Aging-US

BUFFALO, NY — April 2, 2026 — A new #research paper was #published in Volume 18 of Aging-US on March 24, 2026, titled “Age-specific relationship between the modulation of brain dynamics in response to task demands and bimanual performance.” Led by first author Sara Magalhães Ferreira from Hasselt University, with corresponding author Koen Cuypers from Hasselt University and KU Leuven, the study examined how age affects BOLD variability and its modulation with task demands during a bimanual task. The authors used fMRI in 22 younger and 23 older healthy adults who performed three increasingly complex task conditions. The authors found that older adults showed higher BOLD variability in cerebellar lobule VIIIb and greater modulation across task conditions in sensorimotor and cerebellar regions. Modulation of BOLD variability predicted performance in an age- and region-dependent manner: in younger adults, reduced modulation in sensorimotor and visuospatial areas correlated with better performance, whereas in older adults, increased modulation in the inferior and superior parietal lobules was linked to higher performance. Across groups, better outcomes were associated with greater modulation in the middle occipital gyrus but lower modulation in cerebellar Crus I. “In sum, this study highlights the potential role of BOLD variability modulation in shaping bimanual performance during aging.” The authors note that, while the age-related differences in BOLD dynamics were clear, they did not find robust evidence supporting a brain-behavior relationship in bimanual performance, which limits how directly the neural findings can be interpreted behaviorally. They recommend future work using multimodal imaging, longitudinal designs, and studies that examine both cognitive and motor domains within the same participants to determine whether variability modulation reflects aging, experience, intervention, or broader cross-functional signatures of aging. DOI - https://doi.org/10.18632/aging.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

Inflammation is a double-edged sword. It defends the body against infection and injury, yet when it becomes chronic, it can accelerate aging and fuel the very diseases that shorten human life. For decades, scientists have observed that people with higher levels of inflammatory markers like interleukin-6 (IL6) and C-reactive protein (CRP) tend to have shorter lifespans. But the critical question has always been: does inflammation cause mortality, or does it merely reflect underlying disease? A research paper, titled “Causal effects of inflammation on long-term mortality: A mendelian randomization study” was published in Volume 18 of Aging-US by an international team of researchers, provides a definitive answer by using a powerful genetic technique to untangle cause from effect. The team’s investigation demonstrates that the IL6 inflammatory pathway has a direct causal impact on human survival—but with a surprising twist: two components of the same pathway pull in opposite directions. Full blog - https://aging-us.org/2026/04/il6-and-il6r-opposing-forces-of-inflammation-that-shape-human-survival/ DOI - https://doi.org/10.18632/aging.206352 Corresponding author - Eliano P. Navarese - elianonavarese@gmail.com Abstract video - https://www.youtube.com/watch?v=Br1A0jgU-4M Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206352 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, mendelian randomization, inflammatory biomarkers, mortality, cardiovascular 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 — March 31, 2026 — A new #research paper was #published in Volume 18 of Aging-US on March 20, 2026, titled “Plant-based dietary patterns are associated with slower epigenetic aging.” Led by first and corresponding author Hyunju Kim from the Department of Epidemiology and the Cardiovascular Health Research Unit, Department of Medicine, University of Washington, the study examined whether four plant-based diet indices — overall PDI, provegetarian diet, healthy PDI, and unhealthy PDI — were associated with DNA methylation-based measures of epigenetic aging. The authors analyzed data from the Atherosclerosis Risk in Communities (ARIC) Study (n = 2,810) and the National Health and Nutrition Examination Survey (NHANES, n = 2,056), and assessed associations with GrimAge2, HannumAge, and PhenoAge. The researchers found that each standard deviation higher in the overall PDI, provegetarian diet, and healthy PDI was associated with decelerated GrimAge2, while higher overall PDI and provegetarian diet were also associated with decelerated PhenoAge and HannumAge. By contrast, unhealthy PDI was not significantly associated with epigenetic aging. The findings suggest that plant-rich dietary patterns, especially those emphasizing healthier plant foods, may be linked to slower biological aging in largely non-vegetarian populations. “No significant association was observed for unhealthy PDI and any of the DNA methylation-based aging.” The authors note that these are observational data and do not establish causality. They call for longitudinal and interventional studies to determine whether sustained adherence to healthy plant-based dietary patterns can directly influence epigenetic aging and related health outcomes over time. DOI - https://doi.org/10.18632/aging.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 — March 25, 2026 — A new #review was #published in Volume 18 of Aging-US on March 18, 2026, titled “What are the effects of exergames on the mood states of older people? A systematic review of experimental studies, impacts on mental health and recommendations.” Led by Camile de Bem Gaspar and Whyllerton Mayron da Cruz, with corresponding author Alexandro Andrade, all from the Laboratory of Sport and Exercise Psychology, Human Movement Sciences Graduate Program, College of Health and Sport Science of the Santa Catarina State University (UDESC) in Florianópolis, Brazil, the review examined whether exergames can influence mood in older adults. The authors followed systematic review and meta-analysis methods, screened 651 studies, and found nine that met the inclusion criteria, representing 325 participants aged 61 to 78.9 years. The review found that exergames were associated with better mood outcomes, including reductions in tension, anger, fatigue, confusion, and depressive symptoms, while also promoting engagement, immersion, and socialization. In the studies that measured mood more broadly, participants described exergames as improving well-being and emotional state, and no included study reported worsened mood after participation. “The results indicate that the practice of exergames had a positive effect on the mood of older adults.” The authors note, however, that the evidence base remains small and heterogeneous, with only nine eligible trials and several different mood measures used across studies. They call for longer-term interventions, larger and more diverse samples, and additional home-based or low-cost exergame studies to determine how durable the benefits are and how best to recommend them for older adults in real-world settings. DOI - https://doi.org/10.18632/aging.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 — March 23, 2026 — A new #research paper was #published in Volume 18 of Aging-US on March 12, 2026, titled “Blood biochemical and gut microbiotic neural network models forecasting human biological age.” Led by Anastasia A. Kobelyatskaya from the Russian Clinical Research Center for Gerontology, Pirogov Russian National Research Medical University, and the Institute of Biology of Aging and Healthy Longevity Medicine with Preventive Medicine Clinic, Petrovsky Russian Research Centre of Surgery — with corresponding author Alexey Moskalev from the Institute of Biology of Aging and Healthy Longevity Medicine with Preventive Medicine Clinic, Petrovsky Russian Research Centre of Surgery — the study builds a gender-specific biochemical model (seven routine clinical markers, e.g., cystatin-C, IGF-1, DHEAS, plus sex-specific sets) and a microbiota model (45 species measured by full-length 16S sequencing). Both models were trained and tested on the same 637-person dataset and achieved mean absolute errors of around six years and R² values above 0.8. The team emphasised interpretability: they applied SHapley Additive exPlanations (SHAP) to convert each model from a “black box” into a more interpretable tool, showing how individual predictors (for example, DHEAS, cystatin-C, NT-proBNP in the blood model, and species such as Blautia obeum in the microbiota model) shift predicted age in years for a given individual. The biochemical clock yielded a small (clinically accessible) predictor set (7 markers) to ease clinical translation, while the microbiota clock used a 45-species signature and highlighted microbiome taxa whose abundance gradients correlate with predicted microbiotic age. “As the proposed models possess both global and local explainability, they hold future potential for application in monitoring the effectiveness of various interventions in clinical trials.” The authors note limitations and next steps: the cohort was restricted to a Caucasian population, and the microbiota model requires sequencing resources that may limit immediate clinical rollout. They call for external validation in larger, ethnically diverse cohorts, prospective testing to link model predictions to health outcomes, and application of the explainable models to monitor responses in intervention trials (for example, lifestyle, diet, or drug studies) where a change in predicted biological age would be an early, interpretable signal of benefit. DOI - https://doi.org/10.18632/aging.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

Dr. David Gems from University College London joins new host Dr. Yuan Zhao from Queen Mary University of London to discuss a review they co-authored in Volume 17, Issue 12 of Aging-US, titled “Aging as a multifactorial disorder with two stages.” DOI - https://doi.org/10.18632/aging.206339 Corresponding author - David Gems - david.gems@ucl.ac.uk Video interview - https://www.youtube.com/watch?v=JqZuAm7I4oQ Longevity & Aging Series - https://www.aging-us.com/longevity About Dr. Yuan Zhao - https://www.qmul.ac.uk/sbbs/staff/yuan-zhao.html Abstract video - https://www.youtube.com/watch?v=d4TSI4Ot3yM Abstract Aging (senescence) is characterized by development of diverse senescent pathologies and diseases, leading eventually to death. The major diseases of aging, including cardiovascular disease, cancer and chronic obstructive pulmonary disease (COPD), are multifactorial disorders, resulting from complex interactions between multiple etiologies. Here we propose a general account of how different determinants of aging can interact to generate late-life disease. This account, initially drawn from studies of the nematode Caenorhabditis elegans, depicts senescence as the product of a two-stage process. The first stage involves the diverse causes of disease prior to aging, that cause disruption of normal biological function. These include infection, mechanical injury and mutation (somatic and inherited). Second, etiologies largely confined to aging: deleterious, late-life consequences of evolved wild-type gene action, including antagonistic pleiotropy. Prior to aging, diverse insults lead to accumulation of various forms of injury that is largely contained, preventing progression to major pathology. In later life, wild-type gene action causes loss of containment of latent disruptions, which form foci for pathology development. Pathologies discussed here include osteoarthritis, cancer, late-life recrudescence of infection, and consequences of late-acting deleterious mutations. Such latent injury foci are analogous to seeds which in later life, in the context of programmatic senescent changes, germinate and develop into disease. Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206339 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, C. elegans, disease, hyperfunction, multifactorial model 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 — March 18, 2026 — A new #editorial was #published in Volume 18 of Aging-US on March 10, 2026, titled “Healthy life extension: Geroscience’s north star.” Led by David A. Barzilai — who is affiliated with Geneva College of Longevity Science, Healthspan Coaching LLC (Barzilai Longevity Consulting), and Harvard Medical School — the editorial pays tribute to the late Mikhail Blagosklonny and states that geroscience should adopt healthy life extension (measured as health-adjusted survival such as HALE and QALYs) as its primary objective rather than treating lifespan and healthspan as competing goals. Dr. Barzilai urges clearer outcome priorities, disciplined evidence in mammals, and coordinated investment that matches the field’s potential to delay multimorbidity and extend high-quality years of life. The piece reviews data showing that increases in life expectancy have outpaced gains in healthy life expectancy and summarizes calls to measure success by health-adjusted longevity rather than biomarkers alone. It highlights examples where targeting conserved aging pathways produced replicable lifespan gains in mammals (for example, rapamycin in mice) and notes early human-facing signals (for example, mTOR inhibition improving influenza vaccine responses in older adults) that illustrate how aging-biology interventions can be clinically legible on shorter timelines. The editorial also frames the practical challenge: while lifespan evidence is ideal, human trials must use rigorous, meaningful endpoints that map to delayed multimorbidity, preserved function, and resilience. “Geroscience is for healthy life extension. We should stop pretending that lifespan and healthspan compete.” Dr. Barzilai calls for a “moonshot”-level commitment to aging biology that includes larger, better-funded basic programs, clinical trials with health-adjusted survival endpoints, and translational pipelines able to move robust mammalian lifespan findings toward human studies. He stresses the need for replicable mammalian lifespan data paired with human endpoints that reflect quality of life and independence. The editorial closes with a direct pledge in honor of Dr. Blagosklonny’s legacy, in part to make healthy life extension the field’s north star and measure success in years worth living. DOI - https://doi.org/10.18632/aging.206359 Corresponding author - David A. Barzilai - d.barzilai@gcls.study Intro video - https://www.youtube.com/watch?v=_MwFvDg7Ejw Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206359 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, geroscience, longevity, healthspan, longevity medicine, healthy life extension 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

The aging of an organism is reflected not only in the function of its organs but also in the molecular signatures written into its cells. For years, scientists have cataloged the changes in protein-coding genes and various non-coding RNAs that occur as we grow older. However, one class of molecules—circular RNAs originating from the genome of our cellular power plants, the mitochondria—has remained largely unexplored. A new research paper, titled “Aging-associated mitochondrial circular RNAs” published in Volume 18 of Aging-US by a multi-institutional team of researchers, provides the first detailed profile of these molecules and reveals a surprising link to cellular energy metabolism. The team’s investigation demonstrates that a specific mitochondrial circular RNA, circMT-RNR2, is depleted in older individuals and plays a direct role in regulating the TCA cycle, the engine of cellular energy production. Full blog - https://aging-us.org/2026/03/mitochondrial-circular-rnas-new-players-in-human-aging/ Paper DOI - https://doi.org/10.18632/aging.206354 Corresponding authors - Je-Hyun Yoon - jehyun-yoon@ou.edu, and Young-Kook Kim - ykk@jnu.ac.kr Abstract video - https://www.youtube.com/watch?v=f8uZ6_tcOHw Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206354 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, circular RNA, MT-RNR2, GRSF1, TCA cycle 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 – March 16, 2025 – Impact Journals (publisher of Aging-US, Oncotarget, Oncoscience, and Genes & Cancer), is pleased to announce its participation as an exhibitor at the American Association for Cancer Research (AACR) Annual Meeting 2026. The meeting will take place April 17–22, 2026, at the San Diego Convention Center in San Diego, CA. Conference attendees are warmly invited to visit Booth 3641 to meet members of the Impact Journals team, discover notable recent publications, and discuss opportunities for collaboration. The mission of Impact Journals is to maximize research impact through insightful peer review, eliminate borders between specialties by linking different fields of oncology and biomedical science, and foster the application of both basic and clinical science. This mission is grounded in a strong commitment to ethical standards and scientific integrity. At Impact Journals, evolving digital technologies, tools, and ideas are continually integrated into a robust scientific integrity process. The AACR Annual Meeting serves as a focal point for the global cancer research community, bringing together scientists, clinicians, healthcare professionals, survivors, patients, and advocates to share the latest advances in cancer science and medicine. From population science and prevention to cancer biology, translational and clinical studies, survivorship, and advocacy, the AACR Annual Meeting highlights the work of leading researchers from institutions around the world. To learn more about Impact Journals, please visit impactjournals.com. For media inquiries, email media@impactjournals.com.

BUFFALO, NY — March 13, 2026 — A new #research paper was #published in Volume 18 of Aging-US on March 2, 2026, titled “D, L-Buthionine-(S, R)-sulfoximine recapitulates the anti-obesity effects of sulfur amino acid restriction without the associated deleterious effects on bone in male mice.” Led by Naidu B. Ommi from the Orentreich Foundation for the Advancement of Science — with corresponding author Sailendra N. Nichenametla from the same institution — the study tests whether the glutathione (GSH)-lowering compound D, L-buthionine-(S, R)-sulfoximine (BSO) reproduces the anti-obesity effects of sulfur amino acid restriction (SAAR) without causing the bone loss seen with SAAR diets. Using diet-induced obese male C57BL6/NTac mice fed high-fat diets, the authors compared: a control methionine-replete diet, a SAAR diet (low methionine, no cysteine), SAAR plus the GSH precursor N-acetylcysteine (NAC), and control diet plus BSO in drinking water. Using body-composition, micro-CT, histomorphometry, and biomechanical testing, the team confirmed prior work that SAAR reduces body fat but also lowers trabecular and cortical bone mineral density, increases marrow adiposity, reduces osteoblast numbers, and weakens bone biomechanical strength. Crucially, while NAC supplementation reversed the bone defects of SAAR (implicating cysteine/glutathione restriction in bone loss), BSO reproduced the lean, anti-obesity phenotype without producing the deleterious bone effects observed in SAAR mice. In short, BSO recapitulated the anti-obesity benefits of SAAR without causing the same bone loss — a finding with potential relevance to developing anti-obesity strategies that avoid skeletal harm. “Despite its anti-obesity effects, BSO did not exert any detrimental effects on bones.” The authors emphasize next steps and caveats. They call for mechanistic studies to define how GSH lowering drives fat loss yet spares bone under BSO treatment, investigations of age-at-onset, tissue-specific, and sex-specific effects, and long-term safety studies to assess off-target or delayed adverse effects of BSO before any clinical development. The paper frames BSO as a promising tool compound to dissect the beneficial versus deleterious axes of sulfur amino acid biology, but not yet as a human therapy without further preclinical evaluation. DOI - https://doi.org/10.18632/aging.206358 Corresponding author - Sailendra N. Nichenametla - snichenametla@orentreich.org Abstract video - https://www.youtube.com/watch?v=0adFA_b-q1Q Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206358 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - bone, aging, methionine, glutathione, redox 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