Our bodies are quite miraculous machines. We are born with a genome that contains the code for every protein necessary for survival. We develop and produce hormones that allow us to reproduce and have children. But what happens to us as we age? This question has puzzled scientists for years while they offer theory after theory.

In 1957, evolutionary biologist George Williams proposed what he called the antagonistic pleiotropy hypothesis as a theory of how and why we age. He claimed that our bodies express a gene that has benefits for our early life, but that same gene will harm us later on. His hypothesis has inspired aging research and led to a story about a chemical discovered deep within the dirt of an island floating in the Pacific.

In 1964, Canadian researchers, led by Stanley Skoryna from McGill University, set sail out of Halifax for Easter Island—a speck of land floating 2,000 miles off the coast of Chile, where the human population is small but life is diverse. They were hoping to retrieve precious specimens from the island before its land was tarnished with the building of a new airport. Stanley and his team collected hundreds of plant samples, countless animal specimens, and took blood and saliva from all 949 of the island’s residents.

What they found buried in the dirt on Easter Island would turn out to be the biggest treasure of all: a bacteria that would mystify scientists for the next 50 years. This bacteria was found to create a chemical now known as rapamycin, cleverly named after Easter Island’s native name, Rapa Nui.

Read the full article: https://www.impactjournals.com/journals/blog/aging/rapamycin-miracle-chemical-discovered-easter-islands-dirt/

About Aging

Launched in 2009, Aging publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

Please visit our website at http://www.Aging-US.com​​ or connect with us on:

Twitter - https://twitter.com/AgingJrnl​
Facebook - https://www.facebook.com/AgingUS/​
SoundCloud - https://soundcloud.com/aging-us​
YouTube - https://www.youtube.com/agingus​
LinkedIn -  https://www.linkedin.com/company/aging​

Aging is published by Impact Journals, LLC please visit http://www.ImpactJournals.com​​ or connect with @ImpactJrnls

Media Contact
18009220957
MEDIA@IMPACTJOURNALS.COM

Aging

Rapamycin: The Miracle Compound From Easter Island

Listen to a blog summary of the research paper selected as the cover for Volume 14, Issue 4 of Aging (Aging-US):

Aging seems nearly synonymous with brewing cognitive decline, but does it have to be? There are interventions that may help preserve cognitive function with age, however, the first order of business is identifying early biological aging markers that present before symptoms begin emerging. Mid-life biomarkers that can indicate accelerated aging and predict age-related cognitive decline (including Alzheimer’s disease and dementia) may provide humans with enough time to course-correct and improve our quality of life in old age.

The latest to endeavor in search of these early aging markers are researchers from Northwestern University Feinberg School of Medicine, University of Texas Health Science Center at San Antonio, University of Pennsylvania, Boston University School of Medicine, National Institute on Aging from the National Institutes of Health, University of Minnesota, Columbia University Mailman School of Public Health, Kaiser Permanente Division of Research, University of Texas at Austin, University of California San Francisco, and the San Francisco Veterans Affairs Medical Center. Their new research study was published in Aging (Aging-US) as the cover paper in Volume 14, Issue 4, on February 27, 2022. The paper is entitled, “Mid-life epigenetic age, neuroimaging brain age, and cognitive function: coronary artery risk development in young adults (CARDIA) study.”

Full blog - https://aging-us.org/2022/03/trending-with-impact-cognitive-decline-predicted-from-middle-age/

Paper DOI - https://doi.org/10.18632/aging.203918

Corresponding Authors - Yinan Zheng - y-zheng@northwestern.edu, Kristine Yaffe - Kristine.Yaffe@ucsf.edu, and Lifang Hou - l-hou@northwestern.edu

Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.203918

Keywords - cognitive function, epigenetic age, brain age, DNA methylation, magnetic resonance imaging

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

Please visit our website at http://www.Aging-US.com​​ and connect with us:

SoundCloud - https://soundcloud.com/Aging-Us
Facebook - https://www.facebook.com/AgingUS/
Twitter - https://twitter.com/AgingJrnl
Instagram - https://www.instagram.com/agingjrnl/
YouTube - https://www.youtube.com/agingus​
LinkedIn - https://www.linkedin.com/company/aging/
Pinterest - https://www.pinterest.com/AgingUS/

Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com​​

Media Contact
18009220957
MEDIA@IMPACTJOURNALS.COM

Aging (Aging-US)

Trending With Impact: Cognitive Decline Predicted from Middle-Age

BUFFALO, NY- May 11, 2022 – A new research perspective was published in Oncoscience journal by Mikhail Blagosklonny, M.D., Ph.D., entitled, “Altos Labs and the quest for immortality: but can we live longer right now?”

“Here I discuss how combining rapamycin with other modalities may let us live long enough to benefit from future discoveries in cellular reprogramming and what needs to be done at Altos Labs to make this happen.”

Altos Labs—a new anti-aging biotechnology company funded by multiple billionaire investors, including Jeff Bezos and Yuri Milner—has reported a focus on reprogramming cells in order to reverse the trajectory of diseases, and thus, reverse aging.

In his research perspective, Dr. Blagosklonny writes that potential life-extension with rapamycin may allow us to win time while awaiting future discoveries that will reverse aging.

“Rapamycin treatment is rapidly becoming a mainstream anti-aging intervention.” 

However, Dr. Blagosklonny also writes that rapamycin alone is unlikely to extend lifespan sufficiently to benefit from Altos Labs’ future discoveries in our lifetime.

“If Altos Labs would allocate a small percentage of its funding to develop rapamycin based drug combinations, then additional decades of life extension may be available 3–5 years from now.”

“The number of potential combinations with rapamycin is enormous.” 

Read Dr. Blagosklonny’s research perspective: https://www.oncoscience.us/article/552/text/ 

Correspondence to: Mikhail V. Blagosklonny 

Email: Blagosklonny@oncotarget.com, Blagosklonny@rapalogs.com 

Keywords: aging, longevity, lifespan, geroscience, rapalogs, gerostatics

Follow Dr. Blagosklonny on Twitter: https://twitter.com/Blagosklonny

For media inquiries, please contact media@impactjournals.com.

Oncoscience Journal Office
6666 East Quaker Str., Suite 1D
Orchard Park, NY 14127
Phone: 1-800-922-0957, option 4

###

Press Release: Altos Labs Research Perspective by Dr. Blagosklonny

BUFFALO, NY- January 9, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 24, entitled, “Systemic changes induced by autologous stem cell ovarian transplant in plasma proteome of women with impaired ovarian reserves.”

Patients with poor ovarian response (POR) and premature ovarian insufficiency (POI) are challenging to treat, with oocyte donation remaining as the only feasible option to achieve pregnancy in some cases. The Autologous stem cell ovarian transplantation (ASCOT) technique allows follicle development, enabling pregnancies and births of healthy babies in these patients. Previous research suggests that growth factors and cytokines secreted by stem cells are partially responsible for their regenerative properties. Indeed, ASCOT beneficial effects are associated with the presence of different bone marrow derived stem cell- secreted factors in plasma. 

In this new study, researchers Anna Buigues, Noelia Ramírez-Martin, Jessica Martínez, Nuria Pellicer, Marcos Meseguer, Antonio Pellicer, and Sonia Herraiz from IVIRMA Global Research Alliance aimed to assess whether ASCOT induces any modifications in the plasma proteomic profile of patients with impaired ovarian reserves.

“In this study, we aimed to assess if the ASCOT technique modifies the signature of the human plasma proteome, reveal the mechanisms underlying its beneficial effects on the ovary, and identify key regulators of ovarian aging.”

Discriminant analysis highlighted clear distinctions between the plasma proteome before (PRE), during stem cell mobilization and collection (APHERESIS) and three months after ASCOT (POST) in patients with POR and POI. Both the stem cell mobilization and ASCOT technique induced statistically significant modifications in the plasma composition, reversing some age-related protein expression changes. In the POR group, functional analysis revealed an enrichment in processes related to the complement cascade, immune system, and platelet degranulation, while in the POI group, enriched processes were also associated with responses to oxygen-containing compounds and growth hormones, and blood vessel maturation. 

“In conclusion, our findings highlight the potential proteins and biological processes that may promote the follicle activation and growth observed after ASCOT.”

DOI - https://doi.org/10.18632/aging.205400

Corresponding author - Sonia Herraiz - sonia_herraiz@iislafe.es

Sign up for free Altmetric alerts about this article - 
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205400

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

Keywords - aging, plasma proteomic profile, autologous stem cell ovarian transplantation, poor ovarian response, premature ovarian insufficiency

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

Please visit our website at https://www.Aging-US.com​​ and connect with us:

SoundCloud - https://soundcloud.com/Aging-Us
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/
Pinterest - https://www.pinterest.com/AgingUS/

Media Contact
18009220957
MEDIA@IMPACTJOURNALS.COM

Systemic Changes Induced by ASCOT in Plasma Proteome of Women With Impaired Ovarian Reserves

Traditional Chinese medicine has long been explored for its potential in treating various diseases, including cancer. Lithospermum erythrorhizon, or purple gromwell, is a mysterious plant native to East Asia, and its dried root is often referred to as Zicao. Acetylshikonin, a compound derived from Zicao, has shown promise in exhibiting a variety of anti-cancer properties. While the effects of acetylshikonin on lung cancer are not yet fully understood, recent research has shed light on its potential as a therapeutic agent. 

In a new study, researchers Shih-Sen Lin, Tsung-Ming Chang, Augusta I-Chin Wei, Chiang-Wen Lee, Zih-Chan Lin, Yao-Chang Chiang, Miao-Ching Chi, and Ju-Fang Liu from Shin Kong Wu Ho-Su Memorial Hospital, Chang Gung Memorial Hospital, Chang Gung University of Science and Technology, Ming Chi University of Technology, Taipei Medical University, and China Medical University aimed to explore the mechanisms underlying acetylshikonin-induced cell death in non-small cell lung cancer (NSCLC). On December 19, 2023, their research paper was published in Aging’s Volume 15, Issue 24, entitled, “Acetylshikonin induces necroptosis via the RIPK1/RIPK3-dependent pathway in lung cancer.”

Full blog - https://aging-us.org/2024/01/rooted-in-chinese-medicine-zicaos-anti-cancer-effects-on-lung-cancer/

Paper DOI - https://doi.org/10.18632/aging.205316

Corresponding authors - Ju-Fang Liu - jufangliu@tmu.edu.tw

Sign up for free Altmetric alerts about this article - 
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205316

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

Keywords - aging, human lung cancer, acetylshikonin, ROS, necroptosis

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

Please visit our website at https://www.Aging-US.com​​ and connect with us:

SoundCloud - https://soundcloud.com/Aging-Us
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/
Pinterest - https://www.pinterest.com/AgingUS/

Media Contact
18009220957
MEDIA@IMPACTJOURNALS.COM

Rooted in Chinese Medicine: Zicao’s Anti-Cancer Effects on Lung Cancer

The human brain is a complex organ, and its aging process is influenced by a plethora of factors, both genetic and environmental. Aging-related changes in the brain can lead to cognitive decline and susceptibility to neurodegenerative diseases. Therefore, understanding the molecular mechanisms underlying these changes is crucial for developing therapeutic strategies to delay or prevent age-related cognitive decline.

Over the past few years, a myriad of scientific studies have been conducted to understand the intricate relationship between our genes and the aging process. In a new study, researchers Joseph A. Zarrella and Amy Tsurumi from Harvard T.H. Chan School of Public Health, Massachusetts General Hospital, Harvard Medical School, and Shriner’s Hospitals for Children-Boston explored the concept of genome brain age prediction, a groundbreaking area of study that employs advanced bioinformatics tools to analyze changes in gene expression associated with aging. On February 28, 2024, their research paper was published and chosen as the cover paper for Aging’s Volume 16, Issue 5, entitled, “Genome-wide transcriptome profiling and development of age prediction models in the human brain.”

“[…] we aimed to profile transcriptome changes in the aging PFC [prefrontal cortex] overall and compare females and males, and develop prediction models for age.”

Full blog - https://aging-us.org/2024/03/predicting-brain-age-with-machine-learning-and-transcriptome-profiling/

Paper DOI - https://doi.org/10.18632/aging.205609

Corresponding author - Amy Tsurumi - atsurumi@mgh.harvard.edu

Sign up for free Altmetric alerts about this article - 
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205609

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

Keywords - aging, machine learning, prediction model, biomarker, transcriptome

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

Please visit our website at https://www.Aging-US.com​​ and connect with us:

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/
Pinterest - https://www.pinterest.com/AgingUS/
Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc

Media Contact
18009220957
MEDIA@IMPACTJOURNALS.COM

Predicting Brain Age With Machine Learning and Transcriptome Profiling

Bone mass declines with age, and the anabolic effects of skeletal loading decrease. While much research has focused on gene transcription, how bone ages and loses its mechanoresponsiveness at the protein level remains unclear.

Researchers Christopher J. Chermside-Scabbo, John T. Shuster, Petra Erdmann-Gilmore, Eric Tycksen, Qiang Zhang, R. Reid Townsend, Matthew J. Silva from Washington University School of Medicine and Washington University in St. Louis, MO, share their findings which underscore the need for complementary protein-level assays in skeletal biology research.

On October 12, 2024, their research paper was published as the cover of Aging (listed by MEDLINE/PubMed as “Aging (Albany NY)” and “Aging-US” by Web of Science), Volume 16, Issue 19, entitled, “A proteomics approach to study mouse long bones: examining baseline differences and mechanical loading-induced bone formation in young-adult and old mice.”

Full blog - https://aging-us.org/2024/10/exploring-baseline-variations-and-mechanical-loading-induced-bone-formation-in-young-adult-and-aging-mice-through-proteomics/

Paper DOI - https://doi.org/10.18632/aging.206131

Corresponding author - Christopher J. Chermside-Scabbo - ccherms@wustl.edu

Video short - https://www.youtube.com/watch?v=xm6o7gWH8p4

Sign up for free Altmetric alerts about this article - 
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206131

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

Keywords - aging, bone, mechanical loading, proteomics, RNA-seq/transcriptomics

About Aging-US

The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.

The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)

Please visit our website at https://www.Aging-US.com​​ and connect with us:

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/
Pinterest - https://www.pinterest.com/AgingUS/
Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc

Media Contact
18009220957
MEDIA@IMPACTJOURNALS.COM

Baseline Variations and Mechanical Loading-Induced Bone Formation in Mice through Proteomics

Imagine a future where we not only live longer but stay healthy throughout those extra years. Thanks to recent breakthroughs in biotechnology and artificial intelligence (AI) in healthcare, this vision is closer to becoming a reality.

Advancements in Aging Research

Aging research has made significant progress in recent years by combining disciplines like biology, technology, and medicine to tackle the challenges of extending healthspans and reducing age-related diseases. While people today live longer than ever before, extending our “healthspan”—the years we stay active and illness-free—remains challenging. AI and health biomarkers (biological indicators of our body’s condition) are now key tools in the pursuit of longer, healthier lives.

In a recent paper, led by corresponding authors Yu-Xuan Lyu from Southern University of Science and Technology Shenzhen; Alex Zhavoronkov from Insilico Medicine AI Limited, Masdar City, Abu Dhabi; Morten Scheibye-Knudsen and Daniela Bakula from the Center for Healthy Aging, University of Copenhagen, along with numerous other collaborators, the transformative potential of AI in aging research was explored. The research paper, titled “Longevity biotechnology: bridging AI, biomarkers, geroscience and clinical applications for healthy longevity,” was published as the cover paper in Aging’s Volume 16, Issue 20.

Full blog - https://aging-us.org/2024/11/how-ai-and-longevity-biotechnology-are-revolutionizing-healthcare-for-healthier-longer-lives/

Paper DOI - https://doi.org/10.18632/aging.206135

Corresponding authors - Yu-Xuan Lyu - lvyx@sustech.edu.cn, Alex Zhavoronkov - alex@insilico.com, Morten Scheibye-Knudsen - mscheibye@sund.ku.dk, and Daniela Bakula - bakula@sund.ku.dk

Video short - https://www.youtube.com/watch?v=Hpfe5WJ5g7I

Sign up for free Altmetric alerts about this article - 
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206135

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

Keywords - aging, biotechnology, artificial intelligence, healthy longevity

About Aging-US

The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.

The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)

Please visit our website at https://www.Aging-US.com​​ and connect with us:

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/
Pinterest - https://www.pinterest.com/AgingUS/
Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc

MEDIA@IMPACTJOURNALS.COM

How AI and Longevity Biotechnology are Revolutionizing Healthcare for Healthier, Longer Lives

Imagine a simple topical treatment that could help aging skin heal faster, reducing recovery time from wounds and even improving skin quality. Scientists may have found exactly that. A recent study, published in Aging, reveals that a compound called ABT-263 can eliminate aging cells in the skin, boosting its ability to regenerate. 

Understanding How Aging Affects Skin Healing

Aging affects the skin’s structure and function, leading to a reduced ability to heal from wounds. Scientists have long suspected that senescent cells, also known as “zombie cells,” play a major role in this decline. These cells stop dividing but refuse to die, accumulating in tissues and releasing inflammatory molecules that impair the body’s natural repair processes.

Various studies have explored senolytics, a class of drugs designed to eliminate these aging cells and restore tissue function. While these drugs have shown promise in treating diseases like osteoporosis and fibrosis, their impact on skin regeneration and wound healing has been less studied. A new study titled “Topical ABT-263 treatment reduces aged skin senescence and improves subsequent wound healing” now suggests that a topical application of the senolytic ABT-263 could significantly improve wound healing in older individuals.

Full blog - https://aging-us.org/2025/02/a-new-approach-to-healing-aging-skin-insights-from-senolytic-research/

Paper DOI - https://doi.org/10.18632/aging.206165

Corresponding author - Daniel S. Roh - droh@bu.edu

Video short - https://www.youtube.com/watch?v=AKS7sZyEChg

Sign up for free Altmetric alerts about this article - 
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206165

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

Keywords - aging, senolytic, senescence, wound healing, ABT-263

About Aging-US

The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.

The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)

Please visit our website at https://www.Aging-US.com​​ and connect with us:

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/
Pinterest - https://www.pinterest.com/AgingUS/
Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc

MEDIA@IMPACTJOURNALS.COM

A New Approach to Healing Aging Skin: Insights from Senolytic Research

Aging (Aging-US) was proud to sponsor the Muscle Aging Science & Translation (MAST) Symposium, organized by the Aging Initiative at Harvard University on Friday, April 18, 2025. This important event brought together 350 participants—chosen from more than 1,300 applicants—including students, researchers, company founders, investors, and industry leaders. Together, they explored the latest research and innovations in muscle health and aging. The symposium reflected the journal’s strong commitment to supporting collaboration across fields and advancing research in aging.

-Key Highlights from the MAST Symposium- 
Clinical Research Perspectives on Frailty  

The symposium opened with a strong clinical session led by experts from top institutions: Dr. Roger Fielding (Tufts University and Boston Claude D. Pepper Older Americans Independence Center) and Drs. Douglas Kiel, Shivani Sahni, and Yi-Hsiang Hsu (Harvard Medical School and Beth Israel Deaconess Medical Center).

The panel discussed key topics such as the biology of frailty, how bone and muscle health are connected, and the influence of genetics, diet, and exercise on staying strong as we age. By blending real-life patient care with the latest research, the speakers shed light on the challenges of sarcopenia—the gradual loss of muscle strength and mass that occurs with age—and the new scientific approaches being developed to improve treatment.

Full recap - https://aging-us.org/2025/04/agings-ongoing-support-for-scientific-innovation-sponsoring-the-muscle-aging-science-translation-symposium/

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

To learn more about the journal, please visit our website at 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/
Pinterest - https://www.pinterest.com/AgingUS/
Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc

MEDIA@IMPACTJOURNALS.COM

Aging’s Ongoing Support for Scientific Innovation: Sponsoring the Muscle Aging Science & Translation Symposium

Sponsoring the Muscle Aging Science & Translation Symposium

In a world where we are living longer but not always healthier, scientists are searching for ways to add life to our years, not just years to our lives. A recent study published in Aging (Aging-US), Volume 17, Issue 4, led by researchers at the National University of Natural Medicine, suggests that certain common foods, already known for their health benefits, might also help slow or even reverse epigenetic or biological aging. These foods, rich in specific plant compounds, appear to influence our DNA in ways that may slow down the body’s epigenetic clock.

Full blog - https://aging-us.org/2025/05/study-identifies-foods-that-may-reverse-biological-age-and-promote-healthy-aging-in-men/

Paper DOI - https://doi.org/10.18632/aging.206240

Corresponding author - Ryan Bradley - rbradley@nunm.edu

Video short - https://www.youtube.com/watch?v=T6I33AIAIFM

Sign up for free Altmetric alerts about this article - 
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206240

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

Keywords - aging, epigenetics, DNA methylation, diet, biological clock

To learn more about the journal, please visit our website at 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

Study Identifies Foods That May Reverse Biological Age and Promote Healthy Aging in Men

As we age, our brains become more sensitive to stress and disease. A recent study sheds light on a lesser-known risk: reduced oxygen levels. The study, titled “Defining the hypoxic thresholds that trigger blood-brain barrier disruption: the effect of age” and recently published as the cover for Volume 17, Issue 5 of Aging (Aging-US), found that low oxygen—also called hypoxia—can harm the aging brain by disrupting the blood-brain barrier (BBB). This damage may contribute to cognitive decline, memory problems, and an increased risk of dementia.

Understanding Hypoxia in the Brain

The brain relies on a steady supply of oxygen to stay healthy. When oxygen levels fall—a condition known as hypoxia—the brain undergoes changes to adapt. These changes include the remodeling of blood vessels and, importantly, a weakening of the blood-brain barrier. The BBB acts as a filter, protecting brain tissue from harmful substances. When it breaks down, it can lead to inflammation, brain cell damage, and cognitive issues.

Hypoxia is common in older adults, especially those with conditions like sleep apnea, chronic obstructive pulmonary disease (COPD), heart failure, and asthma. That is why understanding the connection between low oxygen and the aging brain is crucial for preventing long-term neurological damage.

Full blog - https://aging-us.org/2025/06/oxygen-deprivation-and-the-aging-brain-a-hidden-trigger-for-cognitive-decline/

Paper DOI - https://doi.org/10.18632/aging.206241

Corresponding author - Richard Milner - rmilner@sdbri.org

Video short - https://www.youtube.com/watch?v=Nr6rTm7aJRo

Sign up for free Altmetric alerts about this article - 
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206241

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

Keywords - aging, blood-brain barrier integrity, endothelial, proliferation, microglia, chronic mild hypoxia, hypoxic threshold

To learn more about the journal, please visit our website at https://www.Aging-US.com​​ and connect with us:

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

Oxygen Deprivation and the Aging Brain: A Hidden Trigger for Cognitive Decline

A new #study published recently in Volume 17, Issue 6, examines a novel treatment for women with ovarian failure. Researchers from IVI Clinics Alicante in Spain investigated a procedure called Stem Cell Regenera, which uses the body’s own stem cells and platelet-rich plasma to activate dormant follicles in the ovaries. This innovative protocol could expand options for patients with ovarian failure who have not responded to conventional fertility therapies.

Understanding Ovarian Failure

Ovarian failure affects women’s ability to conceive by reducing the quantity and quality of eggs in the ovaries. Conditions like Poor Ovarian Response, Diminished Ovarian Reserve, and Premature Ovarian Insufficiency are key reasons for infertility and make it hard to use assisted reproduction methods like in vitro fertilization (IVF).

Standard fertility treatments often fail to improve outcomes for these patients, leaving donor eggs as the primary alternative. However, recent advances in regenerative medicine have raised the possibility of restoring ovarian function using cellular therapies. Emerging research suggests that the right biological conditions could reactivate dormant follicles within the ovaries, potentially helping patients to use their eggs.

Full blog - https://aging-us.org/2025/07/stem-cell-regenera-a-regenerative-approach-to-activating-dormant-ovarian-follicles/

Paper DOI - https://doi.org/10.18632/aging.206274

Corresponding author -Amparo Santamaria - Amparo.santamaria@ivirma.com

Author interview - https://www.youtube.com/watch?v=oRFJNwnXZWI

Sign up for free Altmetric alerts about this article - 
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206274

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

Keywords - aging, Stem Cell Regenera, oocyte activation, ovarian regeneration, G-CSF, SCFE-PRP, ovarian failure

To learn more about the journal, please visit our website at 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

Stem Cell Regenera: A Regenerative Approach to Activating Dormant Ovarian Follicles

As the global population grows older, understanding what drives the aging process is becoming increasingly important. Diseases like Alzheimer’s, cardiovascular conditions, and cancer are more common with age, yet many current treatments only manage symptoms rather than addressing the underlying biological causes.

One contributor to aging is the buildup of “senescent” cells—cells that have stopped dividing but do not die. These cells can harm nearby tissues by releasing molecular signals, a process known as secondary senescence.

Scientists have found that senescent cells release tiny particles called exosomes. A research team from The Buck Institute for Research on Aging recently discovered that these exosomes carry aging-related messages through the bloodstream. Their study, titled “Exosomes released from senescent cells and circulatory exosomes isolated from human plasma reveal aging-associated proteomic and lipid signatures,” was featured as the cover article in Aging (Aging-US), Volume 17, Issue 8.

Full blog - https://aging-us.org/2025/09/how-exosomes-spread-aging-signals-and-could-support-anti-aging-research/

Paper DOI - https://doi.org/10.18632/aging.206292

Corresponding author - Birgit Schilling - bschilling@buckinstitute.org

Video short - https://www.youtube.com/watch?v=tcyAZahw-g8

Sign up for free Altmetric alerts about this article - 
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206292

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

Keywords - aging, proteomics, senescence, exosomes, data-independent acquisitions

To learn more about the journal, please visit our website at https://www.Aging-US.com​​ and connect with us:

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

How Exosomes Spread Aging Signals and Could Support Anti-Aging Research

In this episode of the Longevity & Aging Series, Girish Harinath from AgelessRx joins host Dr. Evgeniy Galimov to discuss a research paper he co-authored in Volume 17, Issue 4 of Aging-US, titled “Influence of rapamycin on safety and healthspan metrics after one year: PEARL trial results.”

DOI - https://doi.org/10.18632/aging.206235

Corresponding author - Stefanie L. Morgan - stefanie@agelessrx.com

Video interview - https://www.youtube.com/watch?v=7-NvskI8Ve0

Longevity & Aging Series - https://www.aging-us.com/longevity

Abstract

Design: This 48-week decentralized, double-blinded, randomized, placebo-controlled trial (NCT04488601) evaluated the long-term safety of intermittent low-dose rapamycin in a healthy, normative-aging human cohort. Participants received placebo, 5 mg or 10 mg compounded rapamycin weekly. The primary outcome measure was visceral adiposity (by DXA scan), secondary outcomes were blood biomarkers, and lean tissue and bone mineral content (by DXA scan). Established surveys were utilized to evaluate health and well-being. Safety was assessed through adverse events and blood biomarker monitoring.

Results: Adverse and serious adverse events were similar across all groups. Visceral adiposity did not change significantly (ηp2 = 0.001, p = 0.942), and changes in blood biomarkers remained within normal ranges. Lean tissue mass (ηp2 = 0.202, p = 0.013) and self-reported pain (ηp2 = 0.168, p = 0.015) improved significantly for women using 10 mg rapamycin. Self-reported emotional well-being (ηp2 = 0.108, p = 0.023) and general health (ηp2 = 0.166, p = 0.004) also improved for those using 5 mg rapamycin. No other significant effects were observed.

Conclusions: Low-dose, intermittent rapamycin administration over 48 weeks is relatively safe in healthy, normative-aging adults, and was associated with significant improvements in lean tissue mass and pain in women. Future work will evaluate benefits of a broader range of rapamycin doses on healthspan metrics for longevity, and will aim to more comprehensively establish efficacy.

Sign up for free Altmetric alerts about this article - 
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206235

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

Keywords - aging, rapamycin, geroscience, longevity, healthspan

To learn more about the journal, please visit our website at 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

Aging-US

Longevity & Aging Series (S3, E6): Girish Harinath

As life expectancy increases, there is growing interest not only in extending lifespan but also in improving the quality of those additional years. To address the physical and cognitive decline that often accompanies aging, researchers have explored a variety of strategies. Many of these focus on a single biological factor, such as reducing inflammation or stimulating stem cell activity. However, aging is a complex process involving multiple, interconnected changes in the body.

Recognizing this, researchers at the University of California, Berkeley proposed a more comprehensive approach: targeting multiple aging-related pathways simultaneously. Their study, titled “Sex-specific longitudinal reversal of aging in old frail mice,” was recently featured on the cover of Aging-US (Volume 17, Issue 9).

Full blog - https://aging-us.org/2025/10/new-anti-aging-combo-boosts-lifespan-in-old-male-mice/

Paper DOI - https://doi.org/10.18632/aging.206304

Corresponding author - Irina M. Conboy - irina@generationlab.co

Abstract video - https://www.youtube.com/watch?v=bpWxDd7hHhM

Sign up for free Altmetric alerts about this article - 
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206304

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

Keywords - aging, lifespan, healthspan, Alk5 inhibitor, oxytocin, sex-specific differences

To learn more about the journal, please visit our website at https://www.Aging-US.com​​ and connect with us:

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

New Anti-Aging Combo Boosts Lifespan in Old Male Mice

BUFFALO, NY — October 9, 2025 — A new #research paper was #published in Volume 17, Issue 9 of Aging-US on August 22, 2025, titled, “The impact of long-term social housing on biconditional association task performance and neuron ensembles in the anterior cingulate cortex and the hippocampal CA3 region of aged rats.”

The research team led by Anne M. Dankert from Providence College and University of North Carolina, Chapel Hill, showed that aged rats who lived in socially enriched environments throughout life retained better memory and cognitive flexibility than those housed alone. This study highlights the importance of social interaction in protecting the aging brain.

Cognitive decline, such as memory loss and reduced problem-solving ability, affects many people over the age of 65. While many factors contribute to age-related cognitive decline, this study suggests that one key factor may be surprisingly simple: long-term social connection. To explore how social interaction might influence memory performance and brain activity, the researchers designed a study using rats as a model for aging in humans.

“Cognitive decline and changes in neuronal activity are hallmarks of aging.”

They compared three groups of rats: young adults, aged rats housed alone, and aged rats housed socially in groups. All groups had access to the same physical enrichment, such as exercise and stimulating objects, but only some experienced lifelong social companionship. The team tested these animals on a complex memory challenge known as the biconditional association task, which requires animals to make context-based decisions—an ability that typically declines with age.

The results showed that aged rats living in social groups performed just as well as young adults on the memory task, while those housed alone showed significant impairments. Socially housed rats also made fewer working memory errors and required less effort to complete cognitive tasks, suggesting not only better performance but more efficient brain function. These benefits were not observed in aged rats who received only environmental enrichment without social interaction.

Brain imaging revealed additional differences between the groups. Socially housed aged rats showed increased activity in the hippocampus, particularly in the CA3 region, which plays a key role in forming and separating memories. In contrast, aged rats that lived alone had lower activity in this region, which may explain their poorer performance. Interestingly, socially housed rats also showed reduced overactivity in the anterior cingulate cortex—a brain area involved in attention and decision-making—suggesting a more balanced and efficient neural response.

This research provides new insight into how lifelong social experiences shape brain health during aging. While earlier studies have shown that physical activity and cognitive stimulation help preserve cognitive function, this study identifies social interaction as an independent and powerful protective factor. The findings are consistent with human studies showing that older adults who remain socially active tend to experience slower cognitive decline and stronger brain function.

Overall, these results emphasize that brain aging is not inevitable but may be influenced by our social environments. This research suggests that fostering lifelong social connections could be a critical, low-cost strategy to protect memory and mental flexibility in older adults.

DOI - https://doi.org/10.18632/aging.206310

Corresponding author - Anne M. Dankert - adankert@unc.edu

Abstract video - https://www.youtube.com/watch?v=poNnPz1ti6Q

https://www.aging-us.com/

MEDIA@IMPACTJOURNALS.COM

Lifelong Companionship Protects Aging Rat Brains from Cognitive Decline

BUFFALO, NY — October 14, 2025 — A new #research paper was #published in Volume 17, Issue 9 of Aging-US on August 30, 2025, titled, “Glycocalyx-targeted therapy prevents age-related muscle loss and declines in maximal exercise capacity.”

In this study, led by Daniel R. Machin from the University of New Mexico School of Medicine and the University of Utah, researchers found that protecting a fragile layer lining blood vessels, known as the glycocalyx, can prevent muscle deterioration and help maintain physical performance during aging. They also discovered that a supplement containing high-molecular-weight hyaluronan (HMW-HA), a key component of the glycocalyx, enabled older mice to preserve muscle mass and exercise capacity. These findings suggest that targeting the glycocalyx may offer a new approach to reduce frailty and support mobility in older adults.

As this layer degrades with age, it contributes to cardiovascular and muscular decline by impairing blood flow and vascular health. The study examined how preserving the glycocalyx using a therapy called Endocalyx™ affects physical function in aging mice.

Researchers first studied genetically modified mice lacking Has2, the enzyme responsible for producing HMW-HA. These mice had a thinner glycocalyx, reduced exercise performance, and lower mitochondrial function in their muscles, even though muscle size remained normal. This indicated that glycocalyx damage alone can directly impair physical performance.

The team then gave older mice a diet containing Endocalyx™ for 10 weeks. Compared to untreated controls, these mice maintained muscle mass and performed better on treadmill tests. Notably, the treated mice did not show the typical age-related decline in muscle strength and endurance. While the supplement did not fully restore youthful performance, it significantly slowed physical deterioration, suggesting a protective benefit. In contrast, untreated older mice lost both body mass and muscle volume during the same period.

“Taken together, these findings provide direct evidence of a role for HMW-HA in the modulation of exercise capacity.”

This research builds on prior evidence that the glycocalyx is essential for healthy blood vessel function. Since muscle health depends on proper blood flow and oxygen delivery, restoring the glycocalyx may help maintain strength and mobility with age. While more research is needed to confirm these results in humans, the findings point to a potential therapeutic approach to promote healthier aging.

DOI - https://doi.org/10.18632/aging.206313

Corresponding author - Daniel R. Machin — dmachin@salud.unm.edu

Abstract video - https://www.youtube.com/watch?v=S7HjCeXT8fU

Sign up for free Altmetric alerts about this article - 
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206313

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

Keywords - aging, glycocalyx, hyaluronan

To learn more about the journal, please visit our website at 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

Supplement That Supports the Glycocalyx in Blood Vessels May Reduce Frailty in Older Adults

As people age, it is common to experience some memory lapses or slower thinking. Although this is often a normal part of aging, it can still affect a person’s quality of life. Scientists have been investigating ways to slow or prevent cognitive decline, and growing evidence points to the potential role of social interaction.

Recently, a study using rats found that long-term social connection may help protect the brain from age-related memory decline. This work, titled “The impact of long-term social housing on biconditional association task performance and neuron ensembles in the anterior cingulate cortex and the hippocampal CA3 region of aged rats,” was recently published in Aging-US (Volume 17, Issue 9).

Full blog - https://aging-us.org/2025/10/how-long-term-social-connection-supports-brain-health-and-memory-in-aging/

Paper DOI - https://doi.org/10.18632/aging.206310

Corresponding author - Anne M. Dankert - adankert@unc.edu

Abstract video - https://www.youtube.com/watch?v=poNnPz1ti6Q

Sign up for free Altmetric alerts about this article - 
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206310

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

Keywords - aging, aging, environmental enrichment, working memory, complex cognition, immediate early genes

To learn more about the journal, please visit our website at 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

How Long-Term Social Connection Supports Brain Health and Memory in Aging

BUFFALO, NY — October 21, 2025 — A new #editorial was #published in Aging-US on October 13, 2025, titled “Longevity clinics: between promise and peril.”

In this editorial, Marco Demaria, Editor-in-Chief of Aging-US, from the European Research Institute for the Biology of Ageing (ERIBA), University Medical Center Groningen (UMCG), University of Groningen (RUG), reviews the rapid rise of longevity clinics worldwide. 

Longevity clinics have emerged globally in response to increasing demand for personalized, preventive healthcare. Located in countries such as the United States, Switzerland, and the United Arab Emirates, these centers offer advanced diagnostic services, including genomic testing, advanced imaging, and multi-omics profiling. Their goal is to extend healthspan—the number of years a person lives in good health—through customized lifestyle interventions, nutritional guidance, and, in some cases, experimental therapies.

“Longevity clinics embody an important vision: healthcare is personalized, preventive, and engaged.”

Although the concept of proactive aging care is attractive, the editorial raises serious concerns about the scientific and ethical foundations of these clinics. Many operate outside conventional medical systems and lack connections to academic geroscience. This disconnection allows them to market expensive interventions without sufficient clinical validation. Program costs can range from €10,000 to over €100,000 per year, limiting access to wealthy individuals while leaving out populations most at risk for premature aging.

Despite these challenges, Dr. Demaria notes that longevity clinics may contribute meaningfully to innovation. By collecting extensive, long-term health data from clients, these clinics have the potential to identify early biomarkers of aging and detect signs of age-related diseases. Unlike traditional clinical trials, which are limited in scope and duration, longevity clinics track a wide range of health data over time. When paired with artificial intelligence tools, this information could help advance the science of healthy aging.

However, several risks remain. Many clinics lack standardized protocols, and the tools they use, such as biological age calculators or hormone therapies, often lack accuracy or clear clinical value. Without proper guidelines, clients may receive advice that is confusing or not scientifically supported. This can reduce public trust in the broader field of longevity research.

To ensure these clinics contribute positively to health innovation, the editorial outlines different key steps: greater collaboration with academic researchers, the adoption of standardized protocols, increased transparency, and work toward regulatory clarity. Broader access must also be considered by developing scalable and more affordable models, possibly through partnerships with public health systems.

Ultimately, longevity clinics represent both a major opportunity and a serious concern. If integrated responsibly with science, policy, and public health, they could support a shift toward personalized, preventive healthcare. Without this alignment, however, they risk reinforcing inequality and weakening the credibility of the science behind aging.

DOI - https://doi.org/10.18632/aging.206330

Corresponding author - Marco Demaria — m.demaria@umcg.nl

Abstract video - https://www.youtube.com/watch?v=Bt84xBdii0s

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

The Rise of Longevity Clinics: Promise, Risk, and the Future of Aging

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

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

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

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

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

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

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

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

Epigenetic Aging Linked to Cognitive Decline in Hispanic/Latino Adults

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

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

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

Alpha-Synuclein Overexpression in Rats Reveals Early Clues to Synucleinopathies

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

Aging-US Supports the Future of Aging Research Mixer 2025

Interest in healthier, longer lives is rising, supported by recent scientific advances in aging research. But turning those discoveries into everyday healthcare solutions remains a work in progress. In this landscape, longevity clinics have attracted attention as personalized alternatives to traditional medicine.

What Are Longevity Clinics?

Longevity clinics are private centers offering tailored programs designed to improve long-term health and slow biological aging. Using advanced diagnostics such as genetic sequencing, full-body imaging, and blood tests, they develop personalized plans that may include exercise, nutrition, hormone therapy, or experimental treatments. Frequently found in countries like the United States, Switzerland, and the United Arab Emirates, these clinics reflect a growing global interest in preventive healthcare, though their high costs and scientific credibility remain subjects of debate.

The Editorial

“Longevity clinics: between promise and peril,” an editorial by Marco Demaria, Editor-in-Chief of Aging-US, from the European Research Institute for the Biology of Ageing (ERIBA), University Medical Center Groningen (UMCG), University of Groningen (RUG), was published in Aging-US (Volume 17, Issue 10). 

Full blog - https://aging-us.org/2025/11/longevity-clinics-balancing-innovation-with-regulation/

Paper DOI - https://doi.org/10.18632/aging.206330

Corresponding author - Marco Demaria — m.demaria@umcg.nl

Abstract video - https://www.youtube.com/watch?v=Bt84xBdii0s

Sign up for free Altmetric alerts about this article - 
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206330

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

Keywords - aging, longevity clinics, biomarkers, frailty, senescence

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/@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

Longevity Clinics: Balancing Innovation with Regulation

BUFFALO, NY — December 1, 2025 — A new #research paper featured on the #cover of Volume 17, Issue 11 of Aging-US was #published on October 30, 2025, titled “SAMP-Score: a morphology-based machine learning classification method for screening pro-senescence compounds in p16 positive cancer cells.”

In this study led by first author Ryan Wallis along with corresponding author Cleo L. Bishop, from Queen Mary University of London, researchers developed a machine learning tool to identify compounds that induce cancer cells into senescence. The tool, called SAMP-Score, offers a new strategy for drug discovery in cancers with poor treatment options like basal-like breast cancer.

Senescence is a process where damaged or aged cells stop dividing. In cancer therapy, inducing senescence is an approach to control tumor growth. However, it is difficult to detect true senescence in cancer cells that already appear aged. These cancers, often called Sen-Mark+ cancers, include basal-like breast cancer and typically lack reliable markers to confirm senescence. SAMP-Score was designed to address this problem.

Instead of relying on traditional markers, the researchers built a machine learning model trained to recognize patterns based on senescent cells’ shape and structure under a microscope. These visual patterns, known as senescence-associated morphological profiles (SAMPs), allowed the model to distinguish real signs of aging from other effects such as toxicity or normal variation. By analyzing thousands of cell images, the model learned to classify whether a cell had truly entered senescence.

“To demonstrate the potential application of SAMP-Score in p16 positive cancer therapeutic discovery, we assessed a diversity screen of 10,000 novel chemical entities in MB-468 cells (p16 positive BLBC).”

The team used SAMP-Score to screen more than 10,000 experimental compounds. One compound, QM5928, consistently triggered senescence in several cancer cell types without killing them, making it a promising candidate for further study. Importantly, it worked in cancers resistant to known drugs like palbociclib, which are often ineffective in cancers with high p16 expression like basal-like breast cancer. 

Further analysis revealed that QM5928 caused the p16 protein to move into the nucleus of cancer cells, a possible sign that the protein is helping stop cell division. This subtle effect was only detectable using the detailed imaging and analysis made possible by SAMP-Score, highlighting the tool’s ability to distinguish true senescence from toxic responses and making it a powerful resource in cancer drug discovery.

By combining machine learning with high-resolution imaging, this study introduces a new way to find and evaluate cancer therapies. SAMP-Score could accelerate efforts to develop treatments that exploit the body’s natural aging processes to fight cancer, especially for patients with resistant tumors. The tool is openly available at GitHub, making it accessible for other researchers exploring senescence-based cancer therapies.

DOI - https://doi.org/10.18632/aging.206333

Corresponding author - Cleo L. Bishop - c.l.bishop@qmul.ac.uk

Abstract video - https://www.youtube.com/watch?v=qXI_KI3EgHE

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

Machine Learning Identifies Senescence-Inducing Compound for p16-Positive Cancer Cells

BUFFALO, NY — December 3, 2025 — A new #essay was #published in Volume 17, Issue 11 of Aging-US on November 19, 2025, titled “On the intergenerational transfer of ideas in aging and cancer research: from the hypothalamus according to V.M. Dilman to the mTOR protein complex according to M.V. Blagosklonny.”

In this work, Aleksei G. Golubev from the N.N. Petrov National Medical Research Center of Oncology reflects on the legacy of two influential Russian scientists, Vladimir M. Dilman and his son Mikhail V. Blagosklonny, who each introduced groundbreaking ideas about aging and cancer. Drawing from his own experience working in Dilman’s lab, Golubev explores how their ideas remain deeply relevant to today’s scientific understanding.

The essay connects Dilman’s “elevation theory” with Blagosklonny’s “hyperfunction theory,” two frameworks that challenge the conventional view of aging as a process of decline. Instead, both propose that aging results from continued biological processes that once supported growth but eventually become harmful when left unchecked.

Dilman believed that aging begins with reduced sensitivity in the hypothalamus, a brain region that regulates the body’s balance. This desensitization disrupts metabolism and hormone levels, setting the stage for many chronic illnesses. Decades later, Blagosklonny expanded on this idea at the molecular level. Central to his theory is the mTOR protein complex, which regulates growth and metabolism and is now a major focus in aging research.

Golubev also explores the historical and personal connections between the two scientists. Dilman, an endocrinologist trained in the Soviet Union, and Blagosklonny, a molecular biologist educated during the post-Soviet period, represent two generations shaped by a shared scientific tradition. 

“Dilman’s scientific legacy is not as well recognized as it should be, partly due to bias in citation practices.”

The essay also draws attention to a troubling trend in science: the tendency to overlook early contributions, especially from non-Western scholars. Many of Dilman’s insights, such as the connection between high blood sugar, insulin resistance, and cancer, have since been validated by modern tools, yet his work is rarely cited. Golubev points out how citation practices, language barriers, and historical isolation have contributed to this lack of recognition.

Finally, Golubev encourages the scientific community to look back and acknowledge the foundational work that shaped modern aging science. It also highlights the importance of cross-generational knowledge in moving science forward. By tracing the intellectual journey from hormonal regulation in the brain to molecular pathways in cells, this essay demonstrated the relevance of old ideas in a new biological era.

DOI - https://doi.org/10.18632/aging.206338

Corresponding author - Aleksei G. Golubev - lxglbv@rambler.ru

Abstract video - https://www.youtube.com/watch?v=LvrdghTKGws

Sign up for free Altmetric alerts about this article - 
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206338

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

Keywords - aging, gerontology, history of science, hyperfunction, mTOR, hypothalamus, cancer, metabolism, immunity

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

How Two Russian Scientists Changed the Way We Understand Aging and Cancer

BUFFALO, NY — December 8, 2025 — A new #research paper was #published in Volume 17, Issue 11 of Aging-US on September 12, 2025, titled “Infusion of blood from young and old mice modulates amyloid pathology.”

This study was led by co-first authors Matias Pizarro from Universidad Adolfo Ibáñez and Ruben Gomez-Gutierrez from The University of Texas Health Science Center at Houston, alongside corresponding authors Claudia Duran-Aniotz from Universidad Adolfo Ibáñez and Rodrigo Morales from The University of Texas Health Science Center at Houston and Universidad Bernardo O’Higgins. The goal was to investigate how blood from young and old mice influences Alzheimer’s-related changes in a transgenic mouse model. The findings indicate that age-dependent circulating factors can either worsen or mitigate brain changes associated with dementia, highlighting blood and its components as potential therapeutic targets.

Alzheimer’s disease is a progressive neurodegenerative disorder characterized by misfolded amyloid proteins, inflammation, and gradual cognitive decline, with aging as its main risk factor. In this work, whole blood from young adult or very old wild-type mice was repeatedly infused into Tg2576 mice, a well-established model of amyloid accumulation and memory impairment. Over several months, recipient mice received 30 weekly blood infusions, followed by behavioral testing and detailed neuropathological analyses.

“Tg2576 mice express the human APP harboring the Swedish mutation.”

Mice that received blood from old donors performed worse in both short- and long-term spatial memory tasks than mice infused with young blood, suggesting that aged blood contains factors that impair cognition. When the team examined brain tissue, they found more cortical amyloid deposits detected by a specific antibody in mice treated with old blood, while overall amyloid levels measured biochemically did not change, suggesting differences in plaque type or compactness rather than total amount. The expression of amyloid precursor protein in the brain was also higher after old-blood infusion, which may partly explain the shift in amyloid pathology.​

Despite these changes in plaques and memory, classical markers of astrocyte activation, a sign of brain inflammation, did not differ between groups, pointing to more subtle molecular shifts. A broad proteomic analysis of brain samples revealed dysregulation of proteins involved in synapse formation, calcium signaling, and the endocannabinoid system, pathways important for neuronal communication and plasticity. Among them, the calcium channel–related protein CACNA2D2 and the signaling protein BRAF were increased in mice that received old blood, confirming that aged blood circulation can reshape key signaling networks linked to neuronal function and degeneration.

Overall, this study supports the idea that blood is not just a passive carrier but a powerful modulator of brain health during aging and disease. While young blood has been associated in previous work with improved synaptic function and reduced amyloid and tau changes, this study emphasizes the harmful impact of old blood, particularly on cortical amyloid patterns and memory. The identification of CACNA2D2 and BRAF as potential mediators of these effects suggests new avenues for targeting blood-borne factors or downstream brain pathways to slow or modify Alzheimer’s-related decline.

DOI - https://doi.org/10.18632/aging.206319

Corresponding authors - Claudia Duran-Aniotz - Claudia.Duran@uai.cl, and Rodrigo Morales - Rodrigo.MoralesLoyola@uth.tmc.edu

Abstract video - https://www.youtube.com/watch?v=zsBDSAipH3w

To learn more about the journal, visit https://www.Aging-US.com​​.

MEDIA@IMPACTJOURNALS.COM

Young and Old Mice Blood Differently Shapes Alzheimer’s-Related Brain Changes

The paper featured on the cover of this issue of Aging-US, published on October 30, 2025, entitled “SAMP-Score: a morphology-based machine learning classification method for screening pro-senescence compounds in p16-positive cancer cells,” represents an important methodological and conceptual advance at the interface of senescence biology, imaging and drug discovery.

In this study, led by first author Ryan Wallis and corresponding author Cleo L. Bishop (Queen Mary University of London), the authors introduce SAMP-Score, a machine-learning–based framework designed to identify bona fide senescence induction in cancer cells where canonical markers fail. This is a timely and much-needed contribution to the field.

Therapy-induced senescence has emerged as a powerful strategy to restrain tumor growth, yet its reliable detection in cancer cells remains a major bottleneckIn these contexts, cells often already display features associated with cellular aging, rendering conventional senescence markers ambiguous or misleading. Distinguishing true senescence from toxicity, stress responses or baseline “aged” phenotypes is therefore a critical unmet need.

Rather than relying on predefined molecular readouts, the authors take a different approach and train a machine-learning model to recognize senescence-associated morphological profiles (SAMPs) which are subtle but reproducible changes in cellular architecture captured through high-content microscopy. By learning directly from image-based phenotypes, SAMP-Score is able to identify senescence with a level of precision that is difficult to achieve using marker-based strategies alone.

The strength of the platform demonstrated through a large-scale screen of over 10,000 novel chemical entities in p16-positive basal-like breast cancer cells. From this screen, the compound QM5928 emerged as a robust inducer of senescence across multiple cancer models, notably without inducing cytotoxicity. Importantly, QM5928 retains activity in cellular contexts that are resistant to CDK4/6 inhibition, including palbociclib-refractory, p16-high tumors.

Mechanistically, the authors show that QM5928 promotes nuclear relocalization of p16, consistent with a functional engagement of cell-cycle arrest pathways. These nuanced phenotypic changes would likely have gone undetected without the resolution and discrimination provided by SAMP-Score, underscoring the platform’s ability to separate true senescence from confounding cellular states.

This work exemplifies how machine learning and quantitative imaging can be harnessed to solve long-standing problems in senescence research, moving the field beyond binary marker expression toward phenotype-driven classification. Beyond its immediate relevance for cancer therapy, SAMP-Score offers a broadly applicable framework for senescence-based screening efforts across biological contexts.

DOI - https://doi.org/10.18632/aging.206333

Corresponding author - Cleo L. Bishop - c.l.bishop@qmul.ac.uk

Abstract video - https://www.youtube.com/watch?v=qXI_KI3EgHE

Sign up for free Altmetric alerts about this article - 
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206333

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:

Bluesky - https://bsky.app/profile/aging-us.bsky.social
ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589
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/
Pinterest - https://www.pinterest.com/AgingUS/
Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc

MEDIA@IMPACTJOURNALS.COM

Aging-US Editors' Choice

Treating aggressive cancers that do not respond to standard therapies remains one of the most significant challenges in oncology. Among these are basal-like breast cancers (BLBC), which lack hormone receptors and HER2 amplification. This makes them unsuitable for many existing targeted treatments. As a result, therapeutic options are limited, and patient outcomes are often poor.

One emerging strategy is to induce senescence, a state in which cancer cells permanently stop dividing but remain metabolically active. This approach aims to slow or stop tumor growth without killing the cells directly. Although promising, the clinical application of senescence-based therapies has been limited by several challenges.

Senescence is typically identified using biomarkers such as p16, p21, and beta-galactosidase activity. However, these markers are often already present in aggressive cancers like BLBC (Sen‑Mark+ tumors), making it difficult to determine whether a treatment is truly inducing senescence or merely reflecting the tumor’s existing biology. Moreover, conventional screening methods may mistake reduced cell growth for senescence, cell death, or temporary growth arrest, leading to inaccurate assessments. This is especially problematic in large-scale drug screening, where thousands of compounds must be evaluated quickly and reliably.

To overcome these issues, researchers from Queen Mary University of London and the University of Dundee have developed a new machine learning–based method to improve the detection of senescence in cancer cells. Their findings were recently published in Aging-US.

The Study: Developing the SAMP-Score

The study, titled “SAMP-Score: a morphology-based machine learning classification method for screening pro-senescence compounds in p16-positive cancer cells,” was led by Ryan Wallis and corresponding author Cleo L. Bishop from Queen Mary University of London. This paper was featured on the cover of Aging-US Volume 17, Issue 11, and highlighted as our Editors’ Choice.

Full blog - https://aging-us.org/2025/12/using-machine-learning-to-identify-senescence-inducing-drugs-for-resistant-cancers/

Paper DOI - https://doi.org/10.18632/aging.206333

Corresponding author - Cleo L. Bishop - c.l.bishop@qmul.ac.uk

Abstract video - https://www.youtube.com/watch?v=qXI_KI3EgHE

Sign up for free Altmetric alerts about this article - 
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206333

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

Keywords - aging, SAMP-Score, senescence, senescent marker positive cancer cells, Sen-Mark+, machine learning, pro-senescence, high-throughput compound screening

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
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/
Pinterest - https://www.pinterest.com/AgingUS/
Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc

MEDIA@IMPACTJOURNALS.COM

Using Machine Learning to Identify Senescence-Inducing Drugs for Resistant Cancers

BUFFALO, NY — December 12, 2025 — A new #research paper was #published in Volume 17, Issue 11 of Aging-US on November 14, 2025, titled “Methylglyoxal-induced glycation stress promotes aortic stiffening: putative mechanistic roles of oxidative stress and cellular senescence.”

The study was led by first authors Parminder Singh of the Buck Institute for Research on Aging and Ravinandan Venkatasubramanian of the University of Colorado Boulder, with senior contributions from corresponding authors Pankaj Kapahi (Buck Institute for Research on Aging) and Zachary S. Clayton (University of Colorado Boulder and University of Colorado Anschutz Medical Campus). The researchers investigated how methylglyoxal (MGO), a toxic byproduct that builds up in blood vessels with age or metabolic dysfunction like diabetes, contributes to artery stiffening. Their findings are especially important to aging and diabetes-related cardiovascular risk.

Aortic stiffening, which reduces the flexibility of the body’s largest artery, is a key predictor of cardiovascular disease in older adults. The research team used young and aged mice to study how MGO affects vascular health. In young mice, chronic exposure to MGO increased aortic stiffness by 21%. However, when treated with Gly-Low, a supplement containing natural compounds such as nicotinamide and alpha-lipoic acid, this stiffening was completely prevented. Gly-Low also reduced the buildup of MGO and its harmful byproducts, particularly MGH-1, in both blood and tissue.

“Aortic stiffness was assessed in vivo via pulse wave velocity (PWV) and ex vivo through elastic modulus.”

The research showed that MGO’s damage goes beyond structural changes. It also caused the endothelial cells that line blood vessels to enter senescence, a state in which cells stop dividing and begin releasing inflammatory signals. This led to lower levels of nitric oxide, a molecule essential for blood vessel relaxation. In human vascular cells in lab culture, Gly-Low reversed these aging-like changes and restored nitric oxide production.

In older mice, which naturally develop stiffer arteries, Gly-Low treatment during four months significantly reduced stiffness and lowered MGO and MGH-1 levels. This suggests that Gly-Low may help slow or even reverse vascular aging by reducing glycation stress.

The study also identified the glyoxalase-1 pathway as a critical mechanism. This is a natural detox system that helps clear harmful molecules like MGO. Gly-Low appeared to boost this pathway. When the pathway was chemically blocked, Gly-Low’s protective effects disappeared, confirming its role in the process.

Overall, the findings highlight glycation stress as a modifiable contributor to vascular aging. The results suggest that natural compound-based therapies, like Gly-Low, may offer a potential strategy to protect arteries from age- and diabetes-related damage.

DOI - https://doi.org/10.18632/aging.206335

Corresponding authors: Pankaj Kapahi - pkapahi@buckinstitute.org; Zachary S. Clayton - Zachary.Clayton@cuanschutz.edu

Abstract video: https://www.youtube.com/watch?v=i_rtq8eIb8c

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:

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

Glycation Stress Promotes Arterial Stiffening and Is Reversed by a Natural Compound in Aging Mice

BUFFALO, NY — December 16, 2025 — A new #research paper was #published in Aging-US on December 10, 2025, titled “Theobromine is associated with slower epigenetic ageing.”

In this study, led by Ramy Saad from King’s College London and Great Ormond Street Hospital for Children NHS Foundation Trust, alongside Jordana T. Bell from King’s College London, researchers found that higher levels of theobromine, a natural compound found in cocoa, are associated with slower biological aging in humans. The findings suggest that theobromine may support healthy aging.

Epigenetic aging refers to biological changes that affect how genes function over time. It is measured using blood-based markers such as DNA methylation and telomere length, which together provide a more accurate picture of aging than chronological age.

In this work, researchers analyzed data from two large European studies. In 509 women from the TwinsUK cohort, they found that higher blood levels of theobromine were associated with slower aging, especially based on GrimAge, an epigenetic clock that predicts the risk of age-related disease and early death. The results were confirmed in 1,160 men and women from the German KORA study.

“We initially tested for the association between six metabolites found in coffee and cocoa, and epigenetic measures of ageing in blood samples from 509 healthy females from the TwinsUK cohort (median age = 59.8, IQR = 12.81, BMI = 25.35).“

Importantly, theobromine’s effects were independent of related compounds such as caffeine. Even after adjusting for these other substances and different lifestyle factors, the association with slower aging remained strong. The study also associated higher theobromine levels with longer telomeres, another marker of healthy aging.

While theobromine is commonly found in cocoa and chocolate, the study does not suggest increasing chocolate intake. However, it highlights the potential of everyday dietary components such as theobromine to influence aging. These findings support growing evidence that certain plant-based compounds may play a role in promoting long-term health. By identifying a connection between theobromine and slower biological aging, the study opens new directions for research into nutritional strategies for healthy aging.

DOI - https://doi.org/10.18632/aging.206344

Corresponding authors - Ramy Saad - ramy.saad@kcl.ac.uk, and Jordana T. Bell - jordana.bell@kcl.ac.uk

Abstract video - https://www.youtube.com/watch?v=S0P1USM8L6E

Sign up for free Altmetric alerts about this article - 
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206344

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

Keywords - aging, theobromine, epigenetic aging, DNA methylation, metabolomics, nutrition

To learn more about the journal, 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
Facebook - https://www.facebook.com/AgingUS/
X - https://twitter.com/AgingJrnl
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

Theobromine From Cocoa Linked to Slower Biological Aging

BUFFALO, NY— December 17, 2025 — We are pleased to announce that we have officially joined ResearchGate, the professional network for scientists and researchers. This collaboration enhances the visibility, accessibility, and impact of research published in Aging-US among the global scientific community.

By integrating ResearchGate, Aging-US offers authors and readers an additional channel to discover, share, and discuss cutting-edge findings in aging research. The journal’s presence on the platform includes a dedicated profile, article listings, author profiles, and metrics that help track readership and engagement.

As the field of aging research continues to grow rapidly, it is essential that high-quality studies are easy to find, access, and share. Joining ResearchGate allows Aging-US authors to connect their work with a wider network of peers, fostering collaboration, advancing understanding of the biology of aging, and helping translate discoveries into better health outcomes.

ResearchGate hosts millions of researchers worldwide and provides tools for sharing publications, asking and answering research questions, and discovering new collaborators across institutions and disciplines. Aging-US’s participation on the platform reinforces its commitment to open scientific dialogue and timely dissemination of rigorously reviewed aging research.

Authors publishing in Aging-US can now:

-Link their publications directly to their ResearchGate profiles.

-Track reads, recommendations, and citations through the platform’s analytics.

-Engage with other scientists interested in aging, geroscience, and translational research.

Readers and researchers can follow Aging-US on ResearchGate to stay updated on newly published articles, special issues, and calls for papers.

To learn more about the journal, 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
Facebook - https://www.facebook.com/AgingUS/
X - https://twitter.com/AgingJrnl
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

Aging-US Now on ResearchGate, Enhancing Visibility for Authors and Readers

BUFFALO, NY — December 19, 2025 — A new #research paper was #published in Volume 17, Issue 11 of Aging-US on November 18, 2025, titled “Epigenetic age predicts depressive symptoms during the COVID-19 pandemic in the Canadian Longitudinal Study on Aging: importance of biological sex.”

This study, led by Cindy K. Barha of the University of Calgary and the University of British Columbia, along with Teresa Liu-Ambrose of the University of British Columbia, found that older women with a younger biological age measured years before the COVID-19 pandemic experienced a greater increase in depressive symptoms during the early lockdown period. These findings could help shape future mental health strategies, particularly for women with high emotional or caregiving demands.

Epigenetic age is a biological marker that reflects how the body is aging and may differ from a person’s actual age. Using long-term data from the Canadian Longitudinal Study on Aging (CLSA), the researchers investigated whether epigenetic age could predict changes in mental health during a major public health crisis. The study included over 600 adults, with an average baseline age of 63, and used two widely accepted epigenetic clocks, the DNAmAge and the Hannum Age, to estimate biological age. Depressive symptoms were tracked at four time points between 2012 and 2020, including during the height of the pandemic.

“The mean participant chronological age at study entry was 63±10 years (46% female).”

The analysis showed that in women, a younger biological age predicted a greater rise in depression during the early phase of the COVID-19 pandemic. This was not observed in men or in individuals with older biological ages.

The study challenges the common belief that a younger biological age always signals better mental or physical resilience. The researchers suggest that women with younger biological profiles may have been more socially or professionally active before the pandemic. When lockdowns disrupted daily routines and social connections, these individuals may have experienced more emotional distress.

Additional factors, such as reduced physical activity, loss of routine, and decreased social interaction, known to affect both mental health and biological aging, may have had a stronger emotional effect on this group. The findings highlight the importance of considering biological sex when studying how aging affects mental well-being during stressful events.

Although the study has some limitations, including the time gap between biological age measurement and the pandemic, it gives valuable insights into how biological and social factors interact during periods of crisis. Future research could use epigenetic clocks to better identify individuals at greater risk of mental health challenges during large-scale public health emergencies.

Overall, this study adds to the growing field of social epigenetics and suggests that biological age may support more targeted public health planning, especially for older adults.

DOI - https://doi.org/10.18632/aging.206337

Corresponding author - Teresa Liu-Ambrose - teresa.ambrose@ubc.ca

Abstract video - https://www.youtube.com/watch?v=DVm78jKsdkY

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:

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

Younger Biological Age May Increase Depression Risk in Older Women During COVID-19

BUFFALO, NY — December 23, 2025 — A new #research paper was #published in Volume 17, Issue 11 of Aging-US on November 25, 2025, titled “A natural language processing–driven map of the aging research landscape.”

In this study, Jose Perez-Maletzki from Universidad Europea de Valencia and Universitat de València, together with Jorge Sanz-Ros from Stanford University School of Medicine, used artificial intelligence (AI) to analyze a century of global aging research, revealing shifts in focus and highlighting underexplored areas.

The team analyzed over 460,000 scientific abstracts published between 1925 and 2023 to identify key themes, trends, and research gaps in the study of aging. Their goal was to provide a comprehensive, unbiased view of how the field has evolved and where future research could have the greatest impact.

The study found that aging research has moved from basic cellular studies and animal models to a growing focus on clinical topics, particularly age-related diseases such as Alzheimer’s and dementia. Using natural language processing and machine learning, the researchers grouped publications into thematic clusters and tracked how interest in each topic changed over time.

“By integrating Latent Dirichlet Allocation (LDA), term frequency-inverse document frequency (TF-IDF) analysis, dimensionality reduction and clustering, we delineate a comprehensive thematic landscape of aging research.”

One key finding was the growing separation between basic biological studies and clinical research. While both areas have grown significantly, they often progress independently with limited overlap. Clinical studies tend to focus on geriatrics, healthcare, and neurodegenerative diseases, while basic science emphasizes cellular mechanisms such as oxidative stress, telomere shortening, mitochondrial dysfunction, and senescence. The authors note that this lack of integration limits the translation of laboratory discoveries into medical applications.

The study also showed that some emerging topics, such as autophagy, RNA biology, and nutrient sensing, are expanding rapidly but remain separated from clinical applications. In contrast, long-established links, such as those between cancer and aging, remain strong. The analysis also highlighted that potentially important associations, such as those between mitochondrial dysfunction and senescence or epigenetics and autophagy, are rarely studied and may be new research opportunities.

This AI-driven analysis offers a new way to guide future research by identifying how different areas of aging science are interconnected or isolated. It also highlights how research priorities may be shaped by policy or funding trends, as seen in the heavy focus on Alzheimer’s disease. 

As the global population continues to age, understanding how biological processes relate to clinical outcomes is critical. This study not only offers a historical map of aging science but also serves as a tool to support more connected, interdisciplinary, and effective future research.

DOI - https://doi.org/10.18632/aging.206340

Corresponding author - Jorge Sanz-Ros - jsanzros@stanford.edu

Abstract video - https://www.youtube.com/watch?v=O4dJUGQ2ZcU

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

To learn more about the journal, 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
Facebook - https://www.facebook.com/AgingUS/
X - https://twitter.com/AgingJrnl
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

AI Tracks Nearly 100 Years of Aging Research, Revealing Key Trends and Gaps

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

Aging-US Podcast

Popular tracks