human expert allows for formulation of de novo hypotheses.
Although searches are non-exhaustive and hypothesis generation is inevitably biased by idiosyncratic expertise and choices of human expert, the relative worth of a generated hypothesis is measured in terms of its practical utility by testing hypothesis’ predictions empirically and/or in silico.
The implications of the proposed systemic nature of Alzheimer’s disease for treatment and prevention of cognitive decline are briefly discussed.
The Kurakinn/Bredesen Research Team concluded in their Aging-US Research Paper that the promising results of an integrative, systemic, precision medicine approach to treating Alzheimer’s disease suggests that evaluating and addressing the individual organism as a whole rather than focusing exclusively on an apparently failing part may represent a promising strategy to approach other complex chronic multifactorial disorders, which warrants further exploration and development.
Full Text - https://doi.org/10.18632/aging.103883
Correspondence to: Alexei Kurakin email: akurakin@mednet.ucla.edu and Dale E. Bredesen email: dbredesen@mednet.ucla.edu
Keywords: Alzheimer’s disease, neurodegeneration, complex chronic disorder, network biology, systems biology
Aging-US published a Special Collection on Eye Disease which included "Loss of NAMPT in aging retinal pigment epithelium reduces NAD+ availability and promotes cellular senescence" which reported that retinal pigment epithelium performs numerous functions critical to retinal health and visual function.
Here, the authors evaluated the temporal expression of key nicotinamide adenine dinucleotide -biosynthetic genes and associated levels of NAD+, a principal regulator of energy metabolism and cellular fate, in mouse RPE.
They simulated in vitro the age-dependent decline in NAD+ and the related increase in RPE senescence in human and mouse primary RPE using the NAMPT inhibitor FK866 and demonstrated the positive impact of NAD+-enhancing therapies on RPE cell viability. This was confirmed in vivo in the RPE of mice injected sub-retinally with FK866 in the presence or absence of nicotinamide mononucleotide.
Dr. Pamela M. Martin and Dr. Ravirajsinh N. Jadeja said, "The retinal pigment epithelium (RPE) performs numerous functions essential to normal retinal health and function."
RPE serves as a physiologic barrier between the photoreceptor cells and the choroidal blood supply and in doing so, plays an essential role in protecting the retina from systemic insults by regulating immune responses and thereby limiting the entry of infectious or otherwise detrimental agents into retina.
This is the premise of a number of recent studies including the present investigation in which we focused on nicotinamide adenine dinucleotide and factors governing its bioavailability in relation to the overall impact on RPE viability. NAD+, a central metabolic cofactor, plays a critical role in regulating cellular metabolism and energy homeostasis. The ratio of NAD+ to NADH regulates the activity of various enzymes essential to metabolic pathways including glycolysis, the Kreb’s cycle, and fatty acid oxidation.
There is a wealth of clinical and experimental data stemming from studies of other primary diseases of aging demonstrating clearly a generalized decline in the availability of NAD+ in association with increased age and the related reduction in the activity of a number of downstream metabolic pathways that contribute to the development and progression of degenerative processes.
Members of the sirtuin family, poly ADP-ribose polymerases and the efficacy of therapies capable of impacting them have been evaluated in the context of aging retina and RPE. However, little attention has been given to upstream factors that regulate NAD+ biosynthesis, particularly in RPE. Given the importance of RPE to retinal health and function, in the present investigation we focused on evaluating the impact of NAD+ and factors that regulate its availability on RPE viability both in vivo and in vitro.
This finding is highly relevant to the clinical management of AMD but perhaps also broadly to the management of other degenerative retinal diseases in which RPE is prominently affected.
The Martin/Jadeja Research Team concluded in their Aging-US Research Output that these present data demonstrating an age-dependent decline in NAMPT expression and in turn, NAD+ generation in RPE which ultimately promotes RPE senescence supports strongly the rationale for enhancing NAMPT expression and associated NAD+ generation therapeutically.
Based upon the present experimental observations, future preclinical studies evaluating NMN or other therapies that have a direct impact on NAMPT expression and NAD+ metabolism in the context of aging and age-related retinal disease development and progression are highly warranted.
Full Text - https://www.aging-us.com/article/101469/text
Correspondence to: Pamela M. Martin email: pmmartin@augusta.edu and Ravirajsinh N. Jadeja email: rjadeja@augusta.edu
Keywords: retinal pigment epithelium (RPE), aging, age-related macular degeneration, NAD+, NAMPT, senescence, SIRT1
The immune system is a vast and intricate network. Seven percent of the entire human genome is composed of immune-specific genes. This complex system has important functional and maintenance roles that involve clearing out foreign pathogens and sweeping away dead or dysfunctional cells. As do most human systems, the immune system experiences degradation with age. This degradation in aging populations results in inadequate immune responses to invading pathogens, self-antigens, undesirable and malfunctioning cells, and even to vaccines.
“Furthermore, the aged immune system elicits an inadequate response to vaccines, leaving the elderly susceptible to pathogens despite being vaccinated against them. This is especially poignant in the wake of an ongoing pandemic where the mortality rate is disproportionately high in the elderly.”
Researchers from the University of Florida authored a well-written review article (with exceptionally vivid figures and illustrations) exploring a potential cause of the aging immune system. They believe therapies that could target this cause may stave off age-related diseases and improve our quality of life as we age. The paper was published by Aging (Aging-US) in 2021, and entitled, “Cellular senescence in lymphoid organs and immunosenescence.”
Full blog - https://www.impactjournals.com/journals/blog/aging/%e2%80%8b%e2%80%8bimmunosenescence-and-the-aging-immune-system/
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DOI - https://doi.org/10.18632/aging.203405
Full text - https://www.aging-us.com/article/203405/text
Correspondence to: Daohong Zhou email: zhoudaohong@cop.ufl.edu
Keywords: cellular senescence, immunosenescence, immune senescence, senescence associated secretory phenotype (SASP), thymus
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
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At present (September 2021), the direct targets of COVID-19 have been evidently clear. COVID-19 is causing the greatest threat to those of advanced age and with comorbidities. Despite this fact, there may be additional information gleaned from the accumulating stacks of clinical COVID-19 cases being aggregated around the world. A closer look at this data in sum may help researchers learn new insights about this fast spreading and quickly mutating virus. Moreover, learning about COVID-19 and its patterns may help scientists formulate better treatments and more effective vaccines.
Researchers—from Buckingham Browne and Nichols School, Brigham and Women’s Hospital, Harvard Medical School, and Biotein—conducted a new study in an effort to decipher clinical COVID-19 data from multiple countries. Their aim was to learn additional information about the impact of COVID-19 across all age distributions, including childhood. The team wrote a trending research paper that was published by Aging (Aging-US) in August 2021, and entitled, “COVID-19 mortality rate in children is U-shaped.”
Of note, one of the four authors of this research paper is the first author (and prolific teenager) named Nina Khera. This young woman (merely 15 years old) is a student and longevity researcher that is interested in preventing age-related diseases, including those related to brain aging and COVID-19. Khera is also the co-founder of a Canadian biotech company called Biotein.
Full blog - https://www.impactjournals.com/journals/blog/aging/trending-with-impact-data-shows-unique-covid-19-patterns-in-childhood/
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DOI - https://doi.org/10.18632/aging.203442
Full text - https://www.aging-us.com/article/203442/text
Correspondence to: Vadim N. Gladyshev email: vgladyshev@rics.bwh.harvard.edu
Keywords: mortality, COVID-19, SARS-CoV-2, pediatrics, aging
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
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In 2016, researchers—from the University of California, Buck Institute for Research on Aging, Pacific Medical Center, and Brainreader—followed up on the anecdotal results from the 10 patients in this study. They provided objective results from quantitative magnetic resonance imaging (MRI) and neuropsychological testing. The researchers authored another paper on results of the MEND protocol, which was published by Aging and entitled, “Reversal of cognitive decline in Alzheimer’s disease.” To date, this paper has generated an Altmetric Attention score of 263.
“In each of these cases, obvious subjective improvement, noted by the patient, his/her significant other, and his/her co-workers, was accompanied by clear, quantitated, objective improvement.”
The MEND protocol, also known as the Bredesen Protocol (named after the creator of the protocol, Dr. Dale Bredesen), consists of a multifaceted, tailored approach to treating each AD patient for their individual symptoms of cognitive decline—and not only a few symptoms. This strategy uses a combination of diet, lifestyle, and therapeutic interventions. Treatment is based on the hypothesis that AD occurs due to an imbalance in an extensive plasticity network in the brain. The authors note that the MEND protocol is an iterative process and designed to improve with continued patient visits.
“The therapeutic system described in this report derives from basic studies of the role of APP signaling and proteolysis in plasticity, and the imbalance in this receptor proteolysis that reproducibly occurs in Alzheimer’s disease.”
Upon clinical assessment and lab testing, patient physical and cognitive health was evaluated. Based on this assessment, patients were prescribed a lengthy personalized therapeutic system. Among other objectives, the MEND protocol recommends treating diabetes; improving sleep and digestive health; reducing stress, inflammation, and blood sugar; increasing physical exercise, intellectual stimulation, antioxidants, and vitamins; and optimizing hormone balance, synthesis of acetylcholine, nerve growth factors, and mitochondrial function.
“In each of these cases, obvious subjective improvement, noted by the patient, his/her significant other, and his/her co-workers, was accompanied by clear, quantitated, objective improvement.”
Full blog - https://www.impactjournals.com/journals/blog/aging/reversing-alzheimers-disease-symptoms/
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DOI - https://doi.org/10.18632/aging.100981
Full text - https://www.aging-us.com/article/100981/text
Correspondence to: Dale E. Bredesen, MD email: dbredesen@buckinstitute.org
Keywords: neurodegeneration, cognition, biomarkers, dementia, neuropsychology, imaging, Alzheimer's disease, Apolipoprotein E
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
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Aging-US published "Beneficial effects of dietary supplementation with green tea catechins and cocoa flavanols on aging-related regressive changes in the mouse neuromuscular system" which reported that green tea extract (GTE) and cocoa-supplemented diets significantly improved survival rate of mice. GTE increased density of VAChT and VGluT2 afferent synapses on neuromuscular junctions.
Cocoa, but not GTE, reduced aging-associated microgliosis and increased the proportion of neuroprotective microglial phenotypes.
Dr. Jordi Calderó from IRBLleida said, "Sarcopenia, the progressive loss of skeletal muscle mass and function with age, is considered the main causative factor of the physical performance decline in the elderly."
Sarcopenia, the progressive loss of skeletal muscle mass and function with age, is considered the main causative factor of the physical performance decline in the elderly. The compromised muscular function associated to sarcopenia has a negative impact on the life quality of older adults and increases the risk for disability, fall-associated injuries, morbidity, and mortality. The authors have recently reported a marked increase in the microglial and astroglial pro-inflammatory phenotypes (M1 and A1, respectively) in the spinal cord of aged mice. This may be due to the presence of anti-inflammatory and neuroprotective (M2 and A2) glial subpopulations. Caloric restriction, based on a diet low in calories, has been shown to attenuate aging sarcopenia in various species by acting at different levels of the skeletal muscle.
Caloric restriction has also been reported to ameliorate age-related changes in rodent NMJs and to prevent MN and motor axon degeneration found to occur with aging [11, 21]. In a similar way, some dietary supplements have been shown to counteract age related changes that contribute to neuromuscular dysfunction (reviewed by [12) Plant flavonoids have gained particular attention as dietary compounds for keeping good health and preventing a number of diseases, particularly cardiac disorders and cancer.
The Calderó Research Team concluded in their Aging-US Research Output that, green tea and cocoa flavonoids from GTE and cocoa significantly increased survival rate of aged mice. Both diets preserved NMJ innervation and maturity, delayed the senescence process of the skeletal muscle, and enhanced its regenerative capacity. Future research is needed to investigate whether higher doses of flavonoid are needed and/or longer-term interventions can help restore proper motor function.
DOI - https://doi.org/10.18632/aging.203336
Full Text - https://www.aging-us.com/article/203336/text
Correspondence to: Jordi Calderó email: jordi.caldero@udl.cat
Keywords: sarcopenia, green tea, neuromuscular system, neural stem cells, aging, cocoa
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
Media Contact 18009220957x105 MEDIA@IMPACTJOURNALS.COM
Aging-US published "A model of the aged lung epithelium in idiopathic pulmonary fibrosis" which reported that Iiopathic pulmonary fibrosis (IPF) is an age-related disorder that carries a universally poor prognosis. By exposing mouse alveolar epithelial cells to repeated, low doses of bleomycin, instead of usual one-time exposures, the authors uncovered changes strikingly similar to those in the IPF lung epithelium.
They propose that this simple yet powerful tool could help uncover new biological mechanisms and assist in developing new pharmacological tools to treat the disease.
Dr. Ross Summer from The Jane and Leonard Korman Respiratory Institute as well as Dr. Freddy Romero from The Baylor College of Medicine said, "Idiopathic pulmonary fibrosis (IPF) represents one of the most aggressive and irreversible lung diseases, has an unknown etiology, and limited therapeutic options."
IPF arises from low-grade insults to the alveolar epithelium, which exhaust stem cell capacity and activate pathways that result in progressive tissue remodeling. Age represents the most significant risk factor for the development of IPF. Senescent cells are believed to drive immune cell and fibroblast activation via their production of secretory proteins (SASP), such as IL-6, TNF-β and TGF-β. Emerging evidence indicates that experimentally-induced pulmonary fibrosis can be ameliorated by targeting senescent cells for destruction [15]. This suggests a role for senolytic therapies in the treatment of IPf.
The Summer/Romero Research Team concluded in their Aging-US Research Output, "we describe a novel model of the IPF lung epithelium that displays many characteristics of the dysfunctional IPF alveolar epithelium. Given its low cost and ease of implementation, we believe our model is ideally suited for uncovering the molecular underpinnings driving mitochondrial dysfunction, cellular senescence and loss of proteostasis in IPF. Further, we believe our model is also ideally suited for high throughput testing of novel pharmacological compounds directed at the alveolar epithelium. This includes drugs aimed at eliminating dysfunction epithelial cells, such as senolytic medications and agents that aim to restore health to the IPF alveolar epithelium"
DOI - https://doi.org/10.18632/aging.203291
Full Text - https://www.aging-us.com/article/203291/text
Correspondence to: Ross Summer email: Ross.Summer@Jefferson.edu and Freddy Romero email: Freddy.RomeroVasquez@bcm.edu
Keywords: aging, IPF, mitochondria, proteostasis, epithelial cells
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
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BUFFALO, NY-August 20, 2021 – Aging is indexed by Web of Science: Science Citation Index Expanded (abbreviated as Aging‑US). In June 2021, Web of Science (Clarivate Analytics) released their 2020 JCR Impact Factor. Aging is pleased to report that our 2020 impact factor is 5.682. This number has increased from last year’s 4.831. Without self-citation, Aging’s 2020 impact factor is 5.279.
Aging is listed in the Web of Science: Science Citation Index Expanded in two categories: Cell Biology and Geriatrics & Gerontology. According to the Journal Citation Indicator (JCI), Aging is ranked in the Q1 quartile in both categories.
Since 2009, Aging has published research papers in all fields of aging research including, but not limited to, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan.
This journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, and prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.
To learn more about Aging, publication standards, and past or current issues, visit www.aging-us.com.
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About Impact Journals:
Impact Journals is an open-access publisher of research journals in biomedical sciences. Our publications focus on topics surrounding cancer research and all fields of aging research. Our mission is to provide scientists with the opportunity to share their exceptional discoveries, offer services that enable rapid dissemination of results, and to present vital findings from the many fields of biomedical science.
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Researchers from Virginia Commonwealth University, Translational Genomics Research Institute, and the Banner Alzheimer’s Institute took part in a research study experimenting with combinations of therapeutic agents which they believe may improve neurodegenerative disorders. In 2021, their paper was published in Aging’s Volume 13, Issue 13, and entitled, “Inhibition of heat shock proteins increases autophagosome formation, and reduces the expression of APP, Tau, SOD1 G93A and TDP-43.”
“In this paper we examined using isogenic colon cancer cells [with] several existing drugs that function by increasing autophagy and degrading misfolded proteins.”
“Aberrant expression of chaperone proteins is found in many human pathologies including cancer, in virology and in AD, ALS and HC.”
In this study, researchers tested drugs that have been used preclinically and clinically in several anticancer studies. The drugs used were: AR12, an antiviral chaperone ATPase inhibitor; Neratinib, a tyrosine kinase inhibitor; a combination of AR12 and Neratinib; Fingolimod, an immunosuppressive sphingosine l-phosphate receptor modulator; MMF, monomethyl fumarate; and a combination of Fingolimod and MMF.
The cells they tested these drug combinations on in vitro included Vero cells (African Green Monkey kidney cells), isogenic HCT116 colon cancer cells (genetically manipulated colon cancer cells), and GBM6 cells (glioblastoma cancer stem cells). They also used plasmids, antibodies, and siRNAs. Researchers acknowledged that the use of non-neuronal cells may be a limitation of this study.
“Our present studies were performed in non-neuronal cells and as a caveat, it is possible that our data in HCT116 and Vero cells will not be reflective of the same processes in neuronal cells.”
Despite this caveat, results from their research were promising. Some combinations of these drugs were capable of knocking down many disease specific proteins that form toxic aggregates inside cells and in extracellular environments via autophagy.
Full blog - https://www.impactjournals.com/journals/blog/aging/trending-with-impact-new-drug-combinations-inhibit-stress-proteins/
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DOI - https://doi.org/10.18632/aging.203297
Full text - https://www.aging-us.com/article/203297/text
Correspondence to: Paul Dent email: paul.dent@vcuhealth.org
Keywords: Alzheimer's, chaperone, GRP78, autophagy, neratinib
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
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Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
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Aging-US published "MiR-513b-5p represses autophagy during the malignant progression of hepatocellular carcinoma by targeting PIK3R3" which reported MiR-513b-5p repressed liver cancer cell proliferation, migration/invasion, and induced apoptosis in vitro.
Crucially, miR-513b-5p attenuated tumor growth of liver cancer cells in vivo.
In the mechanical investigation, the authors identified that PIK3R3 mRNA 3′UTR was targeted by miR-513b-5p and miR-513b-5p suppressed PIK3R3 expression.
PIK3R3 overexpression partly reversed miR-513b-5p-mediated autophagy, proliferation, and apoptosis of liver cancer cells.
Consequently, they concluded in their Aging-US Research Output that miR-513b-5p repressed autophagy during the malignant progression of HCC by targeting PIK3R3. MiR-513b-5p may be applied as a therapeutic target for HCC.
Dr. Rongjun Nie from The Guangxi Medical University said, "Liver cancer is a prevalent malignancy and the principal reason for tumor mortality globally, in which hepatocellular carcinoma (HCC) depicts 70–85% of the entire liver carcinoma weight."
As the previous studies, autophagy is a crucial process during liver cancer development and a potential therapeutic target for liver cancer therapy, but the mechanisms are poorly understood.
PIK3R3 acts as an oncogene of various cancers, containing glioma, lung cancer, and gastric cancer.
As several miRNAs are involved in the modulation of autophagy in HCC and based on the crucial role of miR-513b-5p in cancer development, the authors selected miR-513b-5p as an example to evaluate its function in autophagy during liver cancer progression.
In the present study, they were interested in the miR-513b-5p function in the modulation of autophagy during liver cancer progression.
They demonstrated that miR-513b-5p attenuated autophagy during the malignant progression of liver cancer by targeting PIK3R3.
The Nie Research Team concluded in their study, "miR-513b-5p repressed autophagy during the malignant progression of HCC by targeting PIK3R3. MiR-513b-5p may be applied as a therapeutic target for HCC."
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DOI - https://doi.org/10.18632/aging.203135
Full Text - https://www.aging-us.com/article/203135/text
Correspondence to: Rongjun Nie email: nrj2001@163.com
Keywords: hepatocellular carcinoma, autophagy, progression, miR-513b-5p, PIK3R3
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
Media Contact 18009220957x105 MEDIA@IMPACTJOURNALS.COM
Aging-US published "Identification of RNA binding protein interacting with circular RNA and hub candidate network for hepatocellular carcinoma" which reported that 17 DERBPs, which were commonly dysregulated in HCC from The Clinical Proteomic Tumor Analysis Consortium, The Cancer Genome Atlas and International Cancer Genome Consortium projects, were utilized to construct the RBP-circRNA network.
Additionally, gene set enrichment analysis showed that dysregulated TARDBP might be involved in some pathways related to the HCC pathogenesis.
Therefore, a hub RBP-circRNA network was generated based on TARDBP.
RNA immunoprecipitation and RNA pull-down confirmed that hsa_circ_0004913 binds to TARDBP.
These findings, published in Aging-US, indicated a certain RBP-circRNA regulatory network potentially involved in the pathogenesis of HCC, which provides novel insights into the mechanism of study and biomarker identification for HCC.
Dr. Yuhan Chen from The Southern Medical University said, "Hepatocellular carcinoma (HCC) is most common types of primary liver cancer."
Previous studies have demonstrated that circRNAs can act as sponges of RNA binding protein, in the meantime RBPs are also able to participate in back-splicing. Therefore, the interaction with RBPs can be also regarded as a crucial element to explore functions of circRNAs.
However, there are very few studies related to the effects of RBP-circRNA interactions on HCC, which requires more exploration.
In this study, the authors screened out the differently expressed circRNA in HCC cases from Gene Expression Omnibus database and predicted the RBPs binding to DEcircRNA.
After evaluating the expression level of RBPs in HCC from The Clinical Proteomic Tumor Analysis Consortium, International Cancer Genome Consortium and The Cancer Genome Atlas projects, they utilized 17 common DERBPs to construct the RBP-circRNA regulatory network in HCC.
These findings indicated that certain RBP-circRNA networks may be closely related to HCC, which provides ideas for the mechanism of study for HCC.
The Chen Research Team concluded in their Aging-US Research Output, "we identified some DERBPs interacting with circRNAs and generated RBP-circRNA regulatory networks for HCC. Among the DERBPs, high TARDBP expression was corelated with high grade, advanced stage and low macrophage fraction of HCC. We also constructed the hub RBP-circRNA network based on TARDBP and confirmed that hsa_circ_0004913 could bind to TARDBP, which may provide new clues for HCC mechanism study. However, there are also some limitations in our study. First, we only used TCGA, ICGC and CPTAC projects for analysis and little data resulted in only one RBP with prognostic significance, which may lead to the loss of some potential functional RBPs. Second, we didn’t classify samples according to the etiology and these identified circRNAs and RBPs may not be representative in HCC with different etiologies. Moreover, the number of HCC cases with circRNA data included in this study is relatively small. Due to our current lack of HCC samples and no survival information of HCC with circRNA expression profiles in GEO, we could not verify the expression and assess the prognostic value of circRNAs for HCC. In summary, our results indicated that some RBP-circRNA networks take a potential part in the pathogenesis of HCC and provide a new perspective for further mechanism study and biomarker development of HCC."
DOI - https://doi.org/10.18632/aging.203139
Full Text - https://www.aging-us.com/article/203139/text
Correspondence to: Yuhan Chen email: cspnr1@126.com
Keywords: hepatocellular carcinoma, autophagy, progression, miR-513b-5p, PIK3R3
Aging-US testimonial from Dr. Kara Fitzgerald ND IFMCP with The Institute for Functional Medicine in Federal Way Washington USA talking about their experience publishing "Potential reversal of epigenetic age using a diet and lifestyle intervention: a pilot randomized clinical trial"
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A groundbreaking clinical trial shows we can reduce biological age (as measured by the Horvath 2013 DNAmAge clock) by more than three years in only eight weeks with diet and lifestyle through balancing DNA methylation.
A first-of-its-kind, peer-reviewed study provides scientific evidence that lifestyle and diet changes can deliver immediate and rapid reduction of our biological age. Since aging is the primary driver of chronic disease, this reduction has the power to help us live better, longer.
The study, released on April 12, utilized a randomized controlled clinical trial conducted among 43 healthy adult males between the ages of 50-72. The 8-week treatment program included diet, sleep, exercise and relaxation guidance, and supplemental probiotics and phytonutrients, resulting in a statistically significant reduction of biological age–over three years younger, compared to controls.
The study was independently conducted by the Helfgott Research Institute, with laboratory assistance from Yale University Center for Genome Analysis, and the results independently analyzed at McGill University and the National University of Natural Medicine.
The study’s lead author, Kara Fitzgerald ND IFMCP, stated that “the combined intervention program was designed to target a specific biological mechanism called DNA methylation, and in particular the DNA methylation patterns that have been identified as highly predictive of biological age. We suspect that this focus was the reason for its remarkable impact. These early results appear to be consistent with, and greatly extend, the very few existing studies that have so far examined the potential for biological age reversal. And it is unique in its use of a safe, non-pharmaceutical dietary and lifestyle program, control group, and the extent of the age reduction. We are currently enrolling participants for a larger study which we expect will corroborate these findings.“
Leading epigeneticist Moshe Szyf PhD of McGill University and co-author on the study adds, “The uniqueness of Dr Fitzgerald approach is that her trial devised a natural but mechanistic driven strategy to target the methylation system of our body. This study provides the first insight into the possibility of using natural alterations to target epigenetic processes and improve our well being and perhaps even longevity and lifespan.”
DNA methylation patterns have become a leading means by which scientists evaluate and track biological aging, a term used to describe the accumulation of damage and loss of function to our cells, tissues and organs. This damage is what drives diseases of aging. “What is extremely exciting,” commented Dr. Fitzgerald, “is that food and lifestyle practices, including specific nutrients and food compounds known to selectively alter DNA methylation, are able to have such an impact on those DNA methylation patterns we know predict aging and age-related disease. I believe that this, together with new possibilities for us all to measure and track our DNA methylation age, will provide significant new opportunities for both scientists and consumers.“
Original Source
https://www.aging-us.com/news_room/three-years-younger-in-just-eight-weeks-a-new-study-suggests-yes
Related Journal Article
http://dx.doi.org/10.18632/aging.202913
Listen to a blog summary of this research paper published by Aging, entitled, "Cdkn1a transcript variant 2 is a marker of aging and cellular senescence."
The phenomenon in which cells are still metabolically active but can no longer proliferate is known as cellular senescence. Cellular senescence is a normal mechanism in development and tissue homeostasis—and a hallmark of aging.
“Most of my lab works on a process called cellular senescence, which is a cellular response to stresses and damage, many of which increase with age,” Dr. Judy Campisi, Professor at the Buck Institute for Research on Aging and Senior Scientist at the Lawrence Berkeley National Lab, said in a recent Aging interview.
An international team of researchers from Dr. Campisi’s lab are in search of new biological markers of cellular senescence and aging. Understanding mechanisms of aging such as senescence is key for developing new, safe interventions that may extend human life—with compounding socioeconomic and cultural impacts. Researchers from this lab come from institutions including the Buck Institute, the University of California, Berkeley’s Lawrence Berkeley National Lab, Universidad de Córdoba, Universidad Mayor, Geroscience Center for Brain Health and Metabolism, and Unity Biotechnology. The team published a trending 2021 paper in Aging‘s Volume 13, Issue 10, entitled, “Cdkn1a transcript variant 2 is a marker of aging and cellular senescence.”
“Our results are, to our knowledge, the first to study Ckdn1a transcript variants in the context of aging.”
There are a number of mechanisms that drive cellular senescence. Previously, mRNA and protein coding gene Cdkn1a transcript variant 1 (p21var1) has been better-studied compared to Cdkn1a transcript variant 2 (p21var2). The authors of this paper explain that this is likely because the encoded protein is identical to that encoded by variant 1, and both variants are regulated by p53. However, neither variants have ever before been studied in the context of aging. In this study, the researchers explored the expression levels of both Cdkn1a transcript variants 1 and 2 in the context of cellular senescence using several tissues from aged mice and a cell culture model of mouse cells.
“The stringent cell growth arrest associated with cellular senescence is determined, among other mechanisms, by activities of cyclin-dependent kinase inhibitor proteins p16Ink4a and p21Cip1/Waf1, encoded by the Cdkn2a and Cdkn1a loci, respectively [1].”
Study results showed that both variants are induced during cellular senescence. They showed that p21var1 and p21var2 are equally sensitive to transcriptional upregulation after p53 stabilization. The in vitro models also found that p21var2 is preferentially induced with age.
“In sum, p21var2 expression is consistently elevated with age, in contrast with an absence of age-related change in p21var1 levels.”
The researchers conducted further tests in vivo to examine the expression pattern of p21var2 and their results suggested that the circadian regulation of p21Cip1/Waf1 is driven solely by expression of Cdkn1a transcript variant 1. The team also induced cellular senescence in vivo with doxorubicin and ABT-263 (navitoclax) and evaluated the variants’ expression. These results confirmed their in vitro findings that p21var2 is more prone to cellular senescence than p21var1, thus making it a better marker for assessing the presence of senescent cells in vivo.
“We show that, although tissue-specific exceptions may arise, p21var2 but not p21var1 is a better candidate marker of aging and senescence in mice.”
DOI - doi.org/10.18632/aging.203110
Full Text - www.aging-us.com/article/203110/text
Correspondence to: Judith Campisi email: jcampisi@buckinstitute.org
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Aging published "Cdkn1a transcript variant 2 is a marker of aging and cellular senescence" which reported that cellular senescence is a cell fate response characterized by a permanent cell cycle arrest driven primarily the by cell cycle inhibitor and tumor suppressor proteins p16Ink4a and p21Cip1/Waf1. In mice, the p21Cip1/Waf1 encoding locus, Cdkn1a, is known to generate two transcripts that produce identical proteins, but one of these transcript variants is poorly characterized.
The authors show that the Cdkn1a transcript variant 2, but not the better-studied variant 1, is selectively elevated during natural aging across multiple mouse tissues.
Importantly, mouse cells induced to senescence in culture by genotoxic stress upregulated both transcripts, but with different temporal dynamics: variant 1 responded nearly immediately to genotoxic stress, whereas variant 2 increased much more slowly as cells acquired senescent characteristics.
Upon treating mice systemically with doxorubicin, which induces widespread cellular senescence in vivo, variant 2 increased to a larger extent than variant 1. Variant 2 levels were also more sensitive to the senolytic drug ABT-263 in naturally aged mice.
Thus, variant 2 is a novel and more sensitive marker than variant 1 or total p21Cip1/Waf1 protein for assessing the senescent cell burden and clearance in mice.
Dr. Judith Campisi from The Buck Institute for Research on Aging as well as The University of California said, "The stringent cell growth arrest associated with cellular senescence is determined, among other mechanisms, by activities of cyclin-dependent kinase inhibitor proteins p16Ink4a and p21Cip1/Waf1, encoded by the Cdkn2a and Cdkn1a loci, respectively."
The increased expression of these proteins is a major hallmark of senescence in most cells, and therefore have become markers of senescence both in culture and in vivo.
Consistent with the fact that senescent cells increase with age in many mouse and human tissues, Cdkn2a mRNA levels also increase with age in these tissues.
To date, possible changes in the expression of Cdkn1a transcript-specific variants during age or cellular senescence have not been explored.
The authors also analyze expression levels in a cell culture model of mouse cells subjected to genotoxic stress-induced senescence to evaluate their relative utility as senescence markers both in culture and in vivo.
The Campisi Research Team concluded in their Aging Research Output that it remains unexplored the possibility that the different transcript variants are preferentially associated with one or other cell fate.
Human cells also express several Cdkn1a transcript variants.
Among the ten human transcript variants currently annotated, at least one shares translational regulatory mechanisms with the murine p21var2.
Interestingly, even though murine variant 2 and human variant 4 do not appear to share sequence homology, the translational regulation in both transcripts is driven by the integrated stress response and results in cell cycle arrest.
The potential relevance of this mechanism for cellular senescence in humans remains unknown, and the functions and interrelations of the different Cdkn1a transcript variants have not been studied in depth.
DOI - https://doi.org/10.18632/aging.203110
Full Text - https://www.aging-us.com/article/203110/text
Correspondence to: Judith Campisi email: jcampisi@buckinstitute.org
Keywords: p21, p53, mouse dermal fibroblast, ionizing radiation, doxorubicin
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
In 2021, researchers from Harvard University and the Broad Institute wrote a theory article that was published in Aging’s Volume 13, Issue 12, and entitled, “Shifting epigenetic contexts influence regulatory variation and disease risk.” The authors described common epigenetic trends throughout human growth, development, and aging. They also aimed to show how changing epigenetic contexts may influence the behavior of evolutionary forces and risk of genetic disease.
FETAL TO ADULT EPIGENETIC SHIFTS The researchers point out that in order to better understand the contribution of epigenetic changes to disease and aging, it is important to understand the developmental changes that occur between fetal and adult tissues, and their interaction with epigenetic aging.
“Furthermore, these fetal to adult epigenetic shifts can be compounded by additional modifications through aging-associated epigenetic changes.”
Characterizing these epigenetic trends and examining their potential interaction with later-in-life epigenetic aging were main goals of this study. In order to do this, the researchers defined genomic regions where, over the course of development and aging, chromatin accessibility consistently shifts. Chromatin can be broadly classified in either of two epigenetic states: activating or repressing modifications. These states refer to chromatin accessibility and the increased or decreased ability of DNA to access gene-regulatory machinery, such as transcription factors. The authors note that they used an accessibility-based definition of epigenetic context, and that there are other marks of epigenetic changes (e.g. methylation, and etc.) that are not captured by this definition.
“Epigenetic marks established during development can persist into adulthood, but they do so in the context of shifts in epigenetic states as tissues transition into their adult forms and functions.” Read the full blog post: https://www.impactjournals.com/journals/blog/aging/trending-with-impact-epigenetic-shifts-aging-and-disease/
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DOI - https://doi.org/10.18632/aging.203194
Full text - https://www.aging-us.com/article/203194/text
Correspondence to: Terence D. Capellini email: tcapellini@fas.harvard.edu
Keywords: development, evolution, GWAS, disease, aging
About Aging
Launched in 2009, Aging publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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Aging published this theory article on November 17, 2018, entitled, “Disease or not, aging is easily treatable,” by Dr. Mikhail V. Blagosklonny from the Department of Cell Stress Biology, Roswell Park Comprehensive Cancer Center, Buffalo, NY.
Abstract: Is aging a disease? It does not matter because aging is already treated using a combination of several clinically-available drugs, including rapamycin. Whether aging is a disease depends on arbitrary definitions of both disease and aging. For treatment purposes, aging is a deadly disease (or more generally, pre-disease), despite being a normal continuation of normal organismal growth. It must and, importantly, can be successfully treated, thereby delaying classic age-related diseases such as cancer, cardiovascular and metabolic diseases, and neurodegeneration.
To date, this study has generated an Altmetric Attention Score of 54. The Altmetric Attention Score provides an at-a-glance indication of the volume and type of online attention the research has received.
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DOI - https://doi.org/10.18632/aging.101647
Full text - https://www.aging-us.com/article/101647/text
Correspondence to: Mikhail V. Blagosklonny email: mikhail.blagosklonny@roswellpark.org
Keywords: gerossuppresants, senolytics, longevity, lifespan, aging
About Aging
Launched in 2009, Aging publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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Our bodies are quite miraculous machines. We are born with a genome that contains the code for every protein necessary for survival. We develop and produce hormones that allow us to reproduce and have children. But what happens to us as we age? This question has puzzled scientists for years while they offer theory after theory.
In 1957, evolutionary biologist George Williams proposed what he called the antagonistic pleiotropy hypothesis as a theory of how and why we age. He claimed that our bodies express a gene that has benefits for our early life, but that same gene will harm us later on. His hypothesis has inspired aging research and led to a story about a chemical discovered deep within the dirt of an island floating in the Pacific.
In 1964, Canadian researchers, led by Stanley Skoryna from McGill University, set sail out of Halifax for Easter Island—a speck of land floating 2,000 miles off the coast of Chile, where the human population is small but life is diverse. They were hoping to retrieve precious specimens from the island before its land was tarnished with the building of a new airport. Stanley and his team collected hundreds of plant samples, countless animal specimens, and took blood and saliva from all 949 of the island’s residents.
What they found buried in the dirt on Easter Island would turn out to be the biggest treasure of all: a bacteria that would mystify scientists for the next 50 years. This bacteria was found to create a chemical now known as rapamycin, cleverly named after Easter Island’s native name, Rapa Nui.
Read the full article: https://www.impactjournals.com/journals/blog/aging/rapamycin-miracle-chemical-discovered-easter-islands-dirt/
About Aging
Launched in 2009, Aging publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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Aging published "Potential reversal of epigenetic age using a diet and lifestyle intervention: a pilot randomized clinical trial" which reported on a randomized controlled clinical trial conducted among 43 healthy adult males between the ages of 50-72. The 8-week treatment program included diet, sleep, exercise and relaxation guidance, and supplemental probiotics and phytonutrients.
Genome-wide DNA methylation analysis was conducted on saliva samples using the Illumina Methylation Epic Array and DNAmAge was calculated using the online Horvath DNAmAge clock (also published in Aging).
The diet and lifestyle treatment was associated with a 3.23 years decrease in DNAmAge compared with controls.
DNAmAge of those in the treatment group decreased by an average 1.96 years by the end of the program compared to the same individuals at the beginning with a strong trend towards significance.
This randomized controlled study, published in Aging, suggests that specific diet and lifestyle interventions may reverse Horvath DNAmAge epigenetic aging in healthy adult males.
The study’s lead author, Kara Fitzgerald ND IFMCP, from The Institute for Functional Medicine said, "Advanced age is the largest risk factor for impaired mental and physical function and many non-communicable diseases including cancer, neurodegeneration, type 2 diabetes, and cardiovascular disease."
Methylation clocks are based on systematic methylation changes with age.
DNAmAge clock specifically demonstrates about 60% of CpG sites losing methylation with age and 40% gaining methylation.
Almost a quarter of the DNAmAge CpG sites are located in glucocorticoid response elements, pointing to a likely relationship between stress and accelerated aging. Cumulative lifetime stress has been shown to be associated with accelerated aging of the methylome.
Other findings include that PTSD contributes to accelerated methylation age; and that greater infant distress is associated with an underdeveloped, younger epigenetic age.
This is to say the authors have tentatively accepted the hypothesis that the methylation pattern from which the DNAmAge clock is computed is a driver of aging, thus they expect that attempting to directly influence the DNA methylome using diet and lifestyle to set back DNAmAge will lead to a healthier, more “youthful” metabolism.
The Fitzgerald Research Team concluded in their Aging Research Output, "it may be that emerging ‘omics’ approaches continue to evolve our understanding of biological age prediction and reversal beyond DNA methylation alone. Integration of our future understanding of multi-omics data should therefore be considered in the future trials of candidate age-delaying interventions."
DOI - https://doi.org/10.18632/aging.202913
Full Text - https://www.aging-us.com/article/202913/text
Correspondence to: Kara N. Fitzgerald email: kf@drkarafitzgerald.com
Keywords: DNA methylation, epigenetic, aging, lifestyle, biological clock
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl
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Aging published this research paper on March 14, 2021, entitled, “Deep longitudinal phenotyping of wearable sensor data reveals independent markers of longevity, stress, and resilience,” by researchers from Gero PTE. LTD., Singapore 409051, Singapore and Moscow Institute of Physics and Technology, Moscow Region 141700, Russia.
Abstract: Biological age acceleration (BAA) models based on blood tests or DNA methylation emerge as a de facto standard for quantitative characterizations of the aging process. We demonstrate that deep neural networks trained to predict morbidity risk from wearable sensor data can provide a high-quality and cheap alternative for BAA determination. The GeroSense BAA model was trained and validated using steps per minute recordings from 103,830 one-week long and 2,599 of up to 2 years-long longitudinal samples and exhibited a superior association with life-expectancy over the average number of steps per day in, e.g., groups stratified by professional occupations. The association between the BAA and effects of lifestyles, the prevalence of future incidence of diseases was comparable to that of BAA from models based on blood test results. Wearable sensors let sampling of BAA fluctuations at time scales corresponding to days and weeks and revealed the divergence of organism state recovery time (resilience) as a function of chronological age. The number of individuals suffering from the lack of resilience increased exponentially with age at a rate compatible with Gompertz mortality law. We speculate that due to the stochastic character of BAA fluctuations, its mean and auto-correlation properties together comprise the minimum set of biomarkers of aging in humans.
To date, this study has generated an Altmetric Attention Score of 43. The Altmetric Attention Score provides an at-a-glance indication of the volume and type of online attention the research has received.
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DOI - https://doi.org/10.18632/aging.202816
Full text - https://www.aging-us.com/article/202816/text
Correspondence to: Timothy V. Pyrkov email: tim.pyrkov@gero.ai and Peter O. Fedichev email: peter.fedichev@gero.ai
Keywords: biological age acceleration (BAA), public health, personalized interventions, Gompertz law, resilience, aging
About Aging
Launched in 2009, Aging publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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Aging published this trending editorial on May 20, 2021, entitled, “When aging switches on Alzheimer’s” by researchers from the Department of Biomedical Engineering, MIND Institute, Center for Neurobiology of Learning and Memory, University of California, Irvine, CA.
In the paper, the researchers discuss the effects of oxidative stress in aging and Alzheimer’s disease. In short, age-related oxidative stress launches a global shift in the epigenetic landscape, and drives metabolic and energetic “switches.” The researchers point out that these "switches" highlight potential epigenetic targets for the treatment of Alzheimer’s disease.
To date, this study has generated an Altmetric Attention Score of 22. The Altmetric Attention Score provides an at-a-glance indication of the volume and type of online attention the research has received.
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DOI - https://doi.org/10.18632/aging.203085
Full text - https://www.aging-us.com/article/203085/pdf (PDF Download)
Correspondence to: Gregory J. Brewer email: gjbrewer@uci.edu
Keywords: Alzheimer’s disease, NAD+/NADH, oxidative shift, mitochondrial impairment, neuroinflammation, aging
About Aging
Launched in 2009, Aging publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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Aging published this high-scoring research paper on June 26, 2020, entitled, “Cognitive enhancement of healthy older adults using hyperbaric oxygen: a randomized controlled trial,” by researchers from the Shamir Medical Center, Zerifin, Israel; Tel-Aviv University, Tel-Aviv, Israel; Bar Ilan University, Ramat-Gan, Israel.
“The aim of the current study was to evaluate whether HBOT affects cognitive function and brain perfusion in normal, non-pathological, aging adults.”
A total of 63 patients were admitted into this study. The participants’ age, gender, right/left hand dominance, education, employment, medical conditions, medications, and other characteristics were collected at the start of the study. The median age was approximately 69 years old. Cognitive function of each participant was evaluated at baseline in terms of memory, attention, information processing speed, motor skills, and a number of other measures of neurocognitive function.
The participants were then assigned either the HBOT arm or the control arm of the study. Both groups had similar characteristics and cognitive function at baseline. Half of the participants received 60 daily sessions of HBOT over the course of three months. All post-intervention measurements were taken at least one week after the last hyperbaric session. The assessors were blind to the assignment each participant was given when reevaluating for cognitive function after HBOT intervention.
“Our protocol included 60 sessions of 100% oxygen at 2 ATA including 3 air breaks during each session in order to utilize the hyperoxic hypoxic paradox and minimize the risk for oxygen toxicity.”
To date, this study has generated an Altmetric Attention Score of 111. The Altmetric Attention Score provides an at-a-glance indication of the volume and type of online attention the research has received.
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DOI - https://doi.org/10.18632/aging.103571
Full text - https://www.aging-us.com/article/103571/text
Correspondence to: Amir Hadanny email: amir.had@gmail.com and Shai Efrati email: efratishai@outlook.com
Keywords: cognitive, hyperbaric oxygen, perfusion, cerebral blood flow, aging
About Aging
Launched in 2009, Aging publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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From 1961 to 1970, healthy U.S. males between the ages of 21 and 81 enrolled in the ongoing Veterans Affairs Normative Aging Study. One of the objectives of the study is to characterize the biomedical and psychosocial parameters of normal aging (distinct from the development of disease). There are a total of 2,280 participants in the Normative Aging Study (NAS). In the current Aging study, researchers included 696 elderly men from the NAS.
“The present study included 696 elderly men with 1,070 visits during years of 1999-2013.”
In search of associations between biomarkers of aging and lung function, the researchers first collected the study participants’ personal characteristics, including age, smoking history, height, weight, BMI, education, blood work, and other measures. They then analyzed lung function using three tests: forced expiratory volume in one second (FEV1), forced expiratory volume in one second / forced vital capacity (FEV1/FVC), and maximum mid-expiratory flow (MMEF).
Next, the team analyzed the participants’ epigenetic biomarkers of age; including GrimAgeAccel, PhenoAgeAccel, intrinsic epigenetic age acceleration (IEAA), extrinsic epigenetic age acceleration (EEAA), and Zhang’s DNAmRiskScore; as well as non-epigenetic biomarkers of age, including telomere length and mitochondrial DNA copy number (mtDNA-CN). They then assessed for associations between these biomarkers and the three measures of lung function.
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DOI - https://doi.org/10.18632/aging.103363
Full text - https://www.aging-us.com/article/103363/text
Correspondence to: Cuicui Wang email: cuicuiwang@hsph.harvard.edu
Keywords: pulmonary health, DNA methylation, biological clock, aging
About Aging
Launched in 2009, Aging publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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Aging published this high-scoring research paper on July 30, 2019, entitled, “Effects of transcutaneous vagus nerve stimulation in individuals aged 55 years or above: potential benefits of daily stimulation,” by researchers from the United Kingdom’s University of Leeds and University of Glasgow.
In 2019, the researchers reported on the results of the effects of tVNS among participants 55 years of age and older in three studies.
In the first study, they observed the effects of acute, single-session tVNS on cardiovascular autonomic function compared with the effects of sham (ear lobe/placebo) stimulation among 14 healthy participants 55 years of age and older. They collected baseline values and measured heart rate variability (HVR) and baroreflex sensitivity.
“Since not all participants responded to tVNS, we examined if it was possible to identify potential tVNS responders from baseline parameters.”
In the second study, the researchers explored the effects of acute, single-session tVNS on autonomic function in the same age group by expanding the sample to 51 participants. The third study examined 26 participants in the same age group when administered tVNS once per day, for 15-minutes, over the course of two weeks. The researchers reported the impacts of daily tVNS in measures of autonomic function, health-related quality of life (QoL), mood, and sleep.
“Transcutaneous vagal nerve stimulation (tVNS) acutely administered to the tragus in healthy volunteers aged ≥ 55 years was associated with improvements in spontaneous cardiac baroreflex sensitivity and HRV.”
To date, this study has generated an Altmetric Attention Score of 350. The Altmetric Attention Score provides an at-a-glance indication of the volume and type of online attention the research has received.
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DOI - https://doi.org/10.18632/aging.102074
Full text - https://www.aging-us.com/article/102074/text
Correspondence to: Jim Deuchars email: J.Deuchars@leeds.ac.uk
Keywords: vagus nerve stimulation, autonomic nervous system, neuromodulation, quality of life, mood, aging
About Aging
Launched in 2009, Aging publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
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Aging is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
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Aging published a trending review paper on May 13, 2021, entitled, “Effects of exercise on cellular and tissue aging” by researchers from Harvard Medical School.
Regular physical exercise provides benefits for both the body and mind, but how exactly does this healthy habit benefit our cells, signaling pathways, organs, and even bones? Furthermore, how can we employ regular exercise as part of an anti-aging strategy to extend our healthspan and lifespan?
The researchers from the Beta Cell Aging Lab at Harvard Medical School authored the review paper which breaks down the currently available research on this very topic, with a special focus on pancreatic beta-cells and Type 2 diabetes. The authors detailed the recorded effects of exercise at systemic and cellular levels, its effects on each of the hallmarks of aging, and a potential molecular regulatory node that may integrate those effects.
“Exercise is a promising lifestyle intervention that has shown antiaging effects by extending lifespan and healthspan through decreasing the nine hallmarks of aging and age-associated inflammation.”
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DOI - https://doi.org/10.18632/aging.203051
Full text - https://www.aging-us.com/article/203051/text
Correspondence to: Cristina Aguayo-Mazzucato email: cristina.aguayo-mazzucato@joslin.harvard.edu
Keywords: exercise, aging, AMPK, type 2 diabetes
About Aging
Launched in 2009, Aging publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
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Aging is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
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A groundbreaking clinical trial shows we can reduce biological age (as measured by the Horvath 2013 DNAmAge clock) by more than three years in only eight weeks with diet and lifestyle through balancing DNA methylation.
A first-of-its-kind, peer-reviewed study provides scientific evidence that lifestyle and diet changes can deliver immediate and rapid reduction of our biological age. Since aging is the primary driver of chronic disease, this reduction has the power to help us live better, longer.
The study, released on April 12, utilized a randomized controlled clinical trial conducted among 43 healthy adult males between the ages of 50-72. The 8-week treatment program included diet, sleep, exercise and relaxation guidance, and supplemental probiotics and phytonutrients, resulting in a statistically significant reduction of biological age--over three years younger, compared to controls.
The study was independently conducted by the Helfgott Research Institute, with laboratory assistance from Yale University Center for Genome Analysis, and the results independently analyzed at McGill University and the National University of Natural Medicine.
The study’s lead author, Kara Fitzgerald ND IFMCP, stated that “the combined intervention program was designed to target a specific biological mechanism called DNA methylation, and in particular the DNA methylation patterns that have been identified as highly predictive of biological age. We suspect that this focus was the reason for its remarkable impact. These early results appear to be consistent with, and greatly extend, the very few existing studies that have so far examined the potential for biological age reversal. And it is unique in its use of a safe, non-pharmaceutical dietary and lifestyle program, control group, and the extent of the age reduction. We are currently enrolling participants for a larger study which we expect will corroborate these findings.”
Leading epigeneticist Moshe Szyf PhD of McGill University and co-author on the study adds, “The uniqueness of Dr Fitzgerald approach is that her trial devised a natural but mechanistic driven strategy to target the methylation system of our body. This study provides the first insight into the possibility of using natural alterations to target epigenetic processes and improve our well being and perhaps even longevity and lifespan.”
DNA methylation patterns have become a leading means by which scientists evaluate and track biological aging, a term used to describe the accumulation of damage and loss of function to our cells, tissues and organs. This damage is what drives diseases of aging. “What is extremely exciting,” commented Dr. Fitzgerald, “is that food and lifestyle practices, including specific nutrients and food compounds known to selectively alter DNA methylation, are able to have such an impact on those DNA methylation patterns we know predict aging and age-related disease. I believe that this, together with new possibilities for us all to measure and track our DNA methylation age, will provide significant new opportunities for both scientists and consumers.”
To read the study: https://www.aging-us.com/article/202913
For background information on aging and DNA methylation: https://www.drkarafitzgerald.com/2021/04/13/biological-aging-and-methylation/
For press/interviews contact: media@drkarafitzgerald.com
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl
Aging: Clinical Trial on Potential reversal of Epigenetic Age using a Diet and Lifestyle
Aging published "Potential reversal of epigenetic age using a diet and lifestyle intervention: a pilot randomized clinical trial" which reported on a randomized controlled clinical trial conducted among 43 healthy adult males between the ages of 50-72. The 8-week treatment program included diet, sleep, exercise and relaxation guidance, and supplemental probiotics and phytonutrients.
Genome-wide DNA methylation analysis was conducted on saliva samples using the Illumina Methylation Epic Array and DNAmAge was calculated using the online Horvath DNAmAge clock (also published in Aging).
The diet and lifestyle treatment was associated with a 3.23 years decrease in DNAmAge compared with controls.
DNAmAge of those in the treatment group decreased by an average 1.96 years by the end of the program compared to the same individuals at the beginning with a strong trend towards significance.
This randomized controlled study, published in Aging, suggests that specific diet and lifestyle interventions may reverse Horvath DNAmAge epigenetic aging in healthy adult males.
The study’s lead author, Kara Fitzgerald ND IFMCP, from The Institute for Functional Medicine said, "Advanced age is the largest risk factor for impaired mental and physical function and many non-communicable diseases including cancer, neurodegeneration, type 2 diabetes, and cardiovascular disease."
Methylation clocks are based on systematic methylation changes with age.
DNAmAge clock specifically demonstrates about 60% of CpG sites losing methylation with age and 40% gaining methylation.
Almost a quarter of the DNAmAge CpG sites are located in glucocorticoid response elements, pointing to a likely relationship between stress and accelerated aging. Cumulative lifetime stress has been shown to be associated with accelerated aging of the methylome.
Other findings include that PTSD contributes to accelerated methylation age; and that greater infant distress is associated with an underdeveloped, younger epigenetic age.
This is to say the authors have tentatively accepted the hypothesis that the methylation pattern from which the DNAmAge clock is computed is a driver of aging, thus they expect that attempting to directly influence the DNA methylome using diet and lifestyle to set back DNAmAge will lead to a healthier, more “youthful” metabolism.
The Fitzgerald Research Team concluded in their Aging Research Output, "it may be that emerging ‘omics’ approaches continue to evolve our understanding of biological age prediction and reversal beyond DNA methylation alone. Integration of our future understanding of multi-omics data should therefore be considered in the future trials of candidate age-delaying interventions."
DOI - https://doi.org/10.18632/aging.202913
Full Text - https://www.aging-us.com/article/202913/text
Correspondence to: Kara N. Fitzgerald email: kf@drkarafitzgerald.com
Keywords: DNA methylation, epigenetic, aging, lifestyle, biological clock
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl
Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
Media Contact 18009220957x105 MEDIA@IMPACTJOURNALS.COM
In a trending research perspective published by Aging on February 24, 2021, entitled, “Aging and rejuvenation - a modular epigenome model,” researchers examined the role that the epigenetic clock may play in the aging process and in rejuvenation as an approach to set back epigenetic age.
A centenarian is a human that has lived as long or longer than one hundred years. These individuals are marvels to aging researchers and have been studied at length in hopes of uncovering clues about the mechanisms that drive aging. Many researchers have crafted views and theories about the roots of gerontology; these curiosities have preceded the development of modern science.
In an effort to describe different views and theories of aging—leading to the emergent view of the epigenome as the driver of aging—researchers from the National University of La Plata, National University of Cordoba, World Academy of Art and Science, and Betterhumans Inc., authored a research perspective published by Aging.
“The hypothesis proposing the epigenome as the driver of aging was significantly strengthened by the converging discovery that DNA methylation at specific CpG sites could be used as a highly accurate biomarker of age defined by the Horvath clock.”
To date, this study has generated an Altmetric Attention Score of 34. The Altmetric Attention Score provides an at-a-glance indication of the volume and type of online attention the research has received.
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DOI - https://doi.org/10.18632/aging.202712
Full text - https://www.aging-us.com/article/202712/text
Correspondence to: Rodolfo G. Goya email: goya@isis.unlp.edu.ar
Keywords: aging, DNA methylation, epigenetic clock, rejuvenation, cell reprogramming
About Aging
Launched in 2009, Aging publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
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Aging is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
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Aging published this trending paper on March 2, 2020, entitled, “ESHRD: deconvolution of brain homogenate RNA expression data to identify cell-type-specific alterations in Alzheimer’s disease” by researchers from Neurogenomics Division, The Translational Genomics Research Institute, Phoenix; Center for Statistical Genetics, Department of Neurology, Gertrude H. Sergievsky Center, Columbia University Medical Center, New York; The University of Sydney School of Medicine, Sydney; University of Miami; Banner Sun Health Research Institute, Sun City.
The researchers conducted brain region cell-specific pathway analysis and Gene Set Enrichment Analysis (GSEA). The team mapped and measured five different cell types in seven different brain regions. The cell types included: microglia, neuron, endothelial, astrocyte, and oligodendrocyte. Endothelial and oligodendrocyte are two cell types that are not easily examined in the brain and only very little gene expression data previously existed for Alzheimer’s disease.
“We conducted RNA expression profiling from both brain homogenates and oligodendrocytes obtained by LCM from the same donor brains and then calculated differential expression.”
The researchers used a dataset of Multiple System Atrophy (MSA) patients (n = 4) and controls (n = 5) to validate their ESHRD method. Homogenate, LCM, and scRNA-Seq results were compared using the ESHRD method. They also compared their findings to other research studies.
To date, this study has generated an Altmetric Attention Score of 10. The Altmetric Attention Score provides an at-a-glance indication of the volume and type of online attention the research has received.
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DOI - https://doi.org/10.18632/aging.102840
Full text - https://www.aging-us.com/article/102840/text
Correspondence to: Matthew J. Huentelman email: mhuentelman@tgen.org
Keywords: RNA sequencing, laser capture microdissection, brain homogenates, endothelial cells, oligodendrocytes, Alzheimer’s disease
About Aging
Launched in 2009, Aging publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
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Aging is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
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In this top-performing research paper published by Aging on November 15, 2017, entitled, “Towards natural mimetics of metformin and rapamycin,” researchers used powerful screening methods to analyze over 800 natural compounds to assess their anti-aging potential and safety profile in an effort to mimic metformin and rapamycin.
In 2017, researchers from the United States’ Insilico Medicine, Inc. and Life Extension, the United Kingdom’s Biogerontology Research Foundation, Canada’s Queen’s University, and Russia’s Russian Academy of Sciences, worked together to test a new strategy to accelerate the development of safe, wide-scale anti-aging nutraceuticals.
“One strategy to hasten the process has been the repurposing of existing, FDA-approved drugs that show off-label anti-cancer and anti-aging potential, and at the top of that list are metformin and rapamycin, two drugs that mimic caloric restriction.”
To date, this paper has generated an Altmetric Attention score of 127. Altmetric Attention scores provide an at-a-glance indication of the volume and type of online attention the research has received.
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DOI - http://doi.org/10.18632/aging.101319
Full text - https://www.aging-us.com/article/101319/text
Correspondence to: Alexander Aliper email: aliper@insilicomedicine.com
Keywords: geroprotector, metformin, rapamycin, deep learning, natural, nutraceutical, compound screening, aging
About Aging
Launched in 2009, Aging publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
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Aging is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM
In this trending research paper published by Aging on April 12, 2021, entitled, “Potential reversal of epigenetic age using a diet and lifestyle intervention: a pilot randomized clinical trial,” researchers from the Institute for Functional Medicine, American Nutrition Association, National University of Natural Medicine, Ariel University, McGill University, and the University of California, conducted a new pilot study on the effects that diet and lifestyle intervention have on aging among a small cohort of healthy males between the ages of 50 and 72.
The researchers organized a cohort of 43 healthy adult males between the ages of 50 and 72. Half of the participants (n=21) completed an eight-week treatment program, and the other half (control group=22) received no intervention. Interventions within the treatment program included regimented diet, sleep, exercise, relaxation guidance, and supplemental probiotics and phytonutrients. The participants were enrolled in a preliminary education week, prior to the treatment program, in order to become acquainted with the researchers’ prescribed dietary and lifestyle interventions.
“To our knowledge, this is the first randomized controlled study to suggest that specific diet and lifestyle interventions may reverse Horvath DNAmAge (2013) epigenetic aging in healthy adult males.”
To date, this study has generated an Altmetric Attention score of 25. Altmetric Attention scores provide an at-a-glance indication of the volume and type of online attention the research has received.
Top Aging publications rated by Altmetric score: https://www.aging-us.com/news_room/altmetric
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DOI - https://doi.org/10.18632/aging.202913
Full text - https://www.aging-us.com/article/202913/text
Correspondence to: Kara N. Fitzgerald email: kf@drkarafitzgerald.com
Keywords: DNA methylation, epigenetic, aging, lifestyle, biological clock
About Aging
Launched in 2009, Aging publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
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Aging is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM
In this top-performing research perspective published by Aging on February 12, 2021, entitled, “DNA- and telomere-damage does not limit lifespan: evidence from rapamycin,” Dr. Mikhail Blagosklonny — an adjunct faculty member at Roswell Park Comprehensive Cancer Center and the Editor-in-Chief of Aging, Oncotarget, Oncoscience, and Cell Cycle — gleaned an important new perspective from recent aging studies, which some may have overlooked.
Rapamycin is a macrolide antibiotic that has immunosuppressive properties, regulates a key cellular growth pathway (mTOR), and has been at the center of numerous studies of aging since it’s discovery in 1964. Dr. Blagosklonny explains that, based on findings from recent mouse-model studies of rapamycin’s effects on short-lived mice, normal aging is not caused by the accumulation of molecular damage or telomere shortening.
“Here I discussed new evidence that normal aging is not caused by accumulation of molecular damage or telomere shortening: while extending normal lifespan in mice, rapamycin failed to do so in mice dying from molecular damage (Figure 1).”
To date, this research paper has generated an Altmetric Attention score of 43. Altmetric Attention scores, located at the top-left of trending Aging papers, provide an at-a-glance indication of the volume and type of online attention the research has received. Top Aging publications rated by Altmetric score: https://www.aging-us.com/news_room/altmetric
DOI - https://doi.org/10.18632/aging.202674
Full text - https://www.aging-us.com/article/202674/text
Correspondence to: Mikhail V. Blagosklonny email: Blagosklonny@oncotarget.com
Keywords: quasi-programmed aging, hyperfunction theory, antagonistic pleiotropy, natural selection, mTOR, rapamycin
About Aging
Launched in 2009, Aging publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
Twitter - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ SoundCloud - https://soundcloud.com/aging-us YouTube - https://www.youtube.com/agingus LinkedIn - https://www.linkedin.com/company/aging
Aging is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
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In this trending paper published in Aging on February 11, 2021, entitled, “Examining sleep deficiency and disturbance and their risk for incident dementia and all-cause mortality in older adults across 5 years in the United States,” a team of researchers from Brigham and Women’s Hospital, Harvard Medical School, and Boston College, organized a single examination of the relationships between a comprehensive set of sleep characteristics and incident dementia and all-cause mortality.
The researchers collected their baseline data from the National Health and Aging Trends Study (NHATS), which is a nationally-representative longitudinal study of Medicare beneficiaries (65 years and older) in the United States. The data were collected from a randomly selected subset of 2,812 participants from the NHATS population that were administered sleep questionnaires in 2013 and 2014.
“Participants with dementia at baseline (year 2013) were excluded (n = 202) for a sample of 2,812 with sleep data in either 2013 or 2014.”
To date, this research paper has generated an Altmetric Attention Score of 91. Altmetric Attention Scores, located at the top-left of trending Aging papers, provide an at-a-glance indication of the volume and type of online attention the research has received. Top Aging publications rated by Altmetric Attention Score: https://www.aging-us.com/news_room/altmetric
DOI - https://doi.org/10.18632/aging.202591 Full Text - https://www.aging-us.com/article/202591/text#fulltext
Correspondence to: Rebecca Robbins email: rrobbins4@bwh.harvard.edu
Keywords: Alzheimer's Disease, Sleep, Longevity, Preventative Health Care, Aging
About Aging
Launched in 2009, Aging publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
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Aging is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
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Aging is indexed by PubMed/Medline abbreviated as “Aging (Albany NY)”, PubMed Central, ISI/Web of Science: Science Citation Index Expanded (abbreviated as Aging‑US and listed in the Cell Biology category; since June 2017 it has also been listed in the Geriatrics & Gerontology category), and Scopus /Rank Q1 (abbreviated as Aging).
Every year, the American Association for Cancer Research (AACR) organizes a conference program that covers the latest discoveries in cancer research. Topics include population science and prevention, cancer biology, translational and clinical studies, survivorship, and advocacy. This conference aims to highlight work from the best minds in research and medicine from institutions all over the world. The journal Aging, by Impact Journals, will be participating at the AACR Annual Meeting this year. Visit Aging website: https://www.aging-us.com/
Impact Journals is an open-access publisher of rigorously peer-reviewed scientific literature, and owns several medical research journals, including Aging. Aging was launched by Impact Journals in 2009 with the goal of spotlighting high-impact papers, authored by scientists who study the process of aging and age-related diseases—including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Visit Impact Journals website: https://www.impactjournals.com/
Aging has published outstanding papers and reviews by highly-cited authors and award winners, including Andrew V. Schally (Nobel Laureate), Shinya Yamanaka (Nobel Laureate), Lawrence Donehower, Toren Finkel, Stephen Helfand, Gerald Shadel, Andre Nussenzweig, Maurice Burg, Karen Vousden, Leonard Guarente, and Dale Bredesen. Importantly, the Aging Editorial Board also comprises numerous prestigious award winners, including Nobel Laureate Elizabeth H. Blackburn, and many other distinguished scientists, including Cynthia Kenyon, Judith Campisi, Leonard Guarente, Michael Hall, Mikhail Blagosklonny, Vera Gorbunova, David Sinclair, Jan Vijg, and Thomas Rando.
The journal has recently concluded its 12th year of publishing and has become Impact Journals’ featured journal. Learn more about Aging and Impact Journals at the virtual 2021 AACR conference on April 10-15 and May 17-21, 2021. Registration will be open through the beginning of the event.
More About Aging
Launched in 2009, Aging publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
Please visit our website at http://www.Aging-US.com or connect with us on:
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Aging is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls
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Aging-US recently published "From Causes of Aging to Death from COVID-19" by Blagosklonny et al. which reported that COVID-19 is not deadly early in life, but mortality increases exponentially with age - which is the strongest predictor of mortality.
The Review covers:
Age Age-related diseases Male Gender Mortality from aging compared with COVID-19 mortality Age-related diseases Cytokine storm as a hyperfunction Hyperfunction theory of quasi-programmed aging Covid-19 vulnerability as an age-related syndrome Inflamm-aging and immunosenescence Cellular senescence as a continuation of growth Figuratively, rapamycin rejuvenates immunity Anti-aging medicine Rapamycin and everolimus as anti-aging drugs and, Potential applications of rapamycin/everolimus to COVID-19
The author contends that at its deepest level, aging is driven by inappropriately high cellular functioning. The hyperfunction theory of quasi-programmed aging explains why COVID-19 vulnerability is an age-dependent syndrome, linking it to other age-related diseases.
These conditions are typical age-related diseases: hypertension, diabetes, obesity, ischemic heart disease, chronic obstructive pulmonary disease, and other diseases.
This is because pre-existing conditions are manifestations of biological age, ultimately meaning that A. aging and B. diseases are two sides of the same coin.
The Blagosklonny Research Team goes on to highlight that an anti-aging intervention, such as rapamycin, may slow aging and age-related diseases, potentially decreasing COVID-19 vulnerability.
The Aging-US Review also reported that as soon as the COVID-19 epidemic started, it became clear that COVID-19 vulnerability is an aging-dependent condition, and the use of rapamycin was immediately suggested by independent researchers.
By decreasing biological age and preventing age-related diseases, long-term rapamycin therapy may, in theory, decrease the COVID-19 mortality rate in the elderly.
As specifically discussed in the Review section titled “Figuratively, rapamycin rejuvenates immunity”, mTOR inhibitors can improve immunity to viral infections, improve immunization and vaccination to some viruses such as the flu.
The hypothetical graph in the absence of COVID-19. COVID-19 vulnerability increases exponentially with age.
Then as discussed in the section “Cytokine storm is a hyperfunction”, cytokine storm and hyper-inflammation is the main cause of death in COVID-19 pneumonia Rapamycin, an anti-inflammatory agent, inhibits hyper-functions, cellular senescence and decrease secretion of cytokines.
DOI - https://doi.org/10.18632/aging.103493
Full text - https://www.aging-us.com/article/103493/text#fulltext
Correspondence to - Mikhail V. Blagosklonny Blagosklonny@oncotarget.com or Blagosklonny@rapalogs.com
Keywords - aging, mTOR, rapalogs, senolytics, SARS-CoV-2, COVID-19, coronavirus
Roundtable discussion involving Dr. Yunsung Lee, Dr. Anil P.S. Ori, Dr. Ake T. Lu, and Dr. Steve Horvath talking about the connections between Dr. Horvath's two papers submitted to the Journal Aging-US “Epigenome-wide association study of leukocyte telomere length” and “DNA methylation-based estimator of telomere length”
"Epigenome-wide association study of leukocyte telomere length" Full text - https://www.aging-us.com/article/102230/text Press release - https://www.aging-us.com/news_room/epigenome-wide-association-study-of-leukocyte-telomere-length
"DNA methylation-based estimator of telomere length" - Full text - https://www.aging-us.com/article/102173/text Press release - https://www.aging-us.com/news_room/dna-methylation-based-estimator-of-telomere-length
Priority Research Paper Volume 6, Issue 9 pp 707—717
Article has an altmetric score of 351 Reversal of cognitive decline: A novel therapeutic program Dale E. Bredesen 1, 2
1 Mary S. Easton Center for Alzheimer's Disease Research, Department of Neurology, University of California, Los Angeles, CA 90095; 2 Buck Institute for Research on Aging, Novato, CA 94945 received: September 15, 2014 ; accepted: September 26, 2014 ; published: September 27, 2014
https://doi.org/10.18632/aging.100690
Editorial Volume 10, Issue 2 pp 154—155
Glioblastoma in older adults - http://www.aging-us.com/article/101377/text
Matthias Holdhoff 1, 2 , Raphael Rothenberger 2 , Ilene E. Browner 2
1 Brain Cancer Program, Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA 2 Department of Oncology, Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA received: January 11, 2018 ; published: February 1, 2018
https://doi.org/10.18632/aging.101377
Copyright: Holdhoff et al. This is an open‐access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
CORRESPONDING AUTHOR Matthias Holdhoff mholdho1@jhmi.edu
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License (CC BY 3.0).
Editorial Volume 10, Issue 2 pp 164—165
Ketogenic diet in cancer therapy Daniela D. Weber 1 , Sepideh Aminazdeh-Gohari 1 , Barbara Kofler 1
1 Research Program for Receptor Biochemistry and Tumor Metabolism, University Hospital for Pediatrics of the Paracelsus Medical University, Salzburg 5020, Austria received: January 31, 2018 ; published: February 11, 2018
https://doi.org/10.18632/aging.101382
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