A traditional, twice-monthly, peer-reviewed, open-access journal covering all areas of research on aging and age-related diseases, including cancer and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. In June 2022, Web of
A research paper recently published in Aging, titled “Human-relevant Ptpn6 mutation alters immune and hepatic functions during aging,” investigated how a human-relevant mutation in the PTPN6 gene, which encodes the immune and metabolic regulator SHP-1, affects immune and liver function during aging. Using mice carrying the mutation, the researchers found that older mutant mice had improved glucose tolerance and hepatic insulin sensitivity, but also developed liver abnormalities characterized by increased fibrosis and the accumulation of immune cells, particularly B lymphocytes and macrophages. Further analyses indicated that these age-related changes were driven primarily by altered immune activity rather than direct effects within liver cells. The findings identify SHP-1 as an important regulator of liver immune homeostasis and provide new insight into how immune-cell infiltration may contribute to age-related changes in the liver. DOI - https://doi.org/10.18632/aging.206413 Corresponding author - André Marette - andre.marette@criucpq.ulaval.ca Abstract video - https://www.youtube.com/watch?v=lyn__UY9Buk Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206413 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, SHP-1/Ptpn6, B cell, macrophage, aging, Ptpn6Ala457Thr To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — September 16, 2026 — A new #research paper was #published in Volume 18 of Aging on August 28, 2026, titled “Human-relevant Ptpn6 mutation alters immune and hepatic functions during aging.” The study examines how a mutation affecting the immune and metabolic regulator SHP-1 reshapes liver function during aging, revealing that improved glucose metabolism can coexist with immune-cell accumulation and liver fibrosis. The research was led by first author Beisy Laborit Labrada from the Institut Universitaire de Cardiologie et de Pneumologie de Québec (CRIUCPQ), Université Laval, Québec, Canada. André Marette, from CRIUCPQ and the Department of Medicine at Université Laval, is the corresponding author. SHP-1, encoded by the PTPN6 gene, is a protein tyrosine phosphatase that helps regulate both immune responses and metabolic signaling. In immune cells, it generally restrains signaling pathways that control cellular activation, while in metabolic tissues it acts as a negative regulator of insulin signaling. This dual function places SHP-1 at an important intersection between immunity and metabolism, two systems that undergo substantial changes during aging. The study centered on a rare PTPN6Ala455Thr variant originally identified in a French-Canadian family with early-onset severe emphysema. The human mutation moderately reduces SHP-1 phosphatase activity. To investigate its longer-term effects, the researchers used mice carrying the corresponding Ptpn6Ala457Thr mutation and compared young adult mice at 5.6 months with older animals at 16–19 months. Unlike more severe SHP-1-deficient mouse models, these animals have lifespans comparable to wild-type mice, allowing the consequences of partial SHP-1 dysfunction to be examined across aging. Full press release - https://www.aging-us.com/news-room/human-relevant-ptpn6-mutation-reveals-complex-links-between-immunity-metabolism-and-liver-aging DOI - https://doi.org/10.18632/aging.206413 Corresponding author - André Marette - andre.marette@criucpq.ulaval.ca Abstract video - https://www.youtube.com/watch?v=lyn__UY9Buk Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206413 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, SHP-1/Ptpn6, B cell, macrophage, aging, Ptpn6Ala457Thr To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — September 14, 2026 — A new #review was #published in Volume 18 of Aging on August 26, 2026, titled “Assessing mechanisms and evidence of a causal role for cellular senescence and somatic mutations in aging.” The review examines two biological processes strongly associated with aging—cellular senescence and somatic DNA mutations—and evaluates whether the evidence supports their causal contribution to age-related functional decline. The review was authored by Lucrezia A. Trastus and Fabrizio d'Adda di Fagagna from IFOM ETS – The AIRC Institute of Molecular Oncology in Milan, Italy. d'Adda di Fagagna is also affiliated with the Istituto di Genetica Molecolare, Consiglio Nazionale delle Ricerche (IGM-CNR) in Pavia, Italy. Both authors are corresponding authors. Aging involves many interconnected molecular and cellular changes, making it difficult to distinguish processes that actively drive deterioration from those that simply accompany it. Trastus and d'Adda di Fagagna assess cellular senescence and somatic mutations using necessity and sufficiency as key criteria for causal inference. For cellular senescence, the evidence for causality is comparatively strong. Senescent cells undergo stable proliferative arrest, which can impair tissue regeneration, particularly when stem cells are affected. Their influence can extend far beyond individual cells through the senescence-associated secretory phenotype (SASP), a complex secretory program that allows senescent cells to alter surrounding tissues and promote senescence in neighboring cells. Full press release - https://www.aging-us.com/news-room/evidence-for-cellular-senescence-as-a-driver-of-aging-stronger-than-for-somatic-mutations DOI - https://doi.org/10.18632/aging.206414 Corresponding authors - Lucrezia A. Trastus - lucrezia.trastus@ifom.eu, Fabrizio d'Adda di Fagagna - fabrizio.dadda@ifom.eu Abstract video - https://www.youtube.com/watch?v=XHTBAJHjRZU Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206414 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, cellular senescence, somatic mutations, DNA damage, SASP To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
Scientific progress often begins with questioning assumptions that have shaped a field for decades. Few researchers embodied this approach as strongly as Dr. Mikhail “Misha” Blagosklonny, an oncologist and biogerontologist whose unconventional theories challenged traditional explanations of why organisms age. An essay published in Volume 18 of Aging titled “Misha Blagosklonny: a life of ideas,” reflects on Dr. Blagosklonny's life, scientific career, and contributions to the biology of aging. Full blog post - https://aging-us.org/2026/09/misha-blagosklonnys-ideas-reshaped-thinking-about-aging/ Paper DOI - https://doi.org/10.18632/aging.206412 Corresponding author - David Gems - david.gems@ucl.ac.uk Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206412 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, hyperfunction, programmatic theory, disposable soma 2, quasi-program, biogerontology, evolutionary physiology, Mikhail Blagosklonny To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — September 10, 2026 — A new #research paper was #published in Volume 18 of Aging on August 24, 2026, titled “Disruption of the insulin/IGF-1 signaling pathway in Caenorhabditis elegans dramatically increases male longevity and enhances reproductive health late in life.” The research was conducted by Rose S. Al-Saadi, Hannah B. Lewack and Patrick C. Phillips. Al-Saadi and Lewack contributed equally to the study. Al-Saadi and Phillips are from the Institute of Ecology and Evolution at the University of Oregon, while Lewack is affiliated with both the Institute of Ecology and Evolution at the University of Oregon and the Department of Molecular Biology at the University of California, San Diego. Phillips is the corresponding author. Insulin/IGF-1 signaling (IIS) is one of the best-established molecular pathways regulating longevity across animal species. In C. elegans, the gene DAF-2 encodes an insulin/IGF-1 receptor, and reducing its activity can substantially extend lifespan. However, most previous aging studies in this model have focused on hermaphrodites, leaving considerably less known about how males respond to interventions targeting the same pathway. To investigate these sex-specific effects, the researchers used an auxin-inducible degron system to selectively degrade the DAF-2 receptor throughout the body or within particular tissues. When DAF-2 was degraded throughout the body, the effect on male longevity was striking: median lifespan increased by 446%, compared with a 109% increase in hermaphrodites exposed to the same intervention. The age at which 10% of the population remained alive reached 106 days in treated males, compared with 15 days in controls. The authors describe this as one of the largest lifespan extensions reported in C. elegans—or any animal—from a single intervention. Full press release - https://www.aging-us.com/news-room/reduced-insulin-igf-1-signaling-dramatically-extends-male-lifespan-in-c-elegans DOI - https://doi.org/10.18632/aging.206411 Corresponding author - Patrick C. Phillips - pphil@uoregon.edu Abstract video - https://www.youtube.com/watch?v=zQ32BnBwEBI Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206411 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, Insulin/IGF-1 signaling, sex differences, Caenorhabditis elegans, reproductive health To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — September 9, 2026 — A new #research paper was #published in Volume 18 of Aging on August 13, 2026, titled “Protective effects of three herbal extracts on mitochondrial dysfunction in VPS13C-knockdown SH-SY5Y cells: implications for Parkinson's disease.” The study was led by co-first authors Yih-Ru Wu and Chih-Hsin Lin from the Chang Gung Memorial Hospital, Chang Gung University College of Medicine in Taoyuan, Taiwan, and Pei-Syuan Huang from the School of Life Science at National Taiwan Normal University in Taipei, Taiwan. Corresponding authors I-Cheng Chen and Guey-Jen Lee-Chen are from the School of Life Science at National Taiwan Normal University. The paper identifies Wu, Lin, and Huang as equal contributors. Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized primarily by dysfunction and loss of dopaminergic neurons in the substantia nigra. Although its causes are complex, mitochondrial dysfunction and oxidative stress are important biological processes implicated in both sporadic and inherited forms of the disease. The researchers focused on VPS13C, also known as PARK23, a gene associated with a rare autosomal recessive form of early-onset parkinsonism. Loss of VPS13C function has previously been linked to impaired mitochondrial function. The study investigated three extracts used in traditional Chinese medicine: Uncaria rhynchophylla (UR), Gardenia jasminoides (GJ), and Scutellaria baicalensis (SB). Previous experimental studies have reported neuroprotective effects from these plants or their bioactive constituents in models relevant to PD. The researchers examined whether the extracts could protect cells against mitochondrial dysfunction associated with reduced VPS13C expression. Chemical analyses identified several potentially bioactive constituents in the extracts. UR contained rhynchophylline and isorhynchophylline; GJ contained geniposide and crocin; and SB contained several flavonoids, including baicalin, wogonoside, baicalein, wogonin, and oroxylin A. Across the concentrations initially tested, the three extracts maintained greater than 90% viability in SH-SY5Y cells after 24 hours, indicating low cytotoxicity under these experimental conditions. Full press release - https://www.aging-us.com/news-room/three-herbal-extracts-protect-mitochondrial-function-in-a-cellular-model-of-parkinsons-disease DOI - https://doi.org/10.18632/aging.206409 Corresponding authors - I-Cheng Chen - ichen@ntnu.edu.tw, Guey-Jen Lee-Chen - t43019@ntnu.edu.tw Abstract video - https://www.youtube.com/watch?v=kM8hO89d_9k Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206409 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, Parkinson's disease, traditional Chinese medicine, VPS13C knockdown, mitochondrial dysfunction, oxidative stress To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
Dr. Falak Pahwa, Dr. Ranjan Kumar Nanda, and Mr. Ashish Gupta from the International Centre for Genetic Engineering and Biotechnology (ICGEB) in New Delhi, India, discuss their research paper, recently published in Volume 18 of Aging, titled “Host immunosenescence compromises Mycobacterium tuberculosis clearance.” Video interview - https://www.youtube.com/watch?v=bSaJaB751kM DOI - https://doi.org/10.18632/aging.206374 Corresponding author - Ranjan Kumar Nanda - ranjan@icgeb.res.in Abstract video - https://www.youtube.com/watch?v=isPD8ZmUjv8 Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206374 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, tuberculosis, immunosenescence, TFH cells, proteomics To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — September 3, 2026 — A new #research paper was published in Volume 18 of Aging on August 12, 2026, titled “Indy reduction decreases aging-related dysbiosis in Drosophila.” The study was led by first author Danielle N. A. Lesperance from the University of Connecticut. Corresponding authors Blanka Rogina and Nichole A. Broderick are affiliated with the University of Connecticut Health and Johns Hopkins University, respectively. Broderick is also affiliated with the University of Connecticut. The Indy gene—short for “I'm not dead yet”—encodes a plasma membrane citrate transporter in Drosophila melanogaster. Previous research has shown that reducing Indy activity can extend lifespan and preserve metabolic and intestinal health in flies. Because aging is also associated with disruption of the gut microbiota, the researchers investigated whether changes in intestinal microbes contribute to the longevity effects associated with reduced Indy activity. The researchers compared control flies with Indy heterozygous flies under conventional conditions and axenic conditions, in which microbes were absent. They also examined bacterial load and microbiota composition and performed RNA sequencing of the midgut to investigate molecular pathways connecting Indy, the microbiota, intestinal homeostasis, and aging. Full press release - https://www.aging-us.com/news-room/indy-gene-reduction-linked-to-healthier-gut-microbiota-and-longer-lifespan-in-fruit-flies DOI - https://doi.org/10.18632/aging.206408 Corresponding authors - Blanka Rogina - Rogina@uchc.edu, and Nichole A. Broderick - nbroder1@jhu.edu Abstract video - https://www.youtube.com/watch?v=d0PfTj_Pg7U Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206408 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, Indy, host-microbe interactions, lifespan, Drosophila melanogaster To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
Why do we age? For decades, one of the dominant explanations has been that cells and tissues gradually accumulate molecular damage until they can no longer function normally. DNA mutations, damaged proteins, mitochondrial dysfunction, epigenetic alterations, and other forms of cellular wear have all been proposed as major drivers of aging. But another theory offers a very different possibility: some aspects of aging may result not from biological systems breaking down, but from developmental programs continuing to operate after they are no longer beneficial. A research perspective published in Volume 18 of Aging titled “A brief history of the hyperfunction theory of aging and future directions,” traces the development of this idea and examines where the field may go next. The article was written by João Pedro de Magalhães from the Genomics of Ageing and Rejuvenation Lab, Department of Inflammation and Ageing, College of Medicine and Health, University of Birmingham, United Kingdom. Rather than presenting a new experiment, the paper combines historical analysis, evolutionary theory, experimental evidence, and the author's own perspective on how programmatic models could reshape aging research. Full blog post - https://aging-us.org/2026/09/developmental-programs-could-help-drive-the-aging-process/ DOI - https://doi.org/10.18632/aging.206403 Corresponding author - João Pedro de Magalhães - jp@senescence.info Abstract video - https://www.youtube.com/watch?v=VwC6aJoUUQo Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206403 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, antagonistic pleiotropy, longevity, programmatic aging, quasi-program To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — August 31, 2026 — A new research paper was published in Volume 18 of Aging on August 11, 2026, titled “TMAO is associated with higher age, cardiometabolic risk factors and degenerative alterations of the brain in healthy elderly adults.” The study was led by first author Gunter Almer from the Clinical Institute of Medical and Chemical Laboratory Diagnostics at the Medical University of Graz in Austria. The corresponding author is Markus Herrmann from the same institution. Trimethylamine N-oxide (TMAO) is a metabolite linked to the gut microbiome. Its precursor, trimethylamine (TMA), is produced by gut bacteria from dietary compounds such as L-carnitine and choline and is subsequently converted to TMAO in the liver. Higher circulating TMAO concentrations have previously been associated with cardiovascular and metabolic diseases, but evidence concerning its role in aging and neurodegeneration remains inconsistent. To investigate these relationships, the researchers measured serum TMAO in 487 neurologically normal, community-dwelling adults from the Austrian Stroke Prevention Study and Austrian Stroke Prevention Family Study. Participants had a mean age of 67.8 years and underwent cognitive testing assessing memory, executive function, and motor abilities. Brain MRI data were also available for 180 participants, allowing the researchers to examine structural and vascular brain changes. Full press release - https://www.aging-us.com/news-room/higher-tmao-levels-linked-to-cardiometabolic-risk-and-brain-atrophy-in-older-adults Paper DOI: https://doi.org/10.18632/aging.206401 Corresponding author: Markus Herrmann - markus.herrmann@medunigraz.at Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords: TMAO, aging, risk factors, cognitive function, brain atrophy To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — August 26, 2026 — A new #review was #published in Volume 18 of Aging on August 10, 2026, titled “Metformin at the convergence of aging and longevity.” The review was authored by Jarra Manneh, May Alasmar and Nady El Hajj from the College of Health and Life Sciences at Hamad Bin Khalifa University, Qatar Foundation, Doha, Qatar. Corresponding author Nady El Hajj is also affiliated with the College of Science and Engineering at Hamad Bin Khalifa University, Doha, Qatar. Metformin has been used for decades as a first-line treatment for type 2 diabetes, but increasing interest in geroscience has raised a broader question: could this widely used metabolic drug also influence the biological processes that drive aging? The review brings together evidence from cellular studies, animal models, human observational research, and clinical trials examining how metformin interacts with multiple hallmarks of aging. A central mechanism involves AMP-activated protein kinase (AMPK), a major cellular energy sensor. By inhibiting mitochondrial complex I and altering cellular energy balance, metformin can activate AMPK, triggering downstream effects that include suppression of mechanistic target of rapamycin (mTOR) signaling, increased autophagy and mitochondrial biogenesis, and reduced oxidative stress. Metformin also improves insulin sensitivity and reduces hepatic gluconeogenesis, connecting its established metabolic effects with nutrient-sensing pathways involved in aging biology. Full press release - https://www.aging-us.com/news-room/metformin-emerges-as-a-promising-candidate-at-the-intersection-of-aging-and-longevity DOI - https://doi.org/10.18632/aging.206407 Corresponding author - Nady El Hajj - nelhajj@hbku.edu.qa Abstract video - https://www.youtube.com/watch?v=5Ws-x8e1klI Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206407 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, metformin, AMPK, mTOR, epigenetic modifications To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — August 24, 2026 — A new research paper was published in Volume 18 of Aging on August 8, 2026, titled “Investigating POLG-driven modulation of cancer stemness: a pilot study in breast cancer cells.” The study was led by first author Chiara Chinigò from the Italian National Research Center on Aging (IRCCS INRCA), Cosenza, Italy. Corresponding authors Federica Sotgia and Michael P. Lisanti are affiliated with the University of Salford, United Kingdom, and Lunella Biotech in Ottawa, Canada, with Lisanti additionally affiliated with the Institute of Mental Health Research at the University of Ottawa and The Royal Ottawa Hospital, and Université Laval in Québec. Breast cancer stem cells (CSCs) are a small population of tumor cells with self-renewal and differentiation capabilities that are associated with tumor progression, metastasis, and therapy resistance. These cells rely heavily on mitochondrial biogenesis and oxidative metabolism, making mitochondrial function a potential metabolic vulnerability. The researchers focused on mitochondrial DNA polymerase gamma (POLG), the enzyme responsible for mitochondrial DNA (mtDNA) replication and repair. POLG contains a catalytic subunit encoded by POLG1 and an accessory subunit encoded by POLG2. Using estrogen receptor-positive MCF-7 breast cancer cells, the researchers genetically silenced POLG1 and POLG2 to determine whether disrupting mtDNA maintenance would affect cancer stemness. POLG1 knockdown reduced mtDNA content by approximately 80%, while POLG2 knockdown produced an approximately 70% reduction. Both interventions impaired mitochondrial function, lowering the mtDNA-encoded respiratory-chain protein MTCO2, mitochondrial membrane potential, respiration, and ATP production. Full press release - https://www.aging-us.com/news-room/targeting-polg-reduces-breast-cancer-stemness-through-mitochondrial-dysfunction DOI - https://doi.org/10.18632/aging.206406 Corresponding authors - Federica Sotgia - fsotgia@gmail.com (ORCiD: 0000-0003-2826-4529), Michael P. Lisanti - michaelp.lisanti@gmail.com (ORCiD: 0000-0003-2034-1382) Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206406 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, breast cancer, cancer stem cells, cancer metabolism, POLG, mitochondrial DNA To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — August 24, 2026 — Aging is pleased to announce its partnership as a media partner of the 13th Aging Research and Drug Discovery Meeting (ARDD), taking place October 1–3, 2026, at the David Rubenstein Treehouse at Harvard University in Boston, Massachusetts. ARDD brings together leading researchers, clinicians, biotech innovators and industry experts to advance the understanding of aging and accelerate the development of interventions targeting age-related diseases. The partnership reflects Aging's continued commitment to supporting the growth and visibility of research in the fields of aging and longevity. As a media partner, Aging will help promote ARDD and raise awareness of the meeting through its digital and social media channels, connecting the event with the journal's global audience. Together, Aging and ARDD will help bring greater visibility to the growing scientific community working to advance healthy longevity and address age-related diseases. To learn more about the journal, please visit www.Aging-US.com and connect with us on social media at: Bluesky - bsky.app/profile/aging-us.bsky.social ResearchGate - www.researchgate.net/journal/Aging-1945-4589 X - twitter.com/AgingJrnl Facebook - www.facebook.com/AgingUS/ Instagram - www.instagram.com/agingjrnl/ LinkedIn - www.linkedin.com/company/aging/ Reddit - www.reddit.com/user/AgingUS/ Pinterest - www.pinterest.com/AgingUS/ YouTube - www.youtube.com/@Aging-US Spotify - open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
A #Research paper recently #Published in Volume 18 of Aging, titled “Slowing intervertebral disc aging in mice through long-term systemic treatment with the senolytic BCL-2/BCL-xL proteolysis targeting chimera (PROTAC) 753b,” examines whether the senolytic PROTAC 753b can slow age-related intervertebral disc degeneration (IDD) in mice. Long-term systemic treatment with 753b reduced key features of disc degeneration in 22-month-old male mice, including matrix breakdown, loss of disc aggrecan, age-related structural changes, and inflammatory markers such as IL-6 and TNFα. These benefits, however, were not observed in female mice, highlighting potential sex-based differences in the role of cellular senescence in IDD and the response to senolytic therapies. DOI - https://doi.org/10.18632/aging.206394 Corresponding author - Nam Viet Vo - nvv1@pitt.edu Abstract video - https://www.youtube.com/watch?v=t0z4MULDr1A Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206394 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, intervertebral disc aging, cellular senescence, senolytic, anti-apoptosis, PROTAC-753b To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — August 12, 2026 — A new #research paper was #published in Volume 18 of Aging on July 27, 2026, titled “Transcriptomic aging clock analysis identifies key genes in opioid dependence.” The study was led by first author Hai Duc Nguyen from the Division of Microbiology, Tulane National Biomedical Research Center, Tulane University. The corresponding author is Woong-Ki Kim, who is affiliated with the Division of Microbiology, Tulane National Biomedical Research Center, Tulane University, and the Department of Microbiology and Immunology at Tulane University School of Medicine. Opioid dependence is a chronic and relapsing condition associated with substantial health and societal burdens. Chronic opioid exposure can affect neuronal signaling, immune function, metabolism, and other biological processes, yet the molecular mechanisms underlying dependence remain incompletely understood. Increasing evidence also suggests that substance use disorders may be associated with molecular changes related to aging, raising questions about how chronic opioid exposure interacts with age-dependent processes in the brain. To investigate these relationships, the researchers conducted an in silico study integrating three complementary approaches: RNA sequencing-based transcriptomic profiling, transcriptomic aging-clock modeling, and analysis of previously published genome-wide association studies (GWAS). The transcriptomic analysis used a publicly available brain RNA-seq dataset containing 42 samples—21 healthy controls and 21 individuals with opioid dependence—while the genetic analysis incorporated findings from six independent GWAS. Full press release - https://www.aging-us.com/news-room/transcriptomic-aging-clock-reveals-age-related-molecular-patterns-in-opioid-dependence DOI - https://doi.org/10.18632/aging.206405 Corresponding author - Woong-Ki Kim - wkim6@tulane.edu Abstract video - https://www.youtube.com/watch?v=7VwU0mFGkbg Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206405 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, opioids, GWAS, transcriptomic clock To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — August 10, 2026 — A new #essay was #published in Volume 18 of Aging on August 6, 2026, titled “Misha Blagosklonny: a life of ideas.” The article was written by Aging Editorial Board member David Gems from the Institute of Healthy Ageing and Research Department of Genetics, Evolution and Environment, University College London, United Kingdom, along with Aging Editor-in-Chief Marco Demaria from the European Research Institute for the Biology of Ageing (ERIBA), University Medical Center Groningen (UMCG), University of Groningen, the Netherlands. Rather than presenting new experimental findings, the essay examines the life, scientific contributions, and lasting influence of Mikhail (“Misha”) Blagosklonny, whose ideas had a major influence on modern thinking about the biological mechanisms of aging. Dr. Blagosklonny was trained as a physician and experimental scientist before building an influential career in oncology and aging research after moving to the United States. His work combined cancer biology with theoretical biogerontology, leading to the proposal that aging is driven not primarily by the passive accumulation of molecular damage, but by developmental and growth-related programs that continue beyond their beneficial period. Through what he described as conceptual research, Misha synthesized evidence from diverse experimental studies to generate new hypotheses about aging and reinterpret existing biological observations. A central theme of the essay is Dr. Blagosklonny's development of the hyperfunction theory of aging. Building on observations that persistent activation of the mechanistic target of rapamycin (mTOR) pathway can drive cellular senescence, he proposed that many features of aging arise from the continued activity of biological programs that promote growth and reproduction earlier in life. Rather than viewing aging as an adaptive genetic program, Misha argued that it represents a quasi-program—a genetically determined continuation of normal developmental processes that become harmful later in life. This framework provided a mechanistic explanation linking evolutionary concepts such as antagonistic pleiotropy with molecular pathways that regulate growth, metabolism, and cellular senescence. Full press release - https://www.aging-us.com/news-room/misha-blagosklonnys-scientific-legacy-continues-to-shape-modern-aging-research DOI - https://doi.org/10.18632/aging.206412 Corresponding author - David Gems - david.gems@ucl.ac.uk Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206412 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, hyperfunction, programmatic theory, disposable soma 2, quasi-program, biogerontology, evolutionary physiology, Mikhail Blagosklonny To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — August 6, 2026 — A new #research perspective was #published in Volume 18 of Aging on July 24, 2026, titled “A brief history of the hyperfunction theory of aging and future directions.” The article was written by João Pedro de Magalhães from the Genomics of Ageing and Rejuvenation Lab, Department of Inflammation and Ageing, College of Medicine and Health, University of Birmingham, United Kingdom. Rather than presenting new experimental findings, the perspective examines the historical development of the hyperfunction theory of aging, reviews evidence supporting programmatic mechanisms of aging, and discusses future directions for understanding why organisms age and how aging might eventually be modified. For decades, most aging research has been dominated by the idea that aging results primarily from the gradual accumulation of molecular damage, including DNA damage, oxidative stress, mitochondrial dysfunction, and protein deterioration. In contrast, the hyperfunction theory proposes that aging is driven largely by developmental and growth programs that continue operating beyond their beneficial period. Rather than being intentionally programmed, aging is viewed as a consequence of biological pathways that promote growth and reproduction early in life but become harmful when they continue later in adulthood. The perspective traces the historical roots of these ideas from early theories proposed in the nineteenth century through Clive McCay's pioneering caloric restriction experiments and George Williams' concept of antagonistic pleiotropy. Particular attention is given to the contributions of the late Mikhail Blagosklonny, whose hyperfunction theory proposed that aging results from “quasi-programs”—developmental processes that fail to switch off after their normal biological role has ended. The author argues that this framework provides a mechanistic explanation linking evolutionary theory with many biological features of aging. Full press release - https://www.aging-us.com/news-room/hyperfunction-theory-offers-a-new-perspective-on-why-we-age Paper DOI - https://doi.org/10.18632/aging.206403 Corresponding author - João Pedro de Magalhães - jp@senescence.info Abstract video - https://www.youtube.com/watch?v=VwC6aJoUUQo Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206403 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, antagonistic pleiotropy, longevity, programmatic aging, quasi-program To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
In this episode of the Longevity & Aging Series (S4, E5), Dr. Kan Cao of the Department of Cell Biology and Molecular Genetics at the University of Maryland joins host Dr. Yuan Zhao to discuss the research paper she co-authored in Volume 18 of Aging, titled “Methylene blue protects hair follicle stem cells from oxidative and metabolic stress to enhance hair regeneration.” Interview video - https://www.youtube.com/watch?v=2Por-Wh3AWo DOI - https://doi.org/10.18632/aging.206376 Corresponding author - Kan Cao - kcao@umd.edu Longevity & Aging Series - https://www.aging-us.com/longevity About Dr. Yuan Zhao - https://www.qmul.ac.uk/sbbs/staff/yuan-zhao.html Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206376 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, methylene blue, minoxidil, HFSCs, Wnt/β-catenin, GLP-1 RA To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — August 5, 2026 — A new #research paper was #published in Volume 18 of Aging on July 23, 2026, titled “Adipo-neuroinflammation, cognitive impairment and surrogate markers of cardiovascular risk in patients with Metabolic Dysfunction Associated Steatotic Liver Disease (MASLD).” The study was led by co-first authors Gaetano Pacinella from the University of Palermo, and the Internal Medicine and Stroke Care Ward, Policlinico “P. Giaccone”, Palermo, and Alessandro Del Cuore from the same institutions. Gaetano Pacinella also served as the corresponding author. Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as nonalcoholic fatty liver disease, is increasingly recognized as a systemic condition that extends beyond the liver. People with MASLD have an elevated risk of cardiovascular disease, cognitive decline, and other metabolic complications, yet the biological mechanisms connecting these conditions remain incompletely understood. In this study, researchers investigated whether lipocalin-2 (LCN2), a protein involved in inflammatory and metabolic signaling, is associated with early vascular dysfunction, cognitive impairment, and cardiovascular risk in patients with MASLD. Full press release - https://www.aging-us.com/news-room/fatty-liver-disease-linked-to-early-cardiovascular-and-cognitive-changes DOI - https://doi.org/10.18632/aging.206397 Corresponding author - Gaetano Pacinella - gaetano.pacinella@unipa.it Abstract video - https://www.youtube.com/watch?v=CrqTayKl8KI Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206397 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, metabolic dysfunction, cardiovascular risk, lipocalin-2, cognitive impairment, endothelial dysfunction To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
Heart failure remains one of the leading causes of hospitalization among older adults worldwide. During episodes of acute decompensated heart failure (ADHF), excess fluid builds up in the lungs and body, making breathing difficult and increasing the risk of serious complications. Although intravenous loop diuretics such as furosemide are the standard treatment for relieving congestion, many patients continue to experience persistent inflammation, ongoing cardiac remodeling, and worsening heart function despite therapy. A research paper published in Volume 18 of Aging titled “Effects of intravenous furosemide plus small-volume hypertonic saline solutions on inflammatory, remodelling markers and epigenetics signatures of patients with congestive acute decompensated heart failure (ADHF),” investigated whether combining intravenous furosemide with small volumes of hypertonic saline solution (HSS) could improve biological markers associated with heart failure compared with furosemide alone. Full blog post - https://aging-us.org/2026/08/hypertonic-saline-plus-furosemide-improves-heart-failure-biomarkers-in-randomized-trial/ DOI - https://doi.org/10.18632/aging.206364 Corresponding author - Antonino Tuttolomondo - bruno.tuttolomondo@unipa.it Abstract video - https://www.youtube.com/watch?v=EG65XlcDJ3U Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206364 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, heart failure, acute decompensated heart failure, furosemide, hypertonic saline solution To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — August 3, 2026 — A new #research paper was #published in Volume 18 of Aging on July 17, 2026, titled “Selective targeting of cancer and senescence via shared metabolic shifts extends lifespan of old mice.” The study was led by first author Zachery R. Robinson, and corresponding author and Aging editorial board member Irina M. Conboy, both from the Department of Bioengineering and QB3 Institute, University of California, Berkeley. The researchers developed a new combination therapy that selectively targets both cancer cells and senescent cells by exploiting metabolic vulnerabilities shared by these two cell types. In laboratory studies and aged mice, the treatment selectively eliminated senescent cells and reduced cancer cell viability while improving physical performance and extending lifespan without significant toxicity to healthy tissues. Cancer and aging are closely linked. As people age, senescent cells accumulate throughout the body. Although these cells no longer divide, they remain metabolically active and release inflammatory molecules known as the senescence-associated secretory phenotype (SASP), which contributes to chronic inflammation, tissue dysfunction, and tumor progression. Existing therapies such as the BCL-2/BCL-xL inhibitor navitoclax (ABT-263) can eliminate both cancer cells and senescent cells but require doses that frequently cause thrombocytopenia, a potentially serious reduction in platelet counts that has limited their clinical use. Full press release - https://www.aging-us.com/news-room/new-drug-combination-targets-cancer-and-senescent-cells-while-extending-lifespan-in-old-mice DOI - https://doi.org/10.18632/aging.206399 Corresponding author - Irina M. Conboy - irina@generationlab.co Abstract video - https://www.youtube.com/watch?v=7p5JMvy9Twg Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206399 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, senescence, cancer, metabolic shift, ATP To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 30, 2026 — A new #research perspective was #published in Volume 18 of Aging on July 16, 2026, titled “Towards integration of healthspan strategies into the Italian National Health Service.” The article was led by co-first authors Nicola Marino, affiliated with the AEON Foundation and the Women's Brain Foundation, and Matteo Fiore from the University of Bologna, with both serving as corresponding authors. Rather than presenting new clinical trial results, the authors propose a prevention-focused framework for the staged, evidence-based evaluation and integration of healthspan strategies into Italy's National Health Service (Servizio Sanitario Nazionale, SSN) to help address the challenges of an aging population. Italy has one of the oldest populations in the world. Although life expectancy has continued to increase, many older adults spend a substantial portion of those additional years living with chronic disease, disability, or reduced physical and cognitive function. The authors describe this mismatch as the lifespan–healthspan divide and argue that healthcare systems should increasingly focus not only on helping people live longer, but also on extending the years they remain healthy and functionally independent. To address this challenge, the authors outline the concept of longevity medicine, describing it as a prevention-oriented, life-course framework rather than a new medical specialty. The approach integrates principles from geroscience, preventive medicine, and personalized healthcare with the goal of identifying age-related risks earlier and promoting healthy aging before chronic diseases and functional limitations accumulate. At the same time, the paper emphasizes that many emerging tools—including biological-age biomarkers, multi-omic profiling, wearable sensor data, and artificial intelligence-based risk stratification—remain exploratory and should not be adopted routinely until they demonstrate clear clinical utility, cost-effectiveness, and meaningful benefits for patients. Full press release - https://www.aging-us.com/news-room/italy-proposes-a-healthspan-focused-framework-for-healthy-aging DOI - https://doi.org/10.18632/aging.206402 Corresponding authors - Nicola Marino - marino@aeonfoundation.eu, and Matteo Fiore - matteo.fiore@auslromagna.it Abstract video - https://www.youtube.com/watch?v=uc1tGVfiHMw Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206402 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, preventive, longevity, national health system, health span, biomarkers To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 27, 2026 — A new #research paper was #published in Volume 18 of Aging on July 13, 2026, titled “Slowing intervertebral disc aging in mice through long-term systemic treatment with the senolytic BCL-2/BCL-xL proteolysis targeting chimera (PROTAC) 753b.” The study was led by first author Peter G. Alexander from the Ferguson Laboratory for Spine Research, Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine, and corresponding author Nam Viet Vo from the same institution. Intervertebral disc degeneration is a leading cause of chronic low back pain and disability. As discs age, they lose important structural components, become less able to absorb mechanical stress, and accumulate senescent cells—dysfunctional cells that stop dividing but continue releasing inflammatory molecules that contribute to tissue degeneration. Senolytic therapies, which selectively eliminate these cells, have emerged as a promising strategy to slow age-related diseases. In this study, researchers evaluated PROTAC 753b, a next-generation senolytic designed to target the anti-apoptotic proteins BCL-2 and BCL-xL while reducing the platelet toxicity associated with earlier drugs in this class. The researchers treated 16-month-old male and female mice with PROTAC 753b for six months and evaluated their intervertebral discs at 22 months of age using histology, molecular analyses, and measurements of inflammatory markers. The treatment significantly improved several measures of intervertebral disc health in aged male mice, preserving the extracellular matrix protein aggrecan and reducing matrix metalloproteinase (MMP)-mediated aggrecan breakdown, a hallmark of disc degeneration. In contrast, female mice showed little overall improvement, revealing a sex-specific response to treatment. Full press release - https://www.aging-us.com/news-room/senolytic-protac-slows-age-related-intervertebral-disc-degeneration-in-male-mice DOI - https://doi.org/10.18632/aging.206394 Corresponding author - Nam Viet Vo - nvv1@pitt.edu Abstract video - https://www.youtube.com/watch?v=t0z4MULDr1A Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206394 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, intervertebral disc aging, cellular senescence, senolytic, anti-apoptosis, PROTAC-753b To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 23, 2026 — A new #research paper was #published in Volume 18 of Aging on July 8, 2026, titled “TM4SF1 is a surface marker of senescent pancreatic β-cells.” The study was led by first author Ana Beathriz Leite Lorente from Joslin Diabetes Center and Harvard Medical School, and São Paulo State University (UNESP), Brazil, and corresponding author Cristina Aguayo-Mazzucato from Joslin Diabetes Center and Harvard Medical School. Type 2 diabetes is characterized by insulin resistance and the progressive loss of pancreatic β-cell function. With aging and metabolic stress, senescent β-cells accumulate within the pancreas, producing less insulin while releasing inflammatory signals that contribute to disease progression. Although eliminating these dysfunctional cells has emerged as a promising therapeutic strategy, a major challenge has been identifying markers that distinguish senescent β-cells from healthy cells with sufficient precision. This study identifies transmembrane 4 L six family member 1 (TM4SF1) as a highly selective surface marker of senescent β-cells, providing a promising candidate for the future development of more selective therapies for type 2 diabetes. In this study, the researchers searched for cell-surface proteins that specifically identify senescent β-cells. Using RNA sequencing, flow cytometry, immunofluorescence, and analyses of both mouse and human pancreatic tissue, they compared TM4SF1 with the previously established senescence marker urokinase-type plasminogen activator receptor (uPAR/PLAUR). Their findings showed that TM4SF1 is expressed predominantly in senescent β-cells while exhibiting much lower expression in non-senescent β-cells and other tissues, making it a more β-cell-specific surface marker than uPAR. Full press release - https://www.aging-us.com/news-room/new-surface-marker-could-advance-precision-therapies-for-type-2-diabetes DOI - https://doi.org/10.18632/aging.206398 Corresponding author - Cristina Aguayo-Mazzucato - Cristina.aguayo-mazzucato@joslin.harvard.edu Abstract video - https://www.youtube.com/watch?v=tNbFKdleTJo Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206398 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, senescent β-cell, type 2 diabetes, transmembrane 4 l six family member 1, urokinase-type plasminogen activator receptor To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
Coordinating both hands is something most people take for granted. Everyday activities such as buttoning a shirt, preparing a meal, driving, or using a knife and fork all depend on the brain's ability to precisely control movements on both sides of the body. As people age, however, these tasks often become more difficult, especially when they require both hands to perform different movements at the same time. A research paper published in Volume 18 of Aging titled “Age-specific relationship between the modulation of brain dynamics in response to task demands and bimanual performance,” investigated how aging affects the brain's ability to adapt to increasingly complex hand-coordination tasks. The study was led by first author Sara Magalhães Ferreira from Hasselt University, with corresponding author Koen Cuypers from Hasselt University and KU Leuven. Full blog - https://aging-us.org/2026/07/brain-flexibility-is-linked-to-hand-coordination-during-aging/ DOI - https://doi.org/10.18632/aging.206363 Corresponding author - Koen Cuypers - koen.cuypers@uhasselt.be Abstract video - https://www.youtube.com/watch?v=3TbcGFCZV9s Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206363 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, bimanual coordination, Bimanual Tracking Task, BOLD variability, task modulation To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 21, 2026 — A new #research paper was #published in Volume 18 of Aging on July 6, 2026, titled “Inhibition of peroxisomal protein PRX-11 promotes longevity in Caenorhabditis elegans via enhancements to mitochondria.” The study was authored by Yash Flora, Dhriti Shastri, Kathryn R. DeLeo, and K. Adam Bohnert from the Department of Biological Sciences, Louisiana State University. Aging is accompanied by the gradual decline of many cellular structures that help maintain healthy tissues and organs. Among these are peroxisomes, which play essential roles in breaking down toxic molecules and metabolizing lipids, and mitochondria, which generate most of the cell's energy. Although these organelles work closely together, little has been known about how changes in one influence the aging of the other. This new study reveals that preserving peroxisomes helps maintain healthier mitochondria and extends lifespan in the nematode Caenorhabditis elegans, providing new insight into how communication between cellular organelles influences aging. In this study, the researchers investigated the function of PRX-11, a peroxisomal protein involved in peroxisome division. Previous work from the group showed that reducing PRX-11 activity prevents the age-related degradation of peroxisomes through a process known as pexophagy and increases lifespan. The new study explored why preserving peroxisomes produces these beneficial effects and found that maintaining peroxisomes also preserves mitochondrial health during aging. The researchers found that animals with reduced PRX-11 activity retained long, interconnected mitochondrial networks that resembled those seen in young adults, whereas normal aging was associated with progressive mitochondrial fragmentation. These preserved mitochondria also accumulated less calcium, generated lower levels of oxidative stress, maintained higher ATP-to-ADP ratios, and were associated with improved locomotor function in older animals. Together, these findings indicate that preventing age-related peroxisome loss supports multiple aspects of mitochondrial function during aging. Full press release - https://www.aging-us.com/news-room/preserving-peroxisomes-helps-maintain-mitochondrial-health-and-extend-lifespan-in-c-elegans DOI - https://doi.org/10.18632/aging.206395 Corresponding author - K. Adam Bohnert - bohnerta@lsu.edu Abstract video - https://www.youtube.com/watch?v=fbcqBsP90CY Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206395 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, cellular aging, lifespan, pexophagy, mitochondrial tubulation, inter-organelle crosstalk To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
Each month, we will highlight a paper published in Aging chosen as the “Editors' Choice.” These selections are handpicked by our editors and accompanied by a brief summary, showcasing research with significant impact and novel insights in aging and age-related diseases. Cellular senescence is a hallmark of aging and age-related disease, yet the diverse mechanisms that trigger this cellular state remain incompletely understood. The review recently published in Volume 18 of Aging, titled “The multifaceted inducers of cellular senescence,” examines the many intrinsic and extrinsic stimuli that induce senescence, including DNA damage, oxidative and mitochondrial stress, telomere attrition, oncogene activation, cell–cell fusion, and developmental signals. The authors, Hilah Gal and Valery Krizhanovsky, explain how these distinct pathways converge on a stable cell-cycle arrest. By highlighting the complexity and heterogeneity of senescent cells, the authors provide valuable insights that may guide the development of future therapies targeting senescence to promote healthy aging and combat age-related diseases. DOI - https://doi.org/10.18632/aging.206391 Corresponding author - Valery Krizhanovsky - valery.krizhanovsky@weizmann.ac.il Abstract video - https://www.youtube.com/watch?v=5Y7R_8GQ1gk Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206391 Keywords - aging, cell senescence To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 16, 2026 — A new #research paper was #published in Volume 18 of Aging on July 1, 2026, titled “Senescent cells accumulate lipid droplets.” The study was led by first author Noa Rachmian-Cooper and corresponding author Valery Krizhanovsky from the Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel. Cellular senescence is a natural biological process in which damaged or stressed cells permanently stop dividing while remaining metabolically active. Although senescence helps suppress tumor formation and supports normal processes such as tissue repair and development, senescent cells accumulate with age and contribute to chronic inflammation and numerous age-related diseases, including cancer, cardiovascular disease, and Alzheimer's disease. While many of the biological effects of senescent cells have been linked to inflammatory signaling, much less has been understood about the metabolic changes that accompany senescence. In this study, the researchers investigated how cellular metabolism changes during senescence, with a particular focus on lipid metabolism. Using comprehensive metabolic profiling of human fibroblasts, they discovered that senescent cells accumulate high levels of triacylglycerols—the major precursors of lipid droplets—alongside increased glycolytic activity. Additional laboratory experiments confirmed that senescent cells contain significantly more lipid droplets than actively dividing cells. Full press release - https://www.aging-us.com/news-room/senescent-cells-found-to-accumulate-lipid-droplets-across-aging-and-alzheimers-disease DOI - https://doi.org/10.18632/aging.206390 Corresponding author - Valery Krizhanovsky - valery.krizhanovsky@weizmann.ac.il Abstract video - https://www.youtube.com/watch?v=GZbhY3wtGGI Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206390 Keywords - aging, senescence, lipid droplets, metabolism, Alzheimer's disease To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 13, 2026 — A new #review was #published in Volume 18 of Aging on June 26, 2026, titled “Hormonal dimorphism in sarcopenia disease.” The review was led by first author Romain Menard and corresponding author Romain Madelaine from the MDI Biological Laboratory, Kathryn W. Davis Center for Regenerative Biology and Aging, Bar Harbor, Maine, USA. Sarcopenia—the progressive loss of skeletal muscle mass, strength, and physical function with aging—is one of the leading causes of frailty and disability in older adults. Although the condition affects millions of people worldwide and has been recognized as a disease by the World Health Organization since 2016, treatment options remain largely limited to exercise and nutritional interventions, with no approved medications specifically targeting the disease. Growing evidence now suggests that one reason for this limited success is that sarcopenia develops through distinct biological mechanisms in women and men. In this comprehensive review, the authors examine how biological sex influences the hormonal mechanisms underlying muscle aging. They focus on three peptide hormones—apelin, insulin, and oxytocin—and describe how age-related changes in these interconnected signaling networks contribute to muscle decline through distinct biological pathways in women and men. According to the review, women often experience an abrupt decline in muscle health during menopause as estrogen levels fall rapidly. This hormonal transition disrupts apelin signaling, accelerates insulin resistance, reduces oxytocin-mediated muscle regeneration, and impairs the function of satellite cells, the muscle stem cells responsible for repair and regeneration. In contrast, men generally undergo a slower, more gradual decline in muscle function that parallels progressive reductions in testosterone, resulting in different patterns of hormonal dysregulation and disease progression. The review also highlights the central roles of apelin, insulin, and oxytocin in maintaining healthy skeletal muscle. Together, these hormones regulate muscle metabolism, glucose utilization, mitochondrial function, protein homeostasis, inflammation, and satellite-cell activity through overlapping signaling pathways. Disruption of this hormonal network during aging is proposed to contribute to impaired muscle repair, reduced metabolic function, chronic inflammation, and progressive muscle loss. Full press release - https://aging-us.net/2026/07/13/sex-specific-hormones-could-hold-the-key-to-better-sarcopenia-treatments/ DOI - https://doi.org/10.18632/aging.206392 Corresponding author - Romain Madelaine - rmadelaine@mdibl.org Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206392 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, sarcopenia, hormonal dimorphism, muscle aging, sex-stratified medicine, sexual dimorphism To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
In this episode of the Longevity & Aging Series (S4, E4), Dr. Maria Blasco of the Spanish National Cancer Centre (CNIO) joins host Dr. Yuan Zhao to discuss the research paper she co-authored in Volume 18 of Aging, titled “Cross species activity of TERT human telomerase component.” Interview video - https://www.youtube.com/watch?v=DHeysGp9oPg DOI - https://doi.org/10.18632/aging.206372 Corresponding author - Maria A. Blasco - mblasco@cnio.es Longevity & Aging Series: https://www.aging-us.com/longevity About Dr. Yuan Zhao: https://www.qmul.ac.uk/sbbs/staff/yuan-zhao.html Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206372 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, telomeres, telomerase To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 7, 2026 — A new #review was #published in Volume 18 of Aging on June 22, 2026, titled “The multifaceted inducers of cellular senescence.” The review was led by first author Hilah Gal and corresponding author Valery Krizhanovsky from the Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel. Cellular senescence is a fundamental biological process in which damaged or stressed cells permanently stop dividing while remaining metabolically active. This response plays an essential role in suppressing tumor formation, supporting embryonic development, facilitating wound healing, and maintaining tissue integrity. However, as people age, senescent cells accumulate because they are no longer efficiently cleared by the immune system. Their persistence contributes to chronic inflammation, tissue dysfunction, cancer, and many age-related diseases. In this comprehensive review, the authors examine the diverse biological stimuli that trigger cellular senescence and describe how seemingly different stimuli ultimately converge on common molecular pathways that establish stable growth arrest. Rather than viewing senescence as a single process, the review emphasizes its remarkable biological diversity and the importance of understanding how different initiating events shape distinct senescent cell phenotypes. The review discusses several major biological inducers of cellular senescence. One of the best-established mechanisms is telomere attrition, in which repeated cell division gradually shortens chromosome ends until they trigger a persistent DNA damage response. Other important stimuli include direct DNA damage caused by ionizing radiation, ultraviolet light, chemotherapy, and oxidative injury, all of which activate cellular pathways that permanently halt proliferation. Full press release - https://aging-us.net/2026/07/07/multiple-biological-triggers-shape-cellular-senescence-in-aging-and-disease/ DOI - https://doi.org/10.18632/aging.206391 Corresponding author - Valery Krizhanovsky - valery.krizhanovsky@weizmann.ac.il Abstract video - https://www.youtube.com/watch?v=5Y7R_8GQ1gk Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206391 Keywords - aging, cell senescence To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
As people live longer, maintaining good health is becoming just as important as extending lifespan. While chronological age simply reflects the number of years a person has lived, biological age measures how well the body is functioning and may better predict future health. Researchers have increasingly focused on lifestyle factors that may slow biological aging, and diet has emerged as one of the most promising. A research paper published in Volume 18 of Aging titled “Plant-based dietary patterns are associated with slower epigenetic aging,” investigated whether diets emphasizing plant foods are associated with slower biological aging as measured by DNA methylation-based epigenetic clocks. Full blog post - https://aging-us.org/2026/07/plant-based-dietary-patterns-are-associated-with-slower-biological-aging/ DOI - https://doi.org/10.18632/aging.206362 Corresponding author - Hyunju Kim - hyunjuk1@uw.edu Abstract video - https://www.youtube.com/watch?v=FcJ7oEZ-KFk Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206362 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, plant-based diets, DNA methylation, epigenetic aging, all-cause mortality, middle-aged adults To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 6, 2026 — A new systematic #review was #published in Volume 18 of Aging on June 18, 2026, titled “Life expectancy and causes of death in classical laminopathic progeroid syndromes: systematic review with individual-patient data synthesis.” The study was led by co-first authors Carlos López-Vila, Manuel García-Cordeiro, and Luís Estévez-Martínez from the University of Santiago de Compostela, and corresponding author David Araújo-Vilar from the University of Santiago de Compostela and the University Clinical Hospital of Santiago de Compostela, Spain. Classical laminopathic progeroid syndromes are among the rarest inherited disorders known. Caused by mutations affecting the LMNA gene or the ZMPSTE24 enzyme, these conditions lead to premature aging, severe multisystem disease, and markedly shortened life expectancy. Although Hutchinson-Gilford progeria syndrome (HGPS), mandibuloacral dysplasia (MAD), and restrictive dermopathy (RD) all belong to this group, reliable information about survival and causes of death for each disorder has remained limited because most published reports describe only individual patients or small case series. In this study, researchers performed a comprehensive systematic review and individual-patient data analysis to date of classical laminopathic progeroid syndromes. Following PRISMA guidelines, they analyzed data from 169 published studies together with two additional genetically confirmed institutional cases, creating a cohort of 158 genetically confirmed patients for the primary survival analysis. By examining individual patient records rather than pooled summaries, the investigators were able to compare survival patterns and causes of death across each disease subtype with greater precision. Full press release - https://aging-us.net/2026/07/06/comprehensive-individual-patient-analysis-clarifies-life-expectancy-across-rare-progeria-disorders/ DOI - https://doi.org/10.18632/aging.206389 Corresponding author - David Araújo-Vilar - david.araujo@usc.es Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206389 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, progeria, Lamin A/C (LMNA), ZMPSTE24, survival, cause of death To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 1, 2026 — A new #review was #published in Volume 18 of Aging on June 11, 2026, titled “Age-related dysfunctions of the neuroendocrine axes in nonhuman primates with depression-like and anxious behavior.” The review, dedicated to the late Dr. Mikhail (Misha) Blagosklonny, was written by Nadezhda D. Goncharova from the Kurchatov Complex of Medical Primatology, National Research Center “Kurchatov Institute,” Adler, Sochi, Russian Federation. As people grow older, their risk of developing stress-related disorders—including depression, metabolic disease, cardiovascular disease, cognitive decline, and neurodegenerative conditions—increases substantially. However, not everyone ages in the same way. Some individuals appear more resilient to stress, while others develop endocrine and metabolic disturbances that may accelerate aging and disease. Understanding the biological mechanisms behind these differences could help identify people at greater risk and support more personalized approaches to healthy aging. In this review, the author summarizes decades of experimental research investigating how aging affects two major neuroendocrine systems—the hypothalamic-pituitary-adrenal (HPA) axis and the hypothalamic-pituitary-thyroid (HPT) axis—in nonhuman primates displaying either typical adaptive behavior or depression-like and anxiety-like behavior. Because rhesus monkeys closely resemble humans in their physiology, endocrine function, and behavior, they provide a valuable translational model for studying age-related changes that are difficult to examine in people. The research shows that older monkeys with depression-like and anxiety-like behavior develop more pronounced dysfunction of the HPA axis than animals with standard behavior. These animals exhibited impaired negative feedback regulation, higher evening and nighttime cortisol levels, increased responses to acute stress, and greater activation of stress-related hormonal pathways. Together, these findings suggest impaired regulation of stress responses during aging. The review also describes important age-related alterations in thyroid function. Older animals with depression-like and anxiety-like behavior showed lower thyroxine secretion, diminished thyroid responsiveness to hormonal stimulation, and evidence of impaired thyroid gland function. These endocrine changes were accompanied by greater insulin resistance, altered triglyceride metabolism, and reduced insulin secretion in overweight animals, indicating that stress-related neuroendocrine dysfunction may extend well beyond the brain. Importantly, the findings suggest that behavioral characteristics may influence how endocrine systems age. Rather than experiencing identical biological changes over time, individuals with greater vulnerability to stress may develop more severe hormonal disturbances that contribute to age-related disease. Full press - https://aging-us.net/2026/07/01/nonhuman-primate-research-reveals-how-aging-stress-and-behavior-may-interact-to-increase-disease-risk/ DOI - https://doi.org/10.18632/aging.206388 Corresponding author - Nadezhda D. Goncharova - ndgoncharova@mail.ru (ORCID id: 0000-0002-2720-9846) Abstract video - https://www.youtube.com/watch?v=yj8zvthBiA4 To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 29, 2026 — A new #review was #published in Volume 18 of Aging on May 30, 2026, titled “The love and hate relationship between cellular senescence and stemness.” The review was led by first author Angelos Papaspyropoulos and corresponding author Vassilis G. Gorgoulis from the National and Kapodistrian University of Athens and the Biomedical Research Foundation of the Academy of Athens, Greece. Cellular senescence and stemness have traditionally been viewed as biological opposites. Senescent cells permanently stop dividing in response to cellular stress, helping prevent the spread of damaged cells, while stem cells maintain tissue repair by continuously renewing themselves and generating specialized cells. However, growing evidence suggests that the relationship between these two biological processes is far more complex and depends on the tissue type, physiological conditions, and disease context. In this review, the authors summarize recent research examining how senescence and stemness interact across normal tissues, aging, regeneration, and cancer. Rather than always opposing one another, the two processes can either suppress or reinforce each other depending on the biological setting. Under normal physiological conditions, senescence often limits stem cell activity. The review highlights studies showing that excessive senescence can impair the regenerative capacity of mesenchymal stem cells, muscle satellite cells, dental pulp stem cells, and pancreatic β-cell progenitors. In several experimental models, reducing senescence restored stem cell function and improved tissue regeneration. At the molecular level, multiple signaling pathways contribute to this balance, including the p53/p21 and p16INK4A/RB pathways, mTOR signaling, Wnt/β-catenin signaling, and the senescence-associated secretory phenotype (SASP). These pathways help determine whether cells maintain regenerative potential or enter a stable senescent state. The review also emphasizes that the relationship changes dramatically in cancer. In many tumors, senescent cells can promote the emergence of cancer stem cells through inflammatory signals released as part of the SASP or through cells escaping from the senescent state. This interaction has been reported in several malignancies, including B-cell lymphoma, liver cancer, colon cancer, lung cancer, and breast cancer, where stem cell-like properties may contribute to tumor progression, metastasis, and resistance to therapy. Full press release - https://www.aging-us.com/news-room/cellular-senescence-and-stem-cells-share-a-more-complex-relationship-than-previously-recognized DOI - https://doi.org/10.18632/aging.206387 Corresponding author - Vassilis G. Gorgoulis - vgorg@med.uoa.gr Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206387 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, senescence, stemness To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 25, 2026 — A new #research paper was #published in Volume 18 of Aging on May 29, 2026, titled “Short-term responsiveness of DNA methylation–based aging biomarkers to a multimodal intervention comprising exercise and dietary guidance involving daily consumption of yogurt containing Bifidobacterium longum BB536: an exploratory randomized controlled trial.” The study, selected as our Editors' Choice, was led by first author Tatsuki Nishimura and corresponding author Yukihiro Hishida from the R&D Division of Morinaga Milk Industry Co., Ltd., Japan. As researchers continue searching for practical ways to promote healthy aging, increasing attention has focused on interventions that target multiple biological pathways simultaneously. While exercise and healthy eating are widely recognized as important components of healthy aging, scientists are also investigating whether specific dietary components and gut microbes may influence biological aging processes measurable at the molecular level. In this study, researchers evaluated whether a 12-week lifestyle program could affect DNA methylation–based biomarkers of aging in overweight men aged 50 years and older. The intervention combined individualized exercise guidance, dietary counseling, and daily consumption of yogurt containing Bifidobacterium longum BB536, a probiotic strain that has previously been linked to beneficial effects on inflammation and gut health. The randomized controlled trial enrolled 48 participants, who were assigned either to the intervention group or to a control group that maintained their usual lifestyle habits. Participants in the intervention group received dietary counseling focused on reducing overeating, exercise guidance encouraging regular walking or stepper-based activity, and a daily serving of yogurt containing Bifidobacterium longum BB536. To assess biological aging, the investigators measured several DNA methylation–based aging biomarkers before and after the 12-week intervention. Particular attention was given to DunedinPACE, an epigenetic measure designed to estimate the current pace of biological aging rather than biological age itself. Full press release - https://aging-us.net/2026/06/25/lifestyle-intervention-linked-to-slower-biological-aging-markers-in-older-men/ DOI - https://doi.org/10.18632/aging.206386 Corresponding author - Yukihiro Hishida - yukihiro-hishida639@morinagamilk.co.jp Abstract video - https://www.youtube.com/watch?v=7W5sDpGgZtE Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206386 Keywords - aging, DNA methylation clock, DunedinPACE, Multicomponent lifestyle intervention, Bifidobacterium longum BB536 To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 23, 2026 — A new #research paper was #published in Volume 18 of Aging on May 28, 2026, titled “p38MAP kinase regulates senescence in human iPS-derived myocytes.” The study was led by first author Hiroki Sato and corresponding author Ryuichiro Sato from The University of Tokyo, along with corresponding author Makoto Shimizu from The University of Tokyo and Ochanomizu University. As people age, skeletal muscle gradually loses strength, mass, and function, contributing to frailty, reduced mobility, and an increased risk of falls. Although cellular senescence is widely recognized as a major driver of aging, the mechanisms that promote aging within mature muscle fibers remain poorly understood. In this study, researchers developed a human cell-based model to investigate how senescence develops in skeletal muscle cells and identified a signaling pathway that appears to play a central role in the process. The research team used human induced pluripotent stem cell (iPSC)-derived myocytes, specialized muscle cells generated from stem cells. To mimic age-related cellular damage, the investigators exposed the cells to low-dose X-ray irradiation, which induced DNA damage without causing extensive cell death. The treated muscle cells developed several characteristics commonly associated with aging. They exhibited muscle fiber atrophy, reduced contractile activity, and increased expression of p21, a well-established marker of cellular senescence. The researchers also observed elevated production of senescence-associated secretory phenotype (SASP) factors, inflammatory and extracellular signaling molecules that are commonly released by senescent cells. To better understand the molecular changes involved, the investigators performed proteomic, transcriptomic, and functional analyses. These studies revealed activation of p38 mitogen-activated protein kinase (p38MAPK), a signaling pathway previously linked to cellular stress responses and aging in other tissues. Further experiments demonstrated that inhibiting p38MAPK partially attenuated several senescence-associated features in the muscle cells. Treatment with p38MAPK inhibitors reduced muscle fiber atrophy, improved contractile function, and suppressed the expression of several senescence-associated factors. Conversely, activating p38MAPK promoted aging-like changes in the cells, further supporting its role in regulating muscle cell senescence. The study also identified activation of an integrin–FAK/SRC–p38MAPK signaling axis following DNA damage. According to the authors, this pathway may help explain how cellular stress is translated into long-term functional decline in skeletal muscle. Importantly, the findings were supported by analyses of human muscle aging datasets, which showed increased activity of MAPK signaling, focal adhesion pathways, and cytokine-related signaling in older skeletal muscle tissue. Full press release - https://aging-us.net/2026/06/23/researchers-identify-key-signaling-pathway-driving-muscle-cell-aging/ DOI - https://doi.org/10.18632/aging.206385 Corresponding authors - Ryuichiro Sato - roysato@g.ecc.u-tokyo.ac.jp, and Makoto Shimizu - shimizu.makoto@ocha.ac.jp Abstract video - https://www.youtube.com/watch?v=ULm7R74CJx0 Website - https://www.Aging-US.com Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
As people live longer, maintaining mental well-being has become an increasingly important part of healthy aging. While regular physical activity is known to support both physical and psychological health, many older adults face barriers that make traditional exercise programs difficult to sustain. Researchers have therefore been exploring new approaches that combine physical activity with enjoyment, social interaction, and cognitive engagement. A review published in Volume 18 of Aging titled “What are the effects of exergames on the mood states of older people? A systematic review of experimental studies, impacts on mental health and recommendations,” examined whether exergames—video games that require physical movement to play—can improve mood and mental health in older adults. The study was led by authors from the Laboratory of Sport and Exercise Psychology, Human Movement Sciences Graduate Program, College of Health and Sport Science of the Santa Catarina State University (UDESC) in Florianópolis, Brazil. Full blog - https://aging-us.org/2026/06/do-exergames-improve-mood-and-mental-well-being-in-older-adults/ DOI - https://doi.org/10.18632/aging.206361 Corresponding author - Alexandro Andrade - alexandro.andrade.phd@gmail.com Abstract video - https://www.youtube.com/watch?v=mNBh_alqVRI Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206361 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, electronic games, older adults, BRUMS, mental health, physical activity To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 18, 2026 — A new #research paper was #published in Volume 18 of Aging on May 26, 2026, titled “Early-life determinants of cardiometabolic outcomes and accelerated biological ageing in Colombia.” The study was led by first and corresponding author Juan Carlos Rivillas from the Department of Epidemiology and Biostatistics, MRC Centre for Environment and Health, School of Public Health, Imperial College London, United Kingdom. Experiences during childhood can shape health for decades. Adverse childhood experiences (ACEs), such as emotional abuse, domestic violence, food insecurity, poor health, and forced displacement, have long been linked to chronic disease. However, less is known about how these early-life hardships may influence biological aging itself. In this study, researchers examined whether childhood adversity is associated with cardiometabolic disease and accelerated biological aging among older adults in Colombia. The investigators analyzed data from 3,385 adults aged 60 years and older who participated in the nationally representative SABE-Colombia study. Five forms of childhood adversity experienced before age 15 were evaluated: emotional abuse, domestic violence, poor childhood health, food scarcity, and forced migration related to Colombia's armed conflict. Biological aging was estimated using the Klemera-Doubal Method for Biological Age, a biomarker-based measure that compares biological age with chronological age. Full press release - https://aging-us.net/2026/06/18/childhood-adversity-may-leave-lasting-biological-scars-decades-later/ DOI - https://doi.org/10.18632/aging.206384 Corresponding author - Juan Carlos Rivillas - j.rivillas-garcia20@imperial.ac.uk Abstract video - https://www.youtube.com/watch?v=5w6vgFzjcNQ Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206384 Keywords - aging, adverse childhood experiences, forced childhood migration, biological ageing, cardiometabolic outcomes, life course epidemiology To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
Each month, we will highlight a paper published in Aging chosen as the “Editors' Choice.” These selections are handpicked by our editors and accompanied by a brief summary, showcasing research with significant impact and novel insights in aging and age-related diseases. This exploratory randomized controlled trial, titled “Short-term responsiveness of DNA methylation–based aging biomarkers to a multimodal intervention comprising exercise and dietary guidance involving daily consumption of yogurt containing Bifidobacterium longum BB536: an exploratory randomized controlled trial,” investigated whether a 12-week lifestyle intervention combining exercise, dietary guidance, and daily consumption of yogurt containing Bifidobacterium longum BB536 could influence biological aging. The researchers found a significant slowing of the DNA methylation-based pace of aging measure DunedinPACE in overweight men aged 50 and older, suggesting that feasible lifestyle changes may be associated with short-term improvements in selected epigenetic aging biomarkers. DOI - https://doi.org/10.18632/aging.206386 Corresponding author - Yukihiro Hishida - yukihiro-hishida639@morinagamilk.co.jp Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206386 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, DNA methylation clock, DunedinPACE, Multicomponent lifestyle intervention, Bifidobacterium longum BB536 To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 16, 2026 — A new #research paper was #published in Volume 18 of Aging on May 22, 2026, titled “Systemic cancer risk profile in neovascular age-related macular degeneration: insights into shared aging-related mechanisms from a nationwide population-based study.” The study was led by first author Hyeong Min Kim and corresponding author Hyewon Chung from Konkuk University College of Medicine and Konkuk University Medical Center in Seoul, Republic of Korea. Neovascular age-related macular degeneration (nAMD) is one of the leading causes of severe vision loss in older adults. Although the disease primarily affects the retina, researchers increasingly recognize that it may reflect broader biological processes associated with aging, including chronic inflammation, vascular dysfunction, and immune dysregulation. These same mechanisms have also been implicated in the development of several cancers, raising questions about whether the two conditions may be biologically connected. To explore this possibility, investigators analyzed data from the Korean National Health Insurance Service, one of the world's largest population-based healthcare databases. The study included 334,091 individuals aged 50 years and older, including 83,742 patients with nAMD and 250,349 matched controls without the disease. Participants were followed for up to 10 years, allowing researchers to evaluate both overall cancer incidence and risks for specific cancer types. The analysis revealed that individuals with nAMD had a modest but statistically significant increase in overall cancer risk compared with matched controls. However, the increased risk was not observed across all cancers. Instead, patients with nAMD showed elevated risks for several specific malignancies, including thyroid, kidney, pancreatic, lung, bladder, and prostate cancers, while no significant associations were found for many other cancer types. Full press release - https://aging-us.net/2026/06/16/common-aging-mechanisms-may-link-vision-loss-disorder-to-increased-risk-of-certain-cancers/ DOI - https://doi.org/10.18632/aging.206383 Corresponding author - Hyewon Chung - hchung@kuh.ac.kr Abstract video - https://www.youtube.com/watch?v=hViOqGLYr1Y Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206383 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, neovascular age-related macular degeneration, cancer, population cohort, polygenic risk, shared susceptibility To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 11, 2026 — A new #meetingreport was #published in Volume 18 of Aging on May 14, 2026, titled “Foundations of Gerophysics.” The report was led by corresponding authors Maximilian Unfried and Brian K. Kennedy from the National University of Singapore. Aging is often studied through biology, genetics, and medicine. Yet despite tremendous advances, many fundamental questions remain unanswered: Why do organisms age at different rates? Why does resilience decline over time? And can the trajectory of aging be predicted before disease develops? Researchers participating in the inaugural Global Conference on Gerophysics explored whether answering these questions may require integrating biology with the quantitative principles of physics. Held in Singapore on March 5–6, 2025, the conference brought together 160 researchers from physics, biology, computation, and medicine and featured 31 speakers from institutions around the world. The meeting focused on developing a predictive and testable science of aging by applying concepts from dynamical systems, thermodynamics, network theory, stochastic processes, and artificial intelligence to biological aging. Full press release - https://aging-us.net/2026/06/11/physics-meets-aging-researchers-lay-the-foundations-of-gerophysics/ DOI - https://doi.org/10.18632/aging.206378 Corresponding authors - Maximilian Unfried - unfried@nus.edu.sg, and Brian K. Kennedy - bkennedy@nus.edu.sg Abstract video - https://www.youtube.com/watch?v=hgsA8EhjF0U Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206378 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - gerophysics, geroscience, aging biology, longevity, complex systems, theoretical physics To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 10, 2026 — A new #research paper was #published in Volume 18 of Aging on May 18, 2026, titled “Transcriptional programs diverge in aging mouse and human skeletal muscle.” The study was led by co-first authors Charles D. Hwang and Siti Rahmayanti and corresponding author Indranil Sinha from Brigham and Women's Hospital, Harvard University. Aging is widely associated with the gradual loss of muscle mass, strength, and physical function. Much of what scientists know about these changes comes from studies in laboratory mice, which are frequently used to investigate the biological mechanisms of aging and to identify potential therapeutic targets. However, an important question remains: how closely do aging-related changes in mouse muscle reflect what actually occurs in humans? To address this question, researchers performed a detailed comparison of gene expression patterns in skeletal muscle from young and old mice and humans. The team analyzed RNA sequencing data from mouse gastrocnemius muscle and compared it with transcriptomic data from healthy young and older adults obtained through the National Institute on Aging's GESTALT study. The results revealed substantial differences between the two species. Despite both mice and humans experiencing age-related muscle decline, fewer than 5% of significantly altered biological pathways were shared between them. Many of the genetic programs that changed with aging in mice showed little resemblance to those observed in human skeletal muscle. Full press release - https://aging-us.net/2026/06/10/aging-muscle-follows-different-genetic-programs-in-mice-and-humans/ DOI - https://doi.org/10.18632/aging.206382 Corresponding author - Indranil Sinha - isinha@bwh.harvard.edu Abstract video - https://www.youtube.com/watch?v=CYKh4X1w8H0 Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206382 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - hypoxia, angiogenesis, aging, skeletal muscle, regeneration To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
Why do some people appear to age faster than others, even when they are the same age? Researchers increasingly believe that chronological age tells only part of the story. Biological age attempts to capture how well the body's systems are functioning and may provide a more meaningful picture of overall health. A research paper on this topic was published in Volume 18 of Aging titled “Blood biochemical and gut microbiotic neural network models forecasting human biological age.” In the study, Russian researchers explored whether information from routine blood tests and the gut microbiome could be used to estimate biological age. Full blog - https://aging-us.org/2026/06/blood-tests-and-gut-bacteria-may-help-reveal-your-biological-age/ DOI - https://doi.org/10.18632/aging.206360 Corresponding author - Alexey Moskalev - amoskalev@med.ru Abstract video - https://www.youtube.com/watch?v=wg3YEwXMKWY Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206360 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, biological age, blood biochemistry, gut microbiome, neural network To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 5, 2026 — A new #review was #published in Volume 18 of Aging on May 15, 2026, titled “Blue period – features of senescence 30 years after beta-galactosidase.” The review was led by first author Chisaka Kuehnemann and corresponding author Christopher D. Wiley from Tufts University. Cellular senescence has emerged as one of the most important biological processes linked to aging and age-related disease. Senescent cells stop dividing in response to stress or damage, yet they remain metabolically active and release a variety of signaling molecules that can influence surrounding tissues. Over the past three decades, evidence has increasingly shown that the accumulation of these cells contributes to chronic inflammation, tissue dysfunction, and many degenerative conditions associated with aging. In this review, the authors examine how the field has evolved since the landmark discovery of senescence-associated beta-galactosidase (SA-β-gal) in 1995. That finding provided one of the first practical methods for identifying senescent cells and helped establish that these cells accumulate in aging tissues. Since then, researchers have identified numerous additional characteristics of senescence and developed new approaches to study their role in health and disease. The review highlights several major features now recognized as hallmarks of senescent cells. These include stable proliferative arrest, increased lysosomal activity, secretion of inflammatory and signaling molecules collectively known as the senescence-associated secretory phenotype (SASP), mitochondrial dysfunction, alterations in nuclear architecture, accumulation of metals and lipofuscin, and enhanced survival despite exposure to cellular stress. Full press release - https://aging-us.net/2026/06/05/thirty-years-after-the-discovery-of-sa-%ce%b2-gal-researchers-revisit-the-hallmarks-of-cellular-senescence/ DOI - https://doi.org/10.18632/aging.206380 Corresponding author - Christopher D. Wiley - christopher.wiley@tufts.edu Abstract video - https://www.youtube.com/watch?v=lfMPJF6No7M Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206380 Keywords - aging, senescence, biomarkers, SASP, cell death To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 3, 2026 — A new #research paper was #published in Volume 18 of Aging-US on May 15, 2026, titled “Extracellular vesicles released by senescent myoblasts affect recipient cells via miRNA-target interactions.” The study was led by first author Michael Kamal from the Department of Kinesiology at McMaster University and corresponding author Gianni Parise from the same university. As people age, skeletal muscle gradually loses strength, size, and regenerative capacity. Scientists have increasingly linked these changes to cellular senescence—a state in which damaged cells permanently stop dividing but remain metabolically active. These senescent cells release a complex mixture of signaling molecules known as the senescence-associated secretory phenotype (SASP), which can influence neighboring cells and contribute to tissue dysfunction. In this study, the researchers investigated whether extracellular vesicles (EVs)—tiny membrane-bound particles released by cells—play a role in this process. Specifically, they examined EVs released by senescent muscle precursor cells, known as myoblasts, and analyzed the microRNAs (miRNAs) carried within these vesicles. The team found that senescent myoblasts released factors that impaired normal muscle cell development. When healthy muscle cells were exposed to signals from senescent cells, the resulting muscle fibers became significantly smaller and displayed increased expression of genes associated with cellular stress and senescence. Further analysis revealed that EVs released by senescent myoblasts carried a distinct set of miRNAs. The researchers identified 22 significantly altered miRNAs, including several previously linked to cellular senescence, such as miR-34a, miR-34b, miR-34c, and miR-22. The study also identified miR-301a-3p as a potentially novel senescence-associated miRNA. Full press release - https://aging-us.net/2026/06/03/senescent-muscle-cells-send-molecular-messages-that-may-contribute-to-age-related-muscle-decline/ DOI - https://doi.org/10.18632/aging.206379 Corresponding author - Gianni Parise - pariseg@mcmaster.ca Abstract video - https://www.youtube.com/watch?v=HKBbraYg8ew Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206379 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, cellular senescence, extracellular vesicles, myoblasts, miRNA, multi-omics To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — May 27, 2026 — A new #research paper was #published in Volume 18 of Aging-US on May 8, 2026, titled “The mediating role of DNA methylation clocks in associations of race, ethnicity, education, income, and occupation with mortality: findings from NHANES 1999-2002.” The study was led by first and corresponding author Hanyang Shen from the Department of Epidemiology and Population Health at Stanford University. In this study, the authors investigated whether DNA methylation aging biomarkers—often called epigenetic aging clocks—may help explain how social inequalities become biologically embedded and contribute to differences in mortality risk. Social factors such as race, ethnicity, educational attainment, household income, and occupation have long been associated with disparities in health outcomes and life expectancy. However, the biological mechanisms linking these social exposures to long-term disease risk and mortality remain incompletely understood. Using nationally representative data from 2,402 adults in the U.S. National Health and Nutrition Examination Survey (NHANES) 1999–2002 linked to mortality follow-up data through 2019, the researchers examined thirteen different DNA methylation biomarkers alongside traditional clinical and behavioral risk factors. The study evaluated whether these epigenetic aging measures mediated associations between social stratification factors and all-cause mortality. The findings showed that several DNA methylation clocks significantly mediated the relationship between social disadvantage and mortality risk. Among all biomarkers examined, GrimAge2 consistently demonstrated the strongest mediation effects, accounting for up to 52% of mortality disparities in some occupational comparisons. DunedinPoAm, a pace-of-aging biomarker, also demonstrated substantial mediation effects across multiple socioeconomic categories. Importantly, the mediation effects observed for several DNA methylation biomarkers frequently exceeded those of traditional clinical risk factors measured in the study, including C-reactive protein and cholesterol-related markers. The results suggest that epigenetic aging measures may capture the cumulative biological effects of multiple social, environmental, behavioral, and physiological stressors simultaneously. “Among all the 13 DNA methylation biomarkers available in NHANES, GrimAge2 consistently exhibited the strongest positive mediation capturing the social disparities on mortality up to 52% (95%CI: 26%-128%), followed by the DunedinPoAm.” Full press release - https://aging-us.net/2026/05/27/dna-methylation-clocks-may-help-explain-how-social-inequality-influences-mortality/ DOI - https://doi.org/10.18632/aging.206377 Corresponding author - Hanyang Shen - hyshen@stanford.edu Abstract video - https://www.youtube.com/watch?v=XObIyirTJok Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206377 Keywords - aging, race and ethnicity, social position, epigenetic aging, mediation analysis, mortality disparities To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — May 20, 2026 — A new #editorial was #published in Volume 18 of Aging-US on May 18, 2026, titled “Public health in the age of longevity interventions: from prevention to system-wide resilience.” The editorial was authored by Jochen Mierau from the University of Groningen and Aging-US Editor-in-Chief Marco Demaria from the University of Groningen and European Research Institute for the Biology of Ageing (ERIBA). In this editorial, the authors examine how modern public health systems may need to evolve as aging populations increasingly face chronic disease, frailty, multimorbidity, and progressive loss of function rather than the acute infectious diseases that shaped 20th-century medicine. The authors argue that many of the greatest gains in human lifespan historically came not from advanced medical technologies, but from broad public health interventions such as sanitation, vaccination, improved nutrition, occupational safety, safer housing, and access to education. While these measures remain essential, they suggest that modern aging societies now face a different challenge: extending healthspan alongside lifespan. The editorial highlights how today's health risks accumulate gradually across the life course through environmental, metabolic, social, and behavioral exposures. Ultra-processed foods, pollution, tobacco, alcohol, sedentary lifestyles, climate-related stressors, and social isolation are described as contributors to accelerated biological aging and increased vulnerability to chronic disease. The authors emphasize that these interconnected exposures cannot be fully addressed through disease-specific treatment alone. “Rather than representing separate or competing domains, these approaches should be viewed as complementary components of a unified strategy to improve population health across aging societies.” A major focus of the article is the growing scientific interest in longevity-directed interventions that target core biological mechanisms of aging. The authors discuss pathways including cellular senescence, chronic inflammation, metabolic dysfunction, and impaired proteostasis, noting that interventions directed at these processes may help delay or modify multiple age-related diseases simultaneously rather than treating each condition individually after it emerges. Importantly, the editorial emphasizes that longevity interventions should not replace either public health or conventional clinical medicine. Instead, the authors propose a coordinated framework operating across the life course. In this model, public health strategies reduce baseline risk and environmental damage, clinical medicine treats established disease, and longevity-focused therapies may help slow biological decline before major pathology becomes clinically apparent. Figure 1 of the paper (page 2) illustrates this proposed multi-layered framework integrating public health, longevity interventions, and disease-specific care across different stages of life. Full press release - https://www.aging-us.com/news-room/extending-healthspan-through-public-health-and-longevity-medicine DOI - https://doi.org/10.18632/aging.206381 Corresponding author - Marco Demaria - m.demaria@umcg.nl Paper Preview Video - https://www.youtube.com/watch?v=KSjfmxpHer8 To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — May 19, 2026 — A new #research paper was #published in Volume 18 of Aging-US on May 5, 2026, titled “Methylene blue protects hair follicle stem cells from oxidative and metabolic stress to enhance hair regeneration.” The study was led by first author Kavitha Sadashivaiah and corresponding author Kan Cao from the Department of Cell Biology and Molecular Genetics at the University of Maryland, College Park. In this study, the authors investigated how methylene blue (MB), a long-established mitochondrial-targeted antioxidant, affects human hair follicle stem cells (HFSCs) under conditions of oxidative and metabolic stress. Hair follicle stem cells are essential for maintaining hair growth and regeneration, but aging, ultraviolet radiation, oxidative stress, and metabolic dysfunction can impair their regenerative capacity and contribute to hair thinning and scalp aging. Using cultured human HFSCs, the researchers found that methylene blue significantly enhanced stem cell proliferation and viability while reducing intracellular reactive oxygen species (ROS). Importantly, MB also increased activation of β-catenin signaling, a central pathway involved in hair follicle regeneration, stem cell maintenance, and wound repair. Functional scratch-assay experiments further demonstrated that MB accelerated wound closure and regenerative activity in HFSC cultures. The study also explored how methylene blue interacts with other compounds commonly associated with scalp or hair health. While antioxidant vitamins A and C improved oxidative stress scavenging, they unexpectedly reduced MB-induced β-catenin activation when used in combination. In contrast, minoxidil—the widely used hair growth stimulant—worked synergistically with MB to further enhance β-catenin signaling and improve HFSC viability. “Overall, these findings identify methylene blue as a multifunctional therapeutic candidate that reduces oxidative and metabolic stress while supporting HFSC–mediated hair regeneration.” Another major focus of the paper involved glucagon-like peptide-1 receptor agonists (GLP-1 RAs), medications increasingly used for diabetes and weight management. Recent clinical observations have suggested that some patients receiving GLP-1 RA therapy may experience hair thinning or hair loss. The authors demonstrated that increasing GLP-1 RA concentrations caused dose-dependent reductions in HFSC viability in vitro. However, pretreatment with methylene blue substantially protected the stem cells from GLP-1 RA–associated metabolic stress and premature cell death. Beyond stem cell protection, the paper discusses methylene blue's broader potential role in scalp health. Because MB absorbs ultraviolet radiation and has previously demonstrated protective effects against UV-induced DNA damage in skin cells, the authors propose that it may help shield the scalp microenvironment from oxidative injury while supporting regenerative signaling pathways important for hair maintenance. The study also highlights MB's possible antimicrobial properties and its potential influence on scalp microbiome balance. Importantly, the authors emphasize that the findings are based on in vitro cellular models and that further in vivo studies will be necessary before clinical applications can be established. Additional research will be required to define appropriate dosing, pharmacokinetics, long-term safety, and therapeutic efficacy in living systems. Overall, this study identifies methylene blue as a potentially multifunctional therapeutic candidate for supporting hair follicle stem cell health under conditions of oxidative, metabolic, and pharmacologic stress. By combining antioxidant activity with activation of regenerative β-catenin signaling, MB may represent a promising future strategy for protecting scalp health, enhancing hair regeneration, and improving the resilience of aging hair follicle stem cells. DOI - https://doi.org/10.18632/aging.206376
Each month, we will highlight a paper published in Aging-US chosen as the “Editors' Choice.” These selections are handpicked by our editors and accompanied by a brief summary, showcasing research with significant impact and novel insights in aging and age-related diseases. __________ In the research paper, titled “Association of epigenetic age acceleration with MRI biomarkers of aging and Alzheimer's disease neurodegeneration,” researchers investigated whether epigenetic clocks of biological aging are associated with MRI markers of brain aging and Alzheimer's disease-related neurodegeneration in 1,196 older women. While none of the five epigenetic clocks examined were linked to accelerated overall brain aging, one measure (AgeAccelGrim2) was associated with MRI patterns related to neurodegeneration. The findings suggest this relationship was largely driven by DNA methylation markers linked to smoking history and changes in frontal and temporal brain regions rather than areas typically affected early in Alzheimer's disease. Overall, the study indicates that epigenetic aging and brain aging may reflect different aspects of the aging process, while highlighting the potential role of smoking-related biological aging in increasing dementia risk. DOI - https://doi.org/10.18632/aging.206369 Corresponding author - Linda K. McEvoy - linda.k.mcevoy@kp.org Abstract video - https://www.youtube.com/watch?v=kZiRjlKnnsI Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206369 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, epigenetic clocks, brain age, biological aging, smoking, frontal lobe To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — May 15, 2026 — A new #review was #published in Volume 18 of Aging-US on May 4, 2026, titled “Cellular senescence: from pathogenic mechanisms to precision anti-aging interventions.” The study was led by first author Jian Deng and corresponding author Dong Yang from the Department of Targeting Therapy and Immunology, Cancer Center, West China Hospital, Sichuan University, Chengdu, Sichuan, China. In this comprehensive review, the authors examine how cellular senescence contributes to aging and age-related disease across multiple organ systems, while also highlighting the emerging complexity and functional diversity of senescent cell populations. Traditionally, senescent cells have been viewed primarily as harmful byproducts of aging, characterized by irreversible cell-cycle arrest and chronic inflammatory signaling. However, growing evidence suggests that some senescent cells also play beneficial physiological roles in tissue repair, embryonic development, and maintenance of tissue homeostasis. The review outlines how senescence develops in major tissues including the liver, lungs, kidneys, heart, adipose tissue, brain, and skin. Across these organs, aging-related cellular dysfunction is driven by a combination of oxidative stress, mitochondrial dysfunction, DNA damage, chronic inflammation, metabolic stress, telomere shortening, and environmental insults such as ultraviolet radiation and pollution. The authors describe how senescent cells accumulate in highly specialized cell populations—including hepatocytes, endothelial cells, fibroblasts, macrophages, astrocytes, and epithelial cells—where they can disrupt normal tissue architecture and promote chronic disease progression. Importantly, the article emphasizes that senescent cells are highly heterogeneous and should not be treated as a uniform population. Depending on the tissue context and biological environment, senescent cells may exert either protective or harmful effects. For example, certain senescent cells may help limit fibrosis or support wound healing, whereas others drive chronic inflammation, metabolic dysfunction, tissue degeneration, and cancer progression. This growing recognition of functional heterogeneity has prompted a major shift in anti-aging research away from indiscriminate elimination of senescent cells toward more selective and precision-based therapeutic strategies. “Based on these insights, this review summarizes the induction mechanisms of cellular senescence and the subsequent evolution of their functional phenotypes across diverse tissues.” Full press release - https://www.aging-us.com/news-room/precision-anti-aging-strategies-aim-to-target-harmful-senescent-cells-while-preserving-beneficial-ones Paper DOI - https://doi.org/10.18632/aging.206375 Corresponding author - Dong Yang – yangdong@wchscu.cn Abstract video - https://www.youtube.com/watch?v=HkJRwF8mp4A Keywords - cellular senescence, aging mechanisms, functional heterogeneity, precision anti-aging To learn more about the journal, please visit www.Aging-US.com and connect with us on social media at: Bluesky - bsky.app/profile/aging-us.bsky.social ResearchGate - www.researchgate.net/journal/Aging-1945-4589 X - twitter.com/AgingJrnl Facebook - www.facebook.com/AgingUS/ Instagram - www.instagram.com/agingjrnl/ LinkedIn - www.linkedin.com/company/aging/ Reddit - www.reddit.com/user/AgingUS/ Pinterest - www.pinterest.com/AgingUS/ YouTube - www.youtube.com/@Aging-US Spotify - open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
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