Aging-US

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.206240 Corresponding author - Ryan Bradley - rbradley@nunm.edu To learn more about the journal, connect with us on social media at: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Bluesky - https://bsky.app/profile/aging-us.bsky.social Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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.206183 Corresponding author - Shubhankar Suman - ss2286@georgetown.edu Author interview - https://www.youtube.com/watch?v=ClLO0ERwC0M Video short - https://www.youtube.com/watch?v=M_WEht4vy4w Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206183 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, senescence-associated secretory phenotype, senolytic agent, carcinogenesis, inflammation, β-catenin 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Bluesky - https://bsky.app/profile/aging-us.bsky.social Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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.206238 Corresponding author - Keisuke Okawa - k-ookawa@chp-kagawa.jp Video short - https://www.youtube.com/watch?v=YtbYpfVDVDI Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206238 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, Factor Xa inhibitor, atrial fibrillation, older patient, cardiovascular events To 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Bluesky - https://bsky.app/profile/aging-us.bsky.social Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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 Syndrome Werner 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 Syndrome Nicotinamide 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.206236 Corresponding author - Evandro F. Fang - e.f.fang@medisin.uio.no Video short - https://www.youtube.com/watch?v=WpRpi8TYPfU Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206236 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, Werner syndrome, premature aging, NAD+, mitochondria, proliferation 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Bluesky - https://bsky.app/profile/aging-us.bsky.social Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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.206237 Corresponding author: Sailendra N. Nichenametla – snichenametla@orentreich.org Video short - https://www.youtube.com/watch?v=AcCzYTIElGY Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords: aging, buthionine sulfoximine, thiols, serine, anti-obesity drugs To 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Bluesky - https://bsky.app/profile/aging-us.bsky.social Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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.206235 Corresponding author: Stefanie L. Morgan – stefanie@agelessrx.com Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords: rapamycin, aging, healthspan, longevity, geroscience To 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Bluesky - https://bsky.app/profile/aging-us.bsky.social Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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.206233 Corresponding author: Ioana Alesutan – ioana.alesutan@jku.at Keywords: 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Bluesky - https://bsky.app/profile/aging-us.bsky.social Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Bluesky - https://bsky.app/profile/aging-us.bsky.social Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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 translation This 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.206236 Corresponding author - Evandro F. Fang - e.f.fang@medisin.uio.no Video short - https://www.youtube.com/watch?v=WpRpi8TYPfU Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206236 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, Werner syndrome, premature aging, NAD+, mitochondria, proliferation 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Bluesky - https://bsky.app/profile/aging-us.bsky.social Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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.206224 Corresponding authors - Amit Sharma - amit.sharma@sens.org, and Pankaj Kapahi - pkapahi@buckinstitute.org Video short - https://www.youtube.com/watch?v=dRfxQ20O2fQ Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts To 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.206179 Corresponding author - Stephen F. Vatner - vatnersf@njms.rutgers.edu Author interview - https://www.youtube.com/watch?v=-DE4H2DtSZg Video short - https://www.youtube.com/watch?v=n1DvuR7owJQ Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206179 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, brown adipose tissue, white adipose tissue, healthful longevity, exercise, regulator of G protein signaling 14 To 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Bluesky - https://bsky.app/profile/aging-us.bsky.social Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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-alerts To 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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.206223 Corresponding author - Sarah Neal - SJNeal@MDAnderson.org Video short - https://www.youtube.com/watch?v=EFfRMFbAMqk Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206223 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts To 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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.206221 Corresponding author: Varun B. Dwaraka – varun.dwaraka@trudiagnostic.com Keywords: aging, epigenetic age change, physiological age change, epigenetic biomarker proxies, hallmarks of aging, nutraceutical longevity interventions To 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/AgingJrnl Instagram - www.instagram.com/agingjrnl/ YouTube - www.youtube.com/@AgingJournal LinkedIn - www.linkedin.com/company/aging/ Pinterest - www.pinterest.com/AgingUS/ Spotify - open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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.206220 Corresponding author: Matteo Pellegrini - matteope@gmail.com Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206220 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords: entropy, DNA methylation, aging, epigenetics, epigenetic clocks To 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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 Aging Breast 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.206218 Corresponding author - Xiao-Ou Shu - xiao-ou.shu@vumc.org Video short - https://www.youtube.com/watch?v=cfuyzVyDeHY Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206218 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, accelerated aging, PhenoAge, breast cancer, survivors 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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.206219 Corresponding author: Mark E. Kleinman- kleinman@etsu.edu Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords: aging, transcriptome, retinal pigment epithelium, oxidative stress, inflammation, chronological aging To 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc Media Contact 18009220957 MEDIA@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.206198 Corresponding author - José Antonio Sánchez-Alcázar - jasanalc@upo.es Video interview - https://www.youtube.com/watch?v=wIV0lAHPA_M Abstract Multiple 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.206198 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, multiple sclerosis, iron accumulation, lipid peroxidation, inflammasome, mitochondrial dysfunction To 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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.206215 Corresponding author: Pawel Kordowitzki- p.kordowitzki@umk.pl Video short - https://www.youtube.com/watch?v=0JJIOqWadE4 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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.206213 Corresponding authors - Melda Onal - MOnal@uams.edu, and Maria Almeida - schullermaria@uams.edu Video short - https://www.youtube.com/watch?v=fHQhA6rOaDc Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206213 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, Atg7, tibia compressive loading, Sod2, Osx1-Cre, osteocytes Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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 diseases Rapamycin and other pharmacological strategies to extend lifespan Senescence bypass and its implications for cancer and regenerative medicine Personalized medicine approaches in aging and longevity research Theoretical models and evolutionary perspectives on aging The 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, 2025 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 We 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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 Disease Alzheimer'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 Inhibition A 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.206227 Corresponding author - Sultan Darvesh - sultan.darvesh@dal.ca Video short - https://www.youtube.com/watch?v=CJQFpG9Jn6Y Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206227 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, cellular senescence, β-amyloid, acetylcholinesterase, butyrylcholinesterase, cholinesterase inhibitors About Aging-US The 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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.206227 Corresponding author - Sultan Darvesh - sultan.darvesh@dal.ca Video short - https://www.youtube.com/watch?v=CJQFpG9Jn6Y Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206227 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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.206194 Corresponding author - Angelo M. Tedaldi - angelomt1999@gmail.com Video short - https://www.youtube.com/watch?v=C2yXfF7iY6c Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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.206193 Corresponding author - Andreas Koller - a.koller@salk.at Video short - https://www.youtube.com/watch?v=ngnrPJzHlpI Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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.206132 Corresponding Author - Julia M. Sidorova - julias@uw.edu Video interview - https://www.youtube.com/watch?v=3yn8O-JA6GE Abstract Werner 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.206132 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, Werner progeria, heterochromatin, senescence, nuclear lamina, satellite repeats About Aging-US The 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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 Level Aging 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 Aging A 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.206201 Corresponding author - Andres Cardenas - andresca@stanford.edu Video short - https://www.youtube.com/watch?v=WcL-K399a7M Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206201 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, epigenetic aging, environmental exposures, exposome, epigenetics About Aging-US The 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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.206211 Corresponding author - Archana Unnikrishnan - archana-unnikrishnan@ouhsc.edu Video short - https://www.youtube.com/watch?v=RtsqRi2_uAI Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts About Aging-US The 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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.206218 Corresponding author - Xiao-Ou Shu - xiao-ou.shu@vumc.org Video short - https://www.youtube.com/watch?v=cfuyzVyDeHY Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts About Aging-US The 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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-US The 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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.206204 Corresponding author: Deidra R. Fricke — der94@pitt.edu Keywords: aging, ankle-brachial index, peripheral arterial disease, heritability, genomewide linkage analysis, genomewide association study Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts About Aging-US The 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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

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 Gliomas Glioblastoma 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.206212 Corresponding author - Morten Scheibye-Knudsen - mscheibye@sund.ku.dk Video short - https://www.youtube.com/watch?v=j91rzDJHXTE Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206212 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, cancer, biomarkers, radiotherapy, GBM, LGG, survival About Aging-US The 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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.206212 Corresponding author - Morten Scheibye-Knudsen - mscheibye@sund.ku.dk Video short - https://www.youtube.com/watch?v=j91rzDJHXTE Visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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.206201 Corresponding author - Andres Cardenas - andresca@stanford.edu Video short - https://www.youtube.com/watch?v=WcL-K399a7M Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts About Aging-US The 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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.206188 Corresponding author - Moshe Szyf - moshe.szyf@epimedtech.com Author interview - https://www.youtube.com/watch?v=NA8Vctks0gY Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206188 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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.206192 Corresponding author - Albert T. Higgins-Chen - a.higginschen@yale.edu About Aging-US The 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc Media Contact 18009220957 MEDIA@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 #video DOI - https://doi.org/10.18632/aging.206135 Corresponding 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.dk Video interview - https://www.youtube.com/watch?v=VUfNxWdBV5k Video short - https://www.youtube.com/watch?v=Hpfe5WJ5g7I Abstract The 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.206135 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, biotechnology, artificial intelligence, healthy longevity About Aging-US The 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc Media Contact 18009220957 MEDIA@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.206188 Corresponding author - Moshe Szyf - moshe.szyf@epimedtech.com Video interview - https://www.youtube.com/watch?v=NA8Vctks0gY Video transcript - https://www.aging-us.com/interviews/epiage-ngs-based-elovl2-epigenetic-clock-for-biological-age-assessment Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206188 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, epigenetic clock, elovl2, next-generation sequencing, EpiAge, Alzheimer's disease About Aging-US The 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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.206187 Corresponding author - Olimpia Sipak - olimpiasipak-szmigiel@wp.pl Video short - https://www.youtube.com/watch?v=O0VMvqaVsUs Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206187 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, benign prostatic hyperplasia (BPH), metabolic syndrome (MetS), lipid markers, inflammation, fatty acids derivatives About Aging-US The 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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.206183 Corresponding author - Shubhankar Suman - ss2286@georgetown.edu Video short - https://www.youtube.com/watch?v=M_WEht4vy4w Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts About Aging-US The 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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 Healing Aging 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.206165 Corresponding author - Daniel S. Roh - droh@bu.edu Video short - https://www.youtube.com/watch?v=AKS7sZyEChg Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206165 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, senolytic, senescence, wound healing, ABT-263 About Aging-US The 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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.206182 Corresponding author - Brandon L. Pierce - brandonpierce@uchicago.edu Video short - https://www.youtube.com/watch?v=Jz-daRsZO2o Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts About Aging-US The 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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.206180 Corresponding author - Alexandro Andrade - alexandro.andrade.phd@gmail.com Video short - https://www.youtube.com/watch?v=uV4WXq7I_J0 About Aging-US The 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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 Fat The 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.206179 Corresponding author - Stephen F. Vatner - vatnersf@njms.rutgers.edu Video short - https://www.youtube.com/watch?v=n1DvuR7owJQ Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206179 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, brown adipose tissue, white adipose tissue, healthful longevity, exercise, regulator of G protein signaling 14 About Aging-US The 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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.206166 Corresponding author: Jonathan Singer - jonsinge@ttu.edu About Aging-US The 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.206165 Corresponding author - Daniel S. Roh - droh@bu.edu Video short - https://www.youtube.com/watch?v=AKS7sZyEChg About Aging-US The 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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.206174 Corresponding author - Pelin Analay - pelinanalay@yahoo.com Video short - https://www.youtube.com/watch?v=gDcQ9w6mHyE About Aging-US The 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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.206176 Corresponding author - Qinghong Li - qinghong.li@rd.nestle.com Video short - https://www.youtube.com/watch?v=WuEP9PXtx2A Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206176 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, trimethylamine N-oxide, indoxyl sulfate, OAT1, OATP4C1, ABCC2 About Aging-US The 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@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 Age Biological 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.206184 Corresponding author - Andrew E. Teschendorff - andrew@sinh.ac.cn Video short - https://www.youtube.com/watch?v=FjJa5U2-AqQ Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206184 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, DNA methylation, epigenetic clocks, cell-type deconvolution, biological aging, Alzheimer's disease, obesity About Aging-US The 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/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM