Advertise on podcast: Aging-US

BUFFALO, NY — October 1, 2026 — A new #research paper was #published in Volume 18 of Aging on September 10, 2026, titled “Social determinants of health and risk of dementia in people with and without type 2 diabetes – findings from two large national-scale cohorts.” The study found that unfavorable social determinants of health (SDOH) were associated with a higher risk of dementia in adults with and without type 2 diabetes (T2D), with particularly strong associations observed among women with T2D. The research was authored by You Lu and Yilin Yoshida. Both researchers are affiliated with the Section of Endocrinology, Deming Department of Medicine, Tulane University, New Orleans, Louisiana. People with T2D already face an elevated risk of dementia and cognitive impairment. The researchers examined whether social and environmental circumstances could further shape this risk. Rather than evaluating individual social factors separately, they developed a weighted multidomain SDOH score designed to capture the cumulative and unequal contributions of multiple forms of social disadvantage. The primary analysis included 10,071 UK Biobank participants with T2D and 11,780 euglycemic participants. SDOH indicators were weighted using an elastic-net approach and grouped into favorable, medium and unfavorable categories. Associations with incident dementia were examined using multivariable models and further evaluated using data from the U.S. All of Us Research Program. Full press release - https://www.aging-us.com/news-room/adverse-social-determinants-linked-to-higher-dementia-risk-in-people-with-type-2-diabetes DOI - https://doi.org/10.18632/aging.206417 Corresponding author - Yilin Yoshida - [email protected] Abstract video - https://www.youtube.com/watch?v=Aql6kZZDrEI Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206417 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, dementia, SDOH, type 2 diabetes, sex difference 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 [email protected]

Aging is commonly associated with the gradual loss of skeletal muscle mass and function. While preserving muscle mass is important, muscle health also depends on the mitochondria that provide energy for contraction and help muscles respond to physical stress. A new study suggests that a protein called Activating Transcription Factor 5 (ATF5) plays a complex role in balancing these processes during aging. A research paper published in Volume 18 of Aging titled “ATF5 is required for the maintenance of mitochondrial homeostasis and skeletal muscle health during aging,” investigated how ATF5 influences mitochondrial quality control, muscle mass, and endurance as mice age. Full blog - https://aging-us.org/2026/09/atf5-helps-preserve-mitochondrial-quality-and-muscle-endurance-during-aging/ DOI - https://doi.org/10.18632/aging.206365 Corresponding author - David A. Hood - [email protected] Abstract video - https://www.youtube.com/watch?v=u2OeppqIPN4 Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206365 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, skeletal muscle, ATF5, mitochondria, stress response 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 [email protected]

BUFFALO, NY — September 29, 2026 — A new #review was #published in Volume 18 of Aging on September 8, 2026, titled “Developmental senescence misregulation in congenital disorders: CHARGE syndrome as a candidate model.” The article proposes that disruption of developmental senescence—a tightly controlled cellular program involved in embryonic tissue remodeling—may contribute to congenital abnormalities associated with CHARGE syndrome. The review was led by co-first authors Álvaro J. Arana and Pablo Palau-Irisarri, who contributed equally. Arana is affiliated with the Departamento de Zoología, Genética y Antropología Física, Facultad de Veterinaria, Universidad de Santiago de Compostela, Spain, while Palau-Irisarri is affiliated with the Departamento de Biología, Facultad de Ciencias, Universidad Autónoma de Madrid, Spain. Arana is also the corresponding author. Cellular senescence is commonly associated with aging, cellular stress and tumor suppression, but it also occurs naturally during embryonic development. Unlike classical stress-induced senescence, developmental senescence is transient and restricted to particular tissues and developmental stages. These cells can contribute to tissue remodeling and patterning before being cleared, helping shape developing organs. Because this process must occur at the right place and time, the authors propose that excessive, insufficient, prolonged or misplaced senescence could interfere with normal morphogenesis. CHARGE syndrome provides a particularly relevant model for investigating this possibility. The rare developmental disorder can involve coloboma, heart defects, choanal atresia, growth and developmental delay, genitourinary abnormalities and characteristic ear defects. Most patients with CHARGE syndrome carry pathogenic variants in CHD7, which encodes an ATP-dependent chromatin remodeler. Full press release - https://www.aging-us.com/news-room/developmental-senescence-emerges-as-a-candidate-mechanism-in-charge-syndrome DOI - https://doi.org/10.18632/aging.206396 Corresponding author - Álvaro J. Arana - [email protected] Abstract video - https://www.youtube.com/watch?v=QtB5390b1To Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206396 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, CHD7, morphogenesis, p53/p21 pathway, TGFβ signaling, congenital disorders 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 [email protected]

In this episode of the Longevity & Aging Series (S4, E6), Dr. Adam Bohnert from the Department of Biological Sciences at Louisiana State University (Baton Rouge, LA) joins host Dr. Yuan Zhao to discuss the research paper he co-authored in Volume 18 of Aging, titled “Inhibition of peroxisomal protein PRX-11 promotes longevity in Caenorhabditis elegans via enhancements to mitochondria.” DOI - https://doi.org/10.18632/aging.206395 Corresponding author - K. Adam Bohnert - [email protected] Video interview - https://www.youtube.com/watch?v=ztK336BflJ4 Abstract video - https://www.youtube.com/watch?v=fbcqBsP90CY Longevity & Aging Series - https://www.aging-us.com/longevity 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 [email protected]

BUFFALO, NY — September 24, 2026 — A new #review was #published in Volume 18 of Aging on September 8, 2026, titled “How to live for centuries: common denominators of organisms with exceptional longevity.” The review examines what some of the world’s longest-lived organisms may reveal about the biology of exceptional longevity. The review was led by first author Stefania E. Kapsetaki from the Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology-Hellas (FORTH), in Heraklion, Crete, Greece. Corresponding author Nektarios Tavernarakis is affiliated with the same institute and with the Division of Basic Sciences, School of Medicine, University of Crete. Kapsetaki and Tavernarakis surveyed molecular and cellular evidence from 101 multicellular species with maximum lifespans of at least 250 years, including 90 plants and 11 animals. Some reach only slightly beyond 250 years, while others may persist for thousands or even tens of thousands of years. The freshwater planarian Schmidtea mediterranea and the jellyfish Turritopsis dohrnii are even considered potentially immortal. Rather than looking only at why certain species live longer than others, the authors compared two dimensions of longevity: variation within exceptionally long-lived species and variation between long- and shorter-lived species. Their analysis covered genetic, genomic, transcriptomic, proteomic and metabolomic findings, as well as telomere maintenance, stress resistance, regeneration and tumorigenesis. Full press release - https://www.aging-us.com/news-room/exceptional-longevity-across-species-linked-to-dna-maintenance-stemness-and-stress-resistance DOI - https://doi.org/10.18632/aging.206419 Corresponding author - Nektarios Tavernarakis - [email protected] Abstract video - https://www.youtube.com/watch?v=VvzjvzQj-Qk Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206419 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, healthspan, interspecific variation, intraspecific variation, 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 [email protected]

BUFFALO, NY — September 21, 2026 — A new #review was #published in Volume 18 of Aging on August 31, 2026, titled “The guardian paradox: DNA damage response overactivation as an integrative driver of aging – a tumor suppressor–negative regulator framework.” The review presents a new framework proposing that chronic overactivation of the DNA damage response (DDR) may serve as a major integrating driver of biological aging. Rather than framing aging in the same mutation-centered terms often applied to cancer, the framework suggests that many tumor-suppressor pathways remain structurally intact but become persistently overactivated or otherwise dysregulated as tissues age. The review was authored by Patrick E. Sewell from Triple Helix Science in Santa Ana, California. The paper organizes 16 candidate tumor suppressor–negative regulator axes into three evidence tiers and proposes experiments designed to determine whether chronic DDR signaling plays a causal role in aging. The DNA damage response is the cellular surveillance system that detects genomic damage and coordinates repair. In young, healthy tissues, DDR signaling normally activates temporarily following stresses such as DNA double-strand breaks, replication stress or oxidative lesions and subsides after repair. With aging, however, persistent signals associated with telomere attrition, epigenetic erosion, mitochondrial dysfunction and transposable-element activity may maintain DDR activation even without new driver mutations. According to the proposed model, chronic DDR signaling can stabilize p53 and increase p21 and p16INK4a, promoting cell-cycle arrest and cellular senescence. Senescent cells can then produce the senescence-associated secretory phenotype (SASP), releasing inflammatory mediators that may spread senescence to neighboring cells, reduce stem-cell function, disrupt tissue homeostasis and contribute to systemic inflammaging. Importantly, these effects can occur while the underlying tumor-suppressor genes remain intact. Full press release - https://www.aging-us.com/news-room/the-guardian-paradox-links-chronic-dna-damage-response-to-aging DOI - https://doi.org/10.18632/aging.206416 Corresponding author - Patrick E. Sewell - [email protected] Abstract video - https://www.youtube.com/watch?v=rBMe9uWMpBU Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206416 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, biological aging, DNA damage response, tumor suppressor pathways, gene therapy, adeno-associated virus 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 [email protected]

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 - [email protected] 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 [email protected]

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 - [email protected] 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 [email protected]

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 - [email protected], Fabrizio d’Adda di Fagagna - [email protected] 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 [email protected]

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 - [email protected] 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 [email protected]

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 - [email protected] 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 [email protected]

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 - [email protected], Guey-Jen Lee-Chen - [email protected] 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 [email protected]

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 - [email protected] 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 [email protected]

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 - [email protected], and Nichole A. Broderick - [email protected] 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 [email protected]

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 - [email protected] 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 [email protected]