Aging-US

Aging Podcast

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

  1. há 5 h

    Three Herbal Extracts Protect Mitochondrial Function in a Cellular Model of Parkinson’s Disease

    BUFFALO, NY — September 9, 2026 — A new #research paper was #published in Volume 18 of Aging on August 13, 2026, titled “Protective effects of three herbal extracts on mitochondrial dysfunction in VPS13C-knockdown SH-SY5Y cells: implications for Parkinson’s disease.” The study was led by co-first authors Yih-Ru Wu and Chih-Hsin Lin from the Chang Gung Memorial Hospital, Chang Gung University College of Medicine in Taoyuan, Taiwan, and Pei-Syuan Huang from the School of Life Science at National Taiwan Normal University in Taipei, Taiwan. Corresponding authors I-Cheng Chen and Guey-Jen Lee-Chen are from the School of Life Science at National Taiwan Normal University. The paper identifies Wu, Lin, and Huang as equal contributors. Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized primarily by dysfunction and loss of dopaminergic neurons in the substantia nigra. Although its causes are complex, mitochondrial dysfunction and oxidative stress are important biological processes implicated in both sporadic and inherited forms of the disease. The researchers focused on VPS13C, also known as PARK23, a gene associated with a rare autosomal recessive form of early-onset parkinsonism. Loss of VPS13C function has previously been linked to impaired mitochondrial function. The study investigated three extracts used in traditional Chinese medicine: Uncaria rhynchophylla (UR), Gardenia jasminoides (GJ), and Scutellaria baicalensis (SB). Previous experimental studies have reported neuroprotective effects from these plants or their bioactive constituents in models relevant to PD. The researchers examined whether the extracts could protect cells against mitochondrial dysfunction associated with reduced VPS13C expression. Chemical analyses identified several potentially bioactive constituents in the extracts. UR contained rhynchophylline and isorhynchophylline; GJ contained geniposide and crocin; and SB contained several flavonoids, including baicalin, wogonoside, baicalein, wogonin, and oroxylin A. Across the concentrations initially tested, the three extracts maintained greater than 90% viability in SH-SY5Y cells after 24 hours, indicating low cytotoxicity under these experimental conditions. Full press release - https://www.aging-us.com/news-room/three-herbal-extracts-protect-mitochondrial-function-in-a-cellular-model-of-parkinsons-disease DOI - https://doi.org/10.18632/aging.206409 Corresponding authors - I-Cheng Chen - ichen@ntnu.edu.tw, Guey-Jen Lee-Chen - t43019@ntnu.edu.tw Abstract video - https://www.youtube.com/watch?v=kM8hO89d_9k Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206409 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, Parkinson’s disease, traditional Chinese medicine, VPS13C knockdown, mitochondrial dysfunction, oxidative stress To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

    Three Herbal Extracts Protect Mitochondrial Function in a Cellular Model of Parkinson’s Disease
  2. há 5 dias

    Behind the Study: How Aging Impairs Tuberculosis Clearance

    Dr. Falak Pahwa, Dr. Ranjan Kumar Nanda, and Mr. Ashish Gupta from the International Centre for Genetic Engineering and Biotechnology (ICGEB) in New Delhi, India, discuss their research paper, recently published in Volume 18 of Aging, titled “Host immunosenescence compromises Mycobacterium tuberculosis clearance.” Video interview - https://www.youtube.com/watch?v=bSaJaB751kM DOI - https://doi.org/10.18632/aging.206374 Corresponding author - Ranjan Kumar Nanda - ranjan@icgeb.res.in Abstract video - https://www.youtube.com/watch?v=isPD8ZmUjv8 Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206374 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, tuberculosis, immunosenescence, TFH cells, proteomics To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

    Behind the Study: How Aging Impairs Tuberculosis Clearance
  3. há 6 dias

    Indy Gene Reduction Linked to Healthier Gut Microbiota and Longer Lifespan in Fruit Flies

    BUFFALO, NY — September 3, 2026 — A new #research paper was published in Volume 18 of Aging on August 12, 2026, titled “Indy reduction decreases aging-related dysbiosis in Drosophila.” The study was led by first author Danielle N. A. Lesperance from the University of Connecticut. Corresponding authors Blanka Rogina and Nichole A. Broderick are affiliated with the University of Connecticut Health and Johns Hopkins University, respectively. Broderick is also affiliated with the University of Connecticut. The Indy gene—short for “I’m not dead yet”—encodes a plasma membrane citrate transporter in Drosophila melanogaster. Previous research has shown that reducing Indy activity can extend lifespan and preserve metabolic and intestinal health in flies. Because aging is also associated with disruption of the gut microbiota, the researchers investigated whether changes in intestinal microbes contribute to the longevity effects associated with reduced Indy activity. The researchers compared control flies with Indy heterozygous flies under conventional conditions and axenic conditions, in which microbes were absent. They also examined bacterial load and microbiota composition and performed RNA sequencing of the midgut to investigate molecular pathways connecting Indy, the microbiota, intestinal homeostasis, and aging. Full press release - https://www.aging-us.com/news-room/indy-gene-reduction-linked-to-healthier-gut-microbiota-and-longer-lifespan-in-fruit-flies DOI - https://doi.org/10.18632/aging.206408 Corresponding authors - Blanka Rogina - Rogina@uchc.edu, and Nichole A. Broderick - nbroder1@jhu.edu Abstract video - https://www.youtube.com/watch?v=d0PfTj_Pg7U Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206408 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, Indy, host-microbe interactions, lifespan, Drosophila melanogaster To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

    Indy Gene Reduction Linked to Healthier Gut Microbiota and Longer Lifespan in Fruit Flies
  4. 1 de set.

    Developmental Programs Could Help Drive the Aging Process

    Why do we age? For decades, one of the dominant explanations has been that cells and tissues gradually accumulate molecular damage until they can no longer function normally. DNA mutations, damaged proteins, mitochondrial dysfunction, epigenetic alterations, and other forms of cellular wear have all been proposed as major drivers of aging. But another theory offers a very different possibility: some aspects of aging may result not from biological systems breaking down, but from developmental programs continuing to operate after they are no longer beneficial. A research perspective published in Volume 18 of Aging titled “A brief history of the hyperfunction theory of aging and future directions,” traces the development of this idea and examines where the field may go next. The article was written by João Pedro de Magalhães from the Genomics of Ageing and Rejuvenation Lab, Department of Inflammation and Ageing, College of Medicine and Health, University of Birmingham, United Kingdom. Rather than presenting a new experiment, the paper combines historical analysis, evolutionary theory, experimental evidence, and the author’s own perspective on how programmatic models could reshape aging research. Full blog post - https://aging-us.org/2026/09/developmental-programs-could-help-drive-the-aging-process/ DOI - https://doi.org/10.18632/aging.206403 Corresponding author - João Pedro de Magalhães - jp@senescence.info Abstract video - https://www.youtube.com/watch?v=VwC6aJoUUQo Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206403 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, antagonistic pleiotropy, longevity, programmatic aging, quasi-program To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

    Developmental Programs Could Help Drive the Aging Process
  5. 31 de ago.

    Higher TMAO Levels Linked to Cardiometabolic Risk and Brain Atrophy in Older Adults

    BUFFALO, NY — August 31, 2026 — A new research paper was published in Volume 18 of Aging on August 11, 2026, titled “TMAO is associated with higher age, cardiometabolic risk factors and degenerative alterations of the brain in healthy elderly adults.” The study was led by first author Gunter Almer from the Clinical Institute of Medical and Chemical Laboratory Diagnostics at the Medical University of Graz in Austria. The corresponding author is Markus Herrmann from the same institution. Trimethylamine N-oxide (TMAO) is a metabolite linked to the gut microbiome. Its precursor, trimethylamine (TMA), is produced by gut bacteria from dietary compounds such as L-carnitine and choline and is subsequently converted to TMAO in the liver. Higher circulating TMAO concentrations have previously been associated with cardiovascular and metabolic diseases, but evidence concerning its role in aging and neurodegeneration remains inconsistent. To investigate these relationships, the researchers measured serum TMAO in 487 neurologically normal, community-dwelling adults from the Austrian Stroke Prevention Study and Austrian Stroke Prevention Family Study. Participants had a mean age of 67.8 years and underwent cognitive testing assessing memory, executive function, and motor abilities. Brain MRI data were also available for 180 participants, allowing the researchers to examine structural and vascular brain changes. Full press release - https://www.aging-us.com/news-room/higher-tmao-levels-linked-to-cardiometabolic-risk-and-brain-atrophy-in-older-adults Paper DOI: https://doi.org/10.18632/aging.206401 Corresponding author: Markus Herrmann - markus.herrmann@medunigraz.at Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords: TMAO, aging, risk factors, cognitive function, brain atrophy To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

    Higher TMAO Levels Linked to Cardiometabolic Risk and Brain Atrophy in Older Adults
  6. 26 de ago.

    Metformin Emerges as a Promising Candidate at the Intersection of Aging and Longevity

    BUFFALO, NY — August 26, 2026 — A new #review was #published in Volume 18 of Aging on August 10, 2026, titled “Metformin at the convergence of aging and longevity.” The review was authored by Jarra Manneh, May Alasmar and Nady El Hajj from the College of Health and Life Sciences at Hamad Bin Khalifa University, Qatar Foundation, Doha, Qatar. Corresponding author Nady El Hajj is also affiliated with the College of Science and Engineering at Hamad Bin Khalifa University, Doha, Qatar. Metformin has been used for decades as a first-line treatment for type 2 diabetes, but increasing interest in geroscience has raised a broader question: could this widely used metabolic drug also influence the biological processes that drive aging? The review brings together evidence from cellular studies, animal models, human observational research, and clinical trials examining how metformin interacts with multiple hallmarks of aging. A central mechanism involves AMP-activated protein kinase (AMPK), a major cellular energy sensor. By inhibiting mitochondrial complex I and altering cellular energy balance, metformin can activate AMPK, triggering downstream effects that include suppression of mechanistic target of rapamycin (mTOR) signaling, increased autophagy and mitochondrial biogenesis, and reduced oxidative stress. Metformin also improves insulin sensitivity and reduces hepatic gluconeogenesis, connecting its established metabolic effects with nutrient-sensing pathways involved in aging biology. Full press release - https://www.aging-us.com/news-room/metformin-emerges-as-a-promising-candidate-at-the-intersection-of-aging-and-longevity DOI - https://doi.org/10.18632/aging.206407 Corresponding author - Nady El Hajj - nelhajj@hbku.edu.qa Abstract video - https://www.youtube.com/watch?v=5Ws-x8e1klI Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206407 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, metformin, AMPK, mTOR, epigenetic modifications To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

    Metformin Emerges as a Promising Candidate at the Intersection of Aging and Longevity
  7. 24 de ago.

    Targeting POLG Reduces Breast Cancer Stemness Through Mitochondrial Dysfunction

    BUFFALO, NY — August 24, 2026 — A new research paper was published in Volume 18 of Aging on August 8, 2026, titled “Investigating POLG-driven modulation of cancer stemness: a pilot study in breast cancer cells.” The study was led by first author Chiara Chinigò from the Italian National Research Center on Aging (IRCCS INRCA), Cosenza, Italy. Corresponding authors Federica Sotgia and Michael P. Lisanti are affiliated with the University of Salford, United Kingdom, and Lunella Biotech in Ottawa, Canada, with Lisanti additionally affiliated with the Institute of Mental Health Research at the University of Ottawa and The Royal Ottawa Hospital, and Université Laval in Québec. Breast cancer stem cells (CSCs) are a small population of tumor cells with self-renewal and differentiation capabilities that are associated with tumor progression, metastasis, and therapy resistance. These cells rely heavily on mitochondrial biogenesis and oxidative metabolism, making mitochondrial function a potential metabolic vulnerability. The researchers focused on mitochondrial DNA polymerase gamma (POLG), the enzyme responsible for mitochondrial DNA (mtDNA) replication and repair. POLG contains a catalytic subunit encoded by POLG1 and an accessory subunit encoded by POLG2. Using estrogen receptor-positive MCF-7 breast cancer cells, the researchers genetically silenced POLG1 and POLG2 to determine whether disrupting mtDNA maintenance would affect cancer stemness. POLG1 knockdown reduced mtDNA content by approximately 80%, while POLG2 knockdown produced an approximately 70% reduction. Both interventions impaired mitochondrial function, lowering the mtDNA-encoded respiratory-chain protein MTCO2, mitochondrial membrane potential, respiration, and ATP production. Full press release - https://www.aging-us.com/news-room/targeting-polg-reduces-breast-cancer-stemness-through-mitochondrial-dysfunction DOI - https://doi.org/10.18632/aging.206406 Corresponding authors - Federica Sotgia - fsotgia@gmail.com (ORCiD: 0000-0003-2826-4529), Michael P. Lisanti - michaelp.lisanti@gmail.com (ORCiD: 0000-0003-2034-1382) Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206406 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, breast cancer, cancer stem cells, cancer metabolism, POLG, mitochondrial DNA To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

    Targeting POLG Reduces Breast Cancer Stemness Through Mitochondrial Dysfunction
  8. 24 de ago.

    Aging Partners with Aging Research and Drug Discovery Meeting (ARDD) as Media Partner

    BUFFALO, NY — August 24, 2026 — Aging is pleased to announce its partnership as a media partner of the 13th Aging Research and Drug Discovery Meeting (ARDD), taking place October 1–3, 2026, at the David Rubenstein Treehouse at Harvard University in Boston, Massachusetts. ARDD brings together leading researchers, clinicians, biotech innovators and industry experts to advance the understanding of aging and accelerate the development of interventions targeting age-related diseases. The partnership reflects Aging’s continued commitment to supporting the growth and visibility of research in the fields of aging and longevity. As a media partner, Aging will help promote ARDD and raise awareness of the meeting through its digital and social media channels, connecting the event with the journal’s global audience. Together, Aging and ARDD will help bring greater visibility to the growing scientific community working to advance healthy longevity and address age-related diseases. To learn more about the journal, please visit www.Aging-US.com​​ and connect with us on social media at: Bluesky - bsky.app/profile/aging-us.bsky.social ResearchGate - www.researchgate.net/journal/Aging-1945-4589 X - twitter.com/AgingJrnl Facebook - www.facebook.com/AgingUS/ Instagram - www.instagram.com/agingjrnl/ LinkedIn - www.linkedin.com/company/aging/ Reddit - www.reddit.com/user/AgingUS/ Pinterest - www.pinterest.com/AgingUS/ YouTube - www.youtube.com/@Aging-US Spotify - open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

    Aging Partners with Aging Research and Drug Discovery Meeting (ARDD) as Media Partner

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

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