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 (Aging-US) Scientific Integrity Process: https://aging-us.com/scientific-integrity

  1. High Tyrosine Levels Linked to Shorter Lifespan in Men

    3 NGÀY TRƯỚC

    High Tyrosine Levels Linked to Shorter Lifespan in Men

    BUFFALO, NY — November 13, 2025 — A new #research paper was #published in Volume 17, Issue 10 of Aging-US on October 3, 2025, titled “The role of phenylalanine and tyrosine in longevity: a cohort and Mendelian randomization study.” In this study led by Jie V. Zhao, Yitang Sun, Junmeng Zhang, and Kaixiong Ye from the University of Hong Kong and the University of Georgia, researchers investigated whether two amino acids, phenylalanine and tyrosine, affect how long people live (lifespan). The results suggest that higher levels of tyrosine are linked to shorter life expectancy in men, pointing to potential sex-specific approaches to promoting longevity. Phenylalanine and tyrosine are amino acids involved in metabolism and brain function. Both are found in protein-rich foods and dietary supplements, but their long-term effects on aging are not well understood. Tyrosine, in particular, is a building block of neurotransmitters such as dopamine, which regulate mood and cognitive function, making it a molecule of interest in aging research. The study analyzed data from more than 270,000 individuals in the UK Biobank. Using both observational and genetic methods, the researchers examined the associations between blood levels of phenylalanine and tyrosine with overall mortality and predicted lifespan. Although both amino acids were initially linked to higher mortality risk, only tyrosine showed a consistent and potentially causal association with reduced life expectancy in men. Genetic analyses estimated that elevated tyrosine levels could shorten men’s lifespan by nearly one year. No significant effect was observed in women. These findings remained consistent even after adjusting for related factors, including the role of phenylalanine. This suggests that tyrosine may independently influence aging. The researchers also observed that men tend to have higher tyrosine levels than women, which could partly explain the gender gap in lifespan. “Phenylalanine showed no association with lifespan in either men or women after controlling for tyrosine.” The exact mechanisms behind this effect are still under investigation. However, tyrosine’s involvement in insulin resistance and the production of stress-related neurotransmitters may be contributing factors. Insulin resistance is associated with many age-related diseases, and hormone-related pathways influenced by tyrosine may differ between men and women, potentially explaining the sex-specific outcomes. Although tyrosine is commonly marketed as a supplement for enhancing focus and mental performance, the study raises concerns about its long-term impact on lifespan. While the researchers did not directly study tyrosine supplementation, their findings suggest that people with high tyrosine levels may benefit from dietary adjustments. Strategies such as protein restriction could help reduce tyrosine levels and support healthier aging. Further studies are needed to confirm these findings and explore whether diet and lifestyle changes can safely lower tyrosine levels to promote longevity. DOI - https://doi.org/10.18632/aging.206326 Corresponding author - Jie V. Zhao - janezhao@hku.hk Abstract video - https://www.youtube.com/watch?v=rr0G44TD36M Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@Aging-US LinkedIn - https://www.linkedin.com/company/aging/ Bluesky - https://bsky.app/profile/aging-us.bsky.social Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

    4 phút
  2. Aging-US Supports the Future of Aging Research Mixer 2025

    5 NGÀY TRƯỚC

    Aging-US Supports the Future of Aging Research Mixer 2025

    Aging-US proudly sponsored the Future of Aging Research (FAR) Mixer 2025, hosted by the Aging Initiative on November 7 in Cambridge, MA, uniting students, researchers, and biotechnology leaders to advance aging research and shape a healthier, longer-lived future. Highlights from the FAR Mixer 2025 The 2025 FAR Mixer featured keynote speaker Dr. Kristen Fortney, Co-Founder and CEO of BioAge Labs, who shared insights into how translational research and clinical pipelines have evolved over the past decade. Dr. Fortney highlighted how obesity-targeting drugs are opening new avenues for metabolic and aging research. She explained that while obesity and osteoporosis are currently major therapeutic priorities, the next wave of reimbursable diseases will likely focus on muscle loss and chronic inflammation, reflecting their growing recognition as key factors in healthy aging. She also emphasized the importance of human databases in target discovery, cross-sector partnerships between pharma and biotech, and the increasing focus on small-molecule interventions to address age-related diseases. Focus talks showcased the diversity and depth of modern aging research. Full recap - https://aging-us.org/2025/11/aging-us-supports-the-future-of-aging-research-mixer-2025/ To learn more about the journal, please visit www.Aging-US.com​​ and connect with us on social media at: Facebook - www.facebook.com/AgingUS/ X - twitter.com/AgingJrnl Instagram - www.instagram.com/agingjrnl/ YouTube - www.youtube.com/@Aging-US LinkedIn - www.linkedin.com/company/aging/ Bluesky - bsky.app/profile/aging-us.bsky.social Pinterest - www.pinterest.com/AgingUS/ Spotify - open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

    5 phút
  3. Alpha-Synuclein Overexpression in Rats Reveals Early Clues to Synucleinopathies

    5 NGÀY TRƯỚC

    Alpha-Synuclein Overexpression in Rats Reveals Early Clues to Synucleinopathies

    Synucleinopathies are a group of age-related neurological disorders, including Parkinson’s disease, dementia with Lewy bodies, and multiple system atrophy. Most individuals are not diagnosed until these diseases have significantly progressed, as early symptoms, such as a reduced sense of smell, subtle cognitive or motor changes are too vague to serve as reliable indicators. To uncover specific biological signs that appear earlier and clearly point to the disease process, researchers from Saarland University developed a study titled “Brain region-specific and systemic transcriptomic alterations in a human alpha-synuclein overexpressing rat model,” featured as the cover Aging-US, Volume 17, Issue 10. Full blog - https://aging-us.org/2025/11/alpha-synuclein-overexpression-in-rats-reveals-early-clues-to-synucleinopathies/ Paper DOI - https://doi.org/10.18632/aging.206331 Corresponding author - Thomas Hentrich - thomas.hentrich@uni-saarland.de Abstract video - https://www.youtube.com/watch?v=Yl6AfVchkb0 Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206331 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, alpha-synuclein, transgenic rat model, different brain regions, transcriptome analysis To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@Aging-US LinkedIn - https://www.linkedin.com/company/aging/ Bluesky - https://bsky.app/profile/aging-us.bsky.social Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

    5 phút
  4. Exercise and L-BAIBA Supplement Boost Muscle and Bone Health in Aging Mice

    5 NGÀY TRƯỚC

    Exercise and L-BAIBA Supplement Boost Muscle and Bone Health in Aging Mice

    BUFFALO, NY — November 11, 2025 — A new #research paper was #published in Volume 17, Issue 10 of Aging-US on October 1, 2025, titled “L-β-aminoisobutyric acid (L-BAIBA) in combination with voluntary wheel running exercise enhances musculoskeletal properties in middle-age male mice.” In this study led by first author Julian A. Vallejo and corresponding author Michael J. Wacker from the University of Missouri, Kansas City, researchers investigated how L-β-aminoisobutyric acid (L-BAIBA), a natural compound released during exercise, works together with regular physical activity to improve muscle and bone health in middle-aged male mice. The findings may support new strategies to maintain musculoskeletal health in aging populations, especially those at risk for mobility loss or osteoporosis. Muscle and bone strength naturally decline with age, increasing the risk of falls, fractures, and reduced quality of life. While exercise remains the most effective way to counteract this deterioration, it is often difficult for older individuals to maintain sufficient activity levels to see results. L-BAIBA, a molecule naturally produced during physical activity, is known to promote energy metabolism and support muscle and bone cells. This study explored its potential to work in synergy with endurance exercise to maximize health benefits in aging bodies. Researchers studied 12-month-old male mice that were split into different groups. Some remained sedentary, while others exercised freely on running wheels. Half of each group received daily L-BAIBA supplementation. After three months, the mice that received both the supplement and exercise showed greater improvements than those receiving either one alone. The soleus, a slow-twitch muscle essential for endurance and balance, grew larger and stronger only in the combined treatment group. These muscles also shifted to a more fatigue-resistant fiber type and had a larger number of oxidative fibers. “To investigate this hypothesis, we subjected 12-month-old (as a model of middle-age) male C57BL6 mice to voluntary wheel running (VWR) with L-BAIBA (100mg/kg/day) (VWR+L-BAIBA), VWR alone, L-BAIBA alone, or none (CTRL) for three months.” The study also showed significant improvements in bone health. Mice that received both exercise and L-BAIBA developed thicker and denser trabecular bone, along with reduced fat levels in the bone marrow, indicators of stronger, healthier bones. These changes were not observed in the groups that only exercised or only received L-BAIBA. Although the compound caused minor changes in heart electrical activity, it did not affect heart size or overall function, suggesting it is safe in this setting. These findings suggest that L-BAIBA may enhance the benefits of physical activity by supporting muscle strength and bone structure, particularly in slow-twitch muscle fibers. This combination could serve as a therapeutic strategy to help older adults, including those unable to engage in regular exercise, maintain musculoskeletal health. As the aging population grows, there is a growing need for solutions that support muscle and bone health without requiring strenuous activity. This research highlights the potential of natural, exercise-related molecules like L-BAIBA to help maintain mobility and strength throughout aging. DOI - https://doi.org/10.18632/aging.206325 Corresponding author - Michael J. Wacker — wackerm@umkc.edu Abstract video - https://www.youtube.com/watch?v=A-zfrLUikfQ Visit https://www.Aging-US.com​​ and connect with us on social media at: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@Aging-US LinkedIn - https://www.linkedin.com/company/aging/ Bluesky - https://bsky.app/profile/aging-us.bsky.social Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

    4 phút
  5. 5 THG 11

    Epigenetic Aging Linked to Cognitive Decline in Hispanic/Latino Adults

    BUFFALO, NY — November 5, 2025 — A new #research paper was #published in Volume 17, Issue 10 of Aging-US on September 10, 2025, titled “Longitudinal associations of epigenetic aging with cognitive aging in Hispanic/Latino adults from the Hispanic Community Health Study/Study of Latinos.” In this study led by Myriam Fornage, from The University of Texas Health Science Center at Houston, researchers found that faster biological aging, measured by DNA-based epigenetic clocks, is associated with greater cognitive decline and higher risk of mild cognitive impairment (MCI) in Hispanic/Latino adults. The results highlight the potential of epigenetic clocks to track changes in brain health over time, helping improve early detection and monitoring of age-related cognitive problems. Cognitive decline and dementia are major public health concerns, especially among aging populations. In this study, researchers followed 2671 Hispanic/Latino adults (average age 57; 66% women) over a seven-year period. They measured each participant’s biological age using epigenetic clocks and assessed their cognitive performance at two time points. “We evaluated the associations of 5 epigenetic clocks and their between-visit change with multiple measures of cognitive aging that included a global and domain-specific cognitive function score at each visit, between-visit change in global and domain-specific cognitive function score, and MCI diagnosis at visit 2 (V2).” Epigenetic clocks estimate biological age based on DNA chemical modifications, called methylation, that accumulate with age. The study evaluated five different clocks, including newer models like GrimAge and DunedinPACE, which are designed to more accurately reflect health-related aging. The researchers found that individuals with faster biological aging showed lower cognitive function and higher probability of developing MCI over time. Among the five clocks studied, newer models such as GrimAge and DunedinPACE showed the strongest associations with memory, processing speed, and overall brain health. These findings suggest that tracking changes in biological age over time may be more effective than relying on a single measurement to identify those at risk for cognitive impairment. Importantly, the associations between biological aging and cognitive decline remained significant even after accounting for other known risk factors such as education, language preference, and cardiovascular health. This supports the idea that epigenetic clocks capture unique biological processes that influence brain aging. The study also found that the impact of changes in biological age over time was comparable to that of APOE4, a well-established genetic risk factor for Alzheimer’s disease. Overall, this is the first large-scale study to examine these associations in a Hispanic/Latino population, a group that is underrepresented in aging research. By identifying early biological signs of brain aging, this work highlights the potential of epigenetic clocks as tools for routine health assessments. Monitoring changes in these biological markers could help detect individuals at risk for cognitive decline and guide timely interventions to preserve brain health. DOI - https://doi.org/10.18632/aging.206317 Corresponding author - Myriam Fornage - Myriam.Fornage@uth.tmc.edu Abstract video - https://www.youtube.com/watch?v=kG0Y-F_sods To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@Aging-US LinkedIn - https://www.linkedin.com/company/aging/ Bluesky - https://bsky.app/profile/aging-us.bsky.social Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

    4 phút
  6. Alpha-Synuclein Triggers Early Gene Expression Changes in Parkinson’s Disease Model

    3 THG 11

    Alpha-Synuclein Triggers Early Gene Expression Changes in Parkinson’s Disease Model

    BUFFALO, NY — November 3, 2025 — A new #research paper featured on the #cover of Volume 17, Issue 10 of Aging-US was #published on October 20, 2025, titled “Brain region-specific and systemic transcriptomic alterations in a human alpha-synuclein overexpressing rat model.” In this study, led by first author Vivien Hoof and corresponding author Thomas Hentrich from Saarland University, Germany, researchers investigated how excess alpha-synuclein—a protein linked to Parkinson’s disease—affects gene activity in different brain regions and the gut. They found that early, region-specific gene disruptions may contribute to the appearance of disease, with some effects also detected in the gut. These early molecular changes could serve as biomarkers for Parkinson’s and point to new directions for treatment. Alpha-synuclein accumulates in the brains of individuals with Parkinson’s disease and other age-related neurological conditions known as synucleinopathies. To better understand this process, the research team used a genetically modified rat model that overexpresses human alpha-synuclein. They studied gene expression in the striatum, cortex, and cerebellum—three key brain regions involved in movement and cognition—and analyzed how these changes evolved with age. “Transcriptomic analyses were performed on gene and transcript level of striatal, frontocortical, and cerebellar tissue in 5- and 12-month-old transgenic (BAC SNCA) and wild type rats […]” The results showed that gene alterations appeared earlier and were more pronounced in young rats, particularly in the striatum and cortex, before any visible signs of disease manifested. This early disruption challenges the common belief that gene alterations gradually increase with age and suggests that early-life molecular changes may be critical in disease development. The researchers also found that many gene expression changes were unique to individual brain regions. However, they identified a set of genes that were consistently affected across all brain regions and the gut. This suggests that the disease may begin to affect the entire body—not just the brain—long before symptoms become noticeable. Several of the shared genes are involved in synaptic signaling and inflammation—processes known to be altered in Parkinson’s. Others are linked to dopamine production and neuronal plasticity, indicating potential early efforts by the brain to compensate for the harmful effects of the alpha-synuclein buildup. Overall, this study provides a detailed view of how alpha-synuclein affects gene networks early in the disease process. Understanding these changes may help identify biomarkers and develop targeted therapies before irreversible brain damage occurs. DOI - https://doi.org/10.18632/aging.206331 Corresponding author - Thomas Hentrich - thomas.hentrich@uni-saarland.de Abstract video - https://www.youtube.com/watch?v=Yl6AfVchkb0 Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206331 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, alpha-synuclein, transgenic rat model, different brain regions, transcriptome analysis To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@Aging-US LinkedIn - https://www.linkedin.com/company/aging/ Bluesky - https://bsky.app/profile/aging-us.bsky.social Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

    4 phút
  7. TRF1 Protein Loss Reduces Fat and Improves Metabolic Health in Mice Without Shortening Telomeres

    27 THG 10

    TRF1 Protein Loss Reduces Fat and Improves Metabolic Health in Mice Without Shortening Telomeres

    BUFFALO, NY — October 27, 2025 — A new #research paper was #published in Volume 17, Issue 9 of Aging-US on September 17, 2025, titled “Depletion of the TRF1 telomere-binding protein leads to leaner mice with altered metabolic profiles.” In this study led by first author Jessica Louzame Ruano and corresponding author Maria A. Blasco from the Spanish National Cancer Centre (CNIO), researchers investigated the role of TRF1, a protein known for protecting telomeres, in regulating whole-body metabolism. The results suggest that TRF1 influences metabolic health through mechanisms unrelated to its known function in telomere maintenance. Obesity and metabolic disorders are major health concerns, especially as people age. To explore TRF1’s role beyond telomere protection, the research team studied both normal mice and genetically modified mice that lacked TRF1. Mice without TRF1 remained leaner over time, resisted fat accumulation, and showed healthier blood sugar and insulin levels compared to normal mice. Importantly, these benefits occurred without any detectable shortening of telomeres. The leaner body composition in TRF1-deficient mice was not due to reduced food intake or increased physical activity. Instead, the fat loss appeared to result from biological changes in how energy was processed and stored. Male mice without TRF1 gained less weight and had lower LDL cholesterol levels, even on a high-fat diet. Female mice showed milder effects, reflecting known sex-based differences in susceptibility to diet-induced obesity. This highlights the importance of including both sexes in metabolic research. “Major metabolic pathways related with energy production and regulation of metabolism homeostasis were also found downregulated in Trf1-deficient mice.” Gene expression analysis in the liver revealed shifts in several key pathways. Genes related to fat production, energy generation, and muscle growth were downregulated, while genes linked to inflammation and cholesterol synthesis were upregulated. The mice also showed signs of higher energy expenditure and a shift from using fat to protein as an energy source, possibly due to their reduced fat reserves. However, some older mice developed mild liver stress, including fibrosis and DNA damage, suggesting a possible long-term trade-off. Overall, this study expands the understanding of how telomere-related proteins influence more than just cellular aging. By identifying a connection between TRF1 and metabolism, the research opens new possibilities for targeting TRF1 or its pathways to address obesity and related conditions. Still, further studies are needed to clarify how TRF1 affects fat development and whether similar effects occur in humans. DOI - https://doi.org/10.18632/aging.206320 Corresponding author - Maria A. Blasco — mblasco@cnio.es Abstract video - https://www.youtube.com/watch?v=7AG3TBgDZIw Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206320 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, Trf1, metabolism, leaner, fat, telomeres To learn more about the journal, visit https://www.Aging-US.com​​ and connect with us on social media at: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Bluesky - https://bsky.app/profile/aging-us.bsky.social Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

    3 phút
  8. PAI-1 Deficiency Protects Aging Female Mice from Muscle and Bone Loss

    23 THG 10

    PAI-1 Deficiency Protects Aging Female Mice from Muscle and Bone Loss

    BUFFALO, NY — October 23, 2025 — A new #research paper was #published in Volume 17, Issue 9 of Aging-US on September 11, 2025, titled “Roles of plasminogen activator inhibitor-1 in aging-related muscle and bone loss in mice.” In this study led by first author Takashi Ohira and corresponding author Hiroshi Kaji from Kindai University Faculty of Medicine, researchers found that female mice lacking the gene for plasminogen activator inhibitor-1 (PAI-1) were protected from age-related muscle weakness and bone thinning. This suggests that PAI-1 could be a potential target for future treatments to reduce frailty in aging populations. As the global population continues to age, more people are affected by conditions such as sarcopenia and osteoporosis. These disorders involve the progressive loss of skeletal muscle mass and bone density, leading to reduced mobility, a greater risk of falls, and a lower quality of life. To investigate the role of PAI-1 in aging, researchers compared young (6-month-old) and aged (24-month-old) male and female mice, with and without the PAI-1 gene. They found that PAI-1 levels increased with age in both sexes. However, only female mice lacking the PAI-1 gene experienced a significant reduction in age-related muscle and bone loss. Female mice without PAI-1 maintained stronger grip strength and greater muscle mass in their lower limbs. They also showed less cortical bone loss in their femurs and tibias. In contrast, male mice did not experience the same benefits, despite also showing increased levels of PAI-1 with age. These results suggest that PAI-1 contributes to aging-related decline in a sex-specific manner. “The present study found that lower limb muscle mass, gastrocnemius and soleus muscle tissue weights, and grip strength were significantly lower in 24-month-old male and female wild-type mice than in their 6-month-old counterparts.” PAI-1 plays key roles in blood clotting, inflammation, and cellular senescence—a process in which aging cells release harmful molecules that affect nearby tissues. One of these molecules, interleukin-6 (IL-6), is a major driver of inflammation. The researchers found that aged female mice lacking PAI-1 had lower IL-6 levels in both muscle and blood, suggesting that PAI-1 may contribute to muscle and bone loss by promoting inflammation. These protective effects were also not associated with changes in muscle protein turnover or reductions in fibrous tissue, reinforcing the idea that PAI-1’s impact is likely driven by inflammatory signaling. This study highlights PAI-1 as a promising therapeutic target for slowing or preventing age-related declines in muscle and bone health, particularly in women. Since postmenopausal women are especially vulnerable to osteoporosis and frailty, a better understanding of how PAI-1 contributes to aging could lead to new strategies for maintaining strength and mobility in later life. Further research is needed to explore how PAI-1 interacts with other age-related biological changes and why its effects differ between sexes. DOI - https://doi.org/10.18632/aging.206318 Corresponding author - Hiroshi Kaji - hkaji@med.kindai.ac.jp Abstract video - https://www.youtube.com/watch?v=hg4qKf-oO2I Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@Aging-US LinkedIn - https://www.linkedin.com/company/aging/ Bluesky - https://bsky.app/profile/aging-us.bsky.social Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

    4 phút

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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 (Aging-US) Scientific Integrity Process: https://aging-us.com/scientific-integrity

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