Aging-US

Aging-US Podcast

Aging-US is dedicated to advancing our understanding of the biological mechanisms that drive aging and the development of age-related diseases. Our mission is to serve as a platform for high-quality research that uncovers the cellular, molecular, and systemic processes underlying aging, and translates these insights into strategies to extend healthspan and delay the onset of chronic disease. Read about the Aging-US Scientific Integrity Process: https://aging-us.com/scientific-integrity

  1. Extending Healthspan Through Public Health and Longevity Medicine

    21H AGO

    Extending Healthspan Through Public Health and Longevity Medicine

    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

    5 min
  2. Methylene Blue May Help Protect Hair Follicle Stem Cells from Aging and Metabolic Stress

    2D AGO

    Methylene Blue May Help Protect Hair Follicle Stem Cells from Aging and Metabolic Stress

    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

    5 min
  3. EDITORS’ CHOICE: Epigenetic age acceleration with MRI biomarkers of aging and Alzheimer’s...

    2D AGO

    EDITORS’ CHOICE: Epigenetic age acceleration with MRI biomarkers of aging and Alzheimer’s...

    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

    2 min
  4. Anti-Aging Strategies Aim to Target Harmful Senescent Cells While Preserving Beneficial Ones

    6D AGO

    Anti-Aging Strategies Aim to Target Harmful Senescent Cells While Preserving Beneficial Ones

    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

    5 min
  5. Glutathione Pathway May Hold the Key to Safer Anti-Obesity Interventions

    MAY 13

    Glutathione Pathway May Hold the Key to Safer Anti-Obesity Interventions

    Efforts to improve metabolic health through dietary interventions often come with trade-offs. Some approaches that reduce obesity or extend lifespan in laboratory models can also negatively affect other tissues, including bone. One example is sulfur amino acid restriction (SAAR), a diet low in methionine and lacking cysteine that has repeatedly shown strong anti-obesity effects in animal studies. However, despite these promising metabolic benefits, SAAR has also been associated with reduced bone mineral density, weaker bones, and increased marrow fat accumulation. This has led researchers to ask whether the metabolic benefits of SAAR can be separated from its harmful skeletal effects. A new research paper was published in Volume 18 of Aging-US, titled “D, L-Buthionine-(S, R)-sulfoximine recapitulates the anti-obesity effects of sulfur amino acid restriction without the associated deleterious effects on bone in male mice.” The researchers investigated whether those metabolic benefits could be achieved without the same harmful effects on bone. The study was led by first author Naidu B. Ommi and corresponding author Sailendra N. Nichenametla from the Orentreich Foundation for the Advancement of Science Inc., in collaboration with Dwight A. L. Mattocks from the same institution and Mark C. Horowitz from the Yale University School of Medicine. Full blog - https://aging-us.org/2026/05/glutathione-pathway-may-hold-the-key-to-safer-anti-obesity-interventions/ Paper DOI - https://doi.org/10.18632/aging.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

    6 min
  6. Aging Immune Systems Show Reduced Ability to Clear Tuberculosis During Treatment

    MAY 12

    Aging Immune Systems Show Reduced Ability to Clear Tuberculosis During Treatment

    BUFFALO, NY — May 12, 2026 — A new #research paper was #published in Volume 18 of Aging-US on May 4, 2026, titled “Host immunosenescence compromises Mycobacterium tuberculosis clearance.” The study was led by first author Falak Pahwa and corresponding author Ranjan Kumar Nanda from the International Centre for Genetic Engineering and Biotechnology (ICGEB), New Delhi, India. In this study, the authors investigated how aging alters immune responses during tuberculosis infection and treatment. Tuberculosis remains one of the world’s deadliest infectious diseases, and older adults are particularly vulnerable due to immunosenescence, the gradual decline of immune function that occurs with aging. Despite the growing burden of tuberculosis in aging populations worldwide, most experimental models continue to rely on young adult animals that do not accurately reflect immune aging. Using multiple age groups of C57BL/6 mice, the researchers examined how aging affects the body’s ability to control Mycobacterium tuberculosis during treatment with rifampicin and isoniazid (RIF-INH), two cornerstone anti-tuberculosis drugs. While young and older mice initially showed similar bacterial burden following infection, older mice demonstrated significantly delayed bacterial clearance in the lungs during the early phase of treatment. Importantly, the study identified several age-associated immune abnormalities linked to impaired bacterial clearance. Older mice exhibited chronic inflammatory signaling, altered T cell responses, accumulation of T-follicular cytotoxic (TFC)-like cells, and evidence of mitochondrial dysfunction within immune cells. Proteomic analysis of splenic CD4+CD44+ T cells further revealed dysregulation of mitochondrial proteins involved in cellular metabolism and immune function. “Collectively, these findings suggest that age-associated immune alterations may disrupt immunometabolic pathways, thereby contributing to the delayed Mtb clearance.” The researchers also observed that older mice maintained elevated inflammatory cytokine levels and developed persistent lung inflammation even after treatment had begun. At the same time, key protective immune responses appeared functionally impaired, suggesting that aging may disrupt the balance between inflammation and effective pathogen control. Together, these findings suggest that age-related immunometabolic dysfunction may play a major role in the reduced treatment response observed in older hosts. Notably, the study found that delayed bacterial clearance in older mice did not appear to result primarily from liver toxicity or impaired drug metabolism. Instead, the evidence suggested that age-related immune dysfunction itself was the dominant factor limiting effective bacterial elimination during therapy. The paper further highlights the emerging importance of mitochondrial health in immune cell function during aging. The authors propose that targeting age-associated immunometabolic defects and mitochondrial dysfunction may represent a promising strategy for improving tuberculosis treatment outcomes in elderly populations. Overall, this study provides new insight into why older adults experience poorer tuberculosis outcomes despite receiving standard therapy. As global populations continue to age, understanding how immunosenescence alters infectious disease responses may become increasingly important for the development of more effective treatment strategies and age-adapted therapeutic interventions. DOI - https://doi.org/10.18632/aging.206374 Corresponding author - Ranjan Kumar Nanda - ranjan@icgeb.res.in Abstract video - https://www.youtube.com/watch?v=isPD8ZmUjv8 Website - https://www.Aging-US.com​​ MEDIA@IMPACTJOURNALS.COM

    4 min
  7. Large-Scale Multi-Omics Study Aims to Decode Aging in the Indian Population

    MAY 7

    Large-Scale Multi-Omics Study Aims to Decode Aging in the Indian Population

    BUFFALO, NY — May 7, 2026 — A new #research paper was #published in Volume 18 of Aging-US on April 24, 2026, titled “The BHARAT study: a multi-modal, multi-omics investigation of aging signatures in the Indian population.” The study was led by first author Suramya Asthana and corresponding author Deepak Kumar Saini from the Indian Institute of Science (IISc). The authors introduce the BHARAT Study (Biomarkers of Healthy Aging, Resilience, Adversity, and Transitions), India’s first large-scale, discovery-driven multi-omics cohort focused on understanding biological aging in the Indian population. The initiative was developed to address a major gap in aging research, as most existing biological age models and aging datasets have been derived primarily from Western populations. The BHARAT study is a multi-center, cross-sectional observational cohort that integrates clinical, molecular, lifestyle, and environmental data from participants across diverse demographic groups in India. The initiative aims to enroll healthy volunteers spanning multiple age groups, with balanced rural-urban and sex representation. Biological samples—including blood, urine, stool, cheek swabs, and hair—will undergo extensive multi-omics profiling, including epigenomics, proteomics, metabolomics, lipidomics, metagenomics, and immune phenotyping. “By generating interoperable, high-resolution data suited for mechanistic modelling and machine learning, BHARAT contributes a resource of global relevance that would be capable of refining universal models of aging biology while revealing novel, population-specific pathways that inform prevention and intervention strategies.” The initiative uses a hub-and-spoke framework centered at the Indian Institute of Science, which serves as the central hub for biobanking, multi-omics analysis, computational integration, and AI-driven modeling. Clinical and community partners across India contribute participant recruitment, clinical assessments, and biological sampling, enabling the study to capture the country’s extraordinary genetic, environmental, dietary, and socioeconomic diversity. A major focus of the study is the development of population-specific biological aging signatures and predictive models tailored to Indian populations. Researchers aim to identify biomarkers associated with resilience, frailty, and age-related decline while also recalibrating biological clocks that may not accurately reflect aging trajectories in non-Western populations. The study further seeks to establish standardized reference datasets and create scalable infrastructure for future longitudinal aging research in India. Importantly, the BHARAT study combines untargeted discovery-based omics technologies with advanced artificial intelligence and machine learning approaches. By integrating molecular data with clinical and lifestyle information, the initiative aims to improve understanding of how biological aging is shaped by genetics, environment, nutrition, infection burden, and social determinants of health. Overall, this study establishes a comprehensive framework for aging research in one of the world’s most diverse populations. By generating large-scale, population-specific biological datasets, the BHARAT initiative may help advance precision aging research, improve risk prediction models, and support the development of more personalized approaches to healthy aging and disease prevention. DOI - https://doi.org/10.18632/aging.206373 Corresponding author - Deepak Kumar Saini - deepaksaini@iisc.ac.in Abstract video - https://www.youtube.com/watch?v=qH2AbitDURQ Website - https://www.Aging-US.com​​ MEDIA@IMPACTJOURNALS.COM

    4 min
  8. Human Telomerase Shows Selective Cross-Species Activity, Revealing Limits of Animal Models

    MAY 5

    Human Telomerase Shows Selective Cross-Species Activity, Revealing Limits of Animal Models

    BUFFALO, NY — May 5, 2026 — A new #research paper was #published in Volume 18 of Aging-US on April 13, 2026, titled “Cross species activity of TERT human telomerase component.” The study was led by co–first authors Raúl Sánchez-Vázquez and Paula Martínez, with María A. Blasco serving as corresponding author, from the Spanish National Cancer Centre (CNIO), Madrid, Spain. In this study, the researchers explored a key question in aging and regenerative medicine: can the human telomerase protein function effectively in other species commonly used in preclinical research? Telomerase plays a central role in maintaining chromosome integrity by preventing telomere shortening—a process closely linked to cellular aging and disease. To investigate this, the team introduced the human telomerase catalytic subunit (TERT) into primary lung fibroblasts from several mammalian species, including monkey, pig, rabbit, rat, dog, and mouse. They then assessed both biochemical activity and the ability of telomerase to extend telomeres over time. The results revealed a clear distinction between biochemical compatibility and true biological function. In vitro, human TERT was able to form active complexes with telomerase RNA from several species, including monkey, pig, rabbit, and rat. However, this activity did not always translate into effective telomere maintenance in living cells. Notably, only human and non-human primate cells showed progressive telomere lengthening over time. In contrast, other species—even those showing initial enzymatic activity—failed to sustain telomere extension during long-term culture. In some cases, telomeres continued to shorten, suggesting that functional integration of telomerase depends on additional species-specific factors. The study also uncovered important limitations in commonly used animal models. Mouse and canine cells did not support human TERT activity, and in some cases, expression of the human enzyme led to reduced cell viability and signs of cellular stress. “These results reveal that only non-human primate cells support full functional activity of the human telomerase protein in a cellular context, underscoring their suitability as preclinical models for telomerase-based therapeutic strategies.” Importantly, the findings highlight that successful telomerase activity in a test tube does not necessarily reflect what happens inside a living cell. The recruitment, regulation, and function of telomerase depend on a complex network of interacting proteins and cellular processes, many of which differ across species. Overall, this study provides important insight into the challenges of translating telomerase-based therapies from preclinical models to humans. By identifying non-human primates as the most compatible system, the work offers a clearer path forward for developing therapies aimed at treating telomere-related diseases and age-associated conditions. DOI - https://doi.org/10.18632/aging.206372 Corresponding author - Maria A. Blasco - mblasco@cnio.es Abstract video - https://www.youtube.com/watch?v=XxjjId5i_Ww 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

    4 min

Ratings & Reviews

4
out of 5
2 Ratings

About

Aging-US is dedicated to advancing our understanding of the biological mechanisms that drive aging and the development of age-related diseases. Our mission is to serve as a platform for high-quality research that uncovers the cellular, molecular, and systemic processes underlying aging, and translates these insights into strategies to extend healthspan and delay the onset of chronic disease. Read about the Aging-US Scientific Integrity Process: https://aging-us.com/scientific-integrity

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