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.

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Aging

Rapamycin: The Miracle Compound From Easter Island

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

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Aging (Aging-US)

Press Release: Altos Labs Research Perspective by Dr. Blagosklonny

It is with great sadness and heavy heart that we announce the recent passing of Dr. Mikhail (Misha) V. Blagosklonny, our beloved Editor-in-Chief. Misha succumbed to metastatic lung cancer after a courageous battle.

Dr. Blagosklonny will be remembered as a brilliant and extraordinary scientist who dedicated his life to science. He was a visionary thinker, who made highly original contributions to cancer and aging research that were often ahead of their time. 

Dr. Blagosklonny was born into a family of scientists. His mother, Professor of Medicine Yanina V. Blagosklonnaya, specialized in endocrinology and was a talented teacher, mentoring several generations of medical students. His father, Professor Vladimir M. Dilman, was a brilliant gerontologist, endocrinologist and oncologist, known for being a very charismatic person. He was the first person to encourage Misha to think about nature, aging, and philosophy. 

Misha was a theorist by nature. While in school, he was deeply interested in physics and dreamed of becoming a theoretical physicist. Eventually, he chose biology, driven to study aging and age-related diseases, including cancer. He started as an experimentalist, but over the years, he became a theoretical biologist. In a way, his dream came true. 

The full tribute to Misha - https://www.aging-us.com/news-room/tribute-to-dr-mikhail-misha-blagosklonny

Tribute to Dr. Mikhail (Misha) Blagosklonny

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

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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:

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

Aging (Aging-US) was a proud sponsor of the “Future of Aging Research Mixer 2024” hosted by the Aging Initiative at Harvard University on November 15 in Boston. This event united a vibrant community of students, researchers and technologists, all driven by a shared mission: advancing innovations in aging research and longevity science.

Key Highlights from the Future of Aging Research Mixer 2024

The event kicked off with inspiring opening remarks and a keynote by George Church, professor at Harvard Medical School, founding member of the Wyss Institute, and co-founder of over 50 biotech companies. He was joined by Kat Kajderowicz, an MIT PhD student and Principal at age1. Together, they highlighted the interdisciplinary nature of aging research and its immense potential to drive transformative advancements.

Jesse Poganik, HMS Instructor in Medicine and Executive Co-Director of the Biomarkers of Aging Consortium, discussed the evolution of aging science and the critical role biomarkers play in understanding aging processes and assessing the effectiveness of interventions aimed at slowing or reversing age-related changes.

Alex Colville, co-founder and general partner at age1, explained how venture capital can accelerate innovation in longevity biotechnology. He shared career advice for aspiring researchers and paid tribute to his mentor, Dr. David Sinclair, a pioneer in aging research.

These talks highlighted the importance of mentorship, interdisciplinary collaboration, and investment in driving progress in the aging research field.

Read the full summary - https://aging-us.org/2024/11/agings-commitment-to-advancing-research-sponsoring-the-future-of-aging-research-mixer/

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:

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Aging’s Commitment to Advancing Research: Sponsoring the “Future of Aging Research Mixer 2024”

Aging’s Commitment to Advancing Research: Sponsoring the “Future of Aging Research Mixer”

Sleep is essential for everyone, but for those living with dementia, it is vital for better health and quality of life. Addressing sleep problems in dementia care is a crucial step toward improving life for both patients and caregivers.

Dementia and Sleep

Sleep is critical for brain health and well-being, but it is often a struggle for people with dementia. Dementia, a condition that affects memory, thinking, and daily life, is frequently complicated by other health issues like heart disease, diabetes, and anxiety. On top of these challenges, sleep problems such as insomnia and sleep apnea are common, making life even harder for patients and their caregivers. 

Addressing sleep issues is key to improving the lives of people with dementia and easing the burden on their support systems. Recognizing this need, researchers Upasana Mukherjee, Ujala Sehar, Malcolm Brownell, and P. Hemachandra Reddy from Texas Tech University Health Sciences Center conducted an extensive review. Published in Aging, Volume 16, Issue 21, their work aims to update healthcare professionals on these issues and promote new practices in dementia care.

The Study: Update on Sleep and Dementia’s Connection

“Sleep deprivation in dementia comorbidities: focus on cardiovascular disease, diabetes, anxiety/depression and thyroid disorders” is a comprehensive review that explores the connections between sleep disturbances, dementia, and related conditions like heart disease, diabetes, and anxiety.

Full blog - https://aging-us.org/2024/12/the-hidden-link-between-sleep-and-dementia-how-better-rest-can-improve-lives/

Paper DOI - https://doi.org/10.18632/aging.206157

Corresponding author - P. Hemachandra Reddy - hemachandra.reddy@ttuhsc.edu

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

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Keywords - aging, dementia and comorbidities, sleep disturbances, cardiovascular disease, diabetes, thyroid disorders, anxiety, insomnia, sleep apnea

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:

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The Hidden Link Between Sleep and Dementia: How Better Rest Can Improve Lives

BUFFALO, NY- December 19, 2024 – We are pleased to announce that Dr. Marco Demaria, a leading expert in aging and cellular senescence, will join Aging (Aging-US) as Editor-in-Chief, starting January 1, 2025. Dr. Demaria will work alongside an esteemed Editorial Board.

Dr. Demaria has an impressive background in aging research. He earned his PhD in Molecular Medicine from the University of Torino, Italy. In 2010, he joined the laboratory of Aging Founding Editor, the late Dr. Judith Campisi, at the Buck Institute for Research on Aging. There he developed cellular and animal models for studying cellular aging, also known as cellular senescence, and its role in tissue repair, cancer, and aging.

Currently, Dr. Demaria leads DemariaLab, whose mission is “to extend human healthspan by pioneering discoveries in molecular and cellular mechanisms that regulate the aging process.” His groundbreaking research has significantly advanced our understanding of cellular senescence and its role in aging and age-related diseases. Dr. Demaria aims to develop new therapeutic approaches to create more effective treatments that mitigate the diseases and extend the healthspan. His work specifically focuses on interfering with the mechanisms of cellular senescence using genetic, pharmacological, and nutraceutical strategies.

“My research is focused on understanding the molecular basis of age-related dysfunctions and disorders, and to identify new molecular and cellular targets to improve health and longevity.” - Marco Demaria

He is also a Full Professor at the European Research Institute for the Biology of Ageing (ERIBA), Director of the Mechanisms of Health, Ageing and Disease (MoHAD) at the University Medical Center Groningen (UMCG), President of the International Cell Senescence Association (ICSA), and Co-Founder of Cleara Biotech. Dr. Demaria also brings valuable editorial experience from his former positions as Editor-in-Chief of npj Aging and Editorial Board member of Aging Cell.

All the above, combined with Dr. Demaria’s academic contributions, commitment, and expertise, align perfectly with Aging’s mission to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. 

For more information about Marco Demaria, PhD, please visit www.demarialab.com and follow him on X (Twitter) @marc_dema or on Bluesky @marcdema.bsky.social.

About Aging-US

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Dr. Marco Demaria Named Editor-In-Chief of Aging (Aging-US)

Imagine being 15 years old but having a body that shows signs of aging as if you are decades older. For some young people with sickle cell disease (SCD), this is a reality. A new study published in Volume 16, Issue 21 of Aging shows that SCD causes the body to age much faster than normal. The research not only explains why this happens but also points to new ways to help people with the disease live healthier, longer lives.

What Is Sickle Cell Disease?

SCD is a genetic condition that changes the shape of red blood cells. Instead of being round, like a doughnut, the cells become curved like a sickle (a farming tool). These misshapen cells struggle to move through blood vessels, often blocking blood flow and leading to pain, organ damage, and other health problems. Even with modern treatments, they can experience complications like those seen in older adults, such as weaker bones, frailty, and organ failure. In the study “Adolescents and young adults with sickle cell disease exhibit accelerated aging with elevated T-cell p16INK4a expression,” researchers wanted to understand why this happens and what it means for people with the disease.

Full blog - https://aging-us.org/?p=6372

Paper DOI - https://doi.org/10.18632/aging.206152

Corresponding author - Samuel R. Wilson - samuel.wilson@med.unc.edu

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

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Keywords - aging, sickle cell disease, p16, adolescents, young adults

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:

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Accelerated Aging in Young People with Sickle Cell Disease

BUFFALO, NY- January 15, 2025 – A new priority #review was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) on January 12, 2025, entitled “Mikhail ‘Misha’ Blagosklonny’s enduring legacy in geroscience: the hyperfunction theory and the therapeutic potential of rapamycin.”

This review, written by Dr. David A. Barzilai, from Geneva College of Longevity Science and Healthspan Coaching LLC, summarizes the outstanding scientific contributions of the late Dr. Mikhail "Misha" Blagosklonny, Founding Editor-in-Chief of Aging. Dr. Blagosklonny’s research changed how researchers and scientists think about aging by introducing a new theory and promoting the use of rapamycin, an mTOR inhibitor, to slow aging and extend healthy life. Published shortly after his passing, this review honors Dr. Blagosklonny’s work and highlights how it challenged the traditional belief that aging is caused mainly by accumulated damage in the body.

Instead of describing aging as an accumulation of cellular damage, Dr. Blagosklonny’s Hyperfunction Theory redefined it as an ongoing biological process that goes into "overdrive" and leads to age-related diseases such as cancer, cardiovascular problems, and memory loss.

He identified the mTOR pathway—an important growth signal in the body—as a key driver of this process. His research showed that by using rapamycin, which slows down mTOR activity, it is possible to reduce aging-related diseases and promote longer, healthier lives.

Research supports many of Dr. Blagosklonny’s predictions about rapamycin’s benefits. Studies show that it can improve immune responses in older adults, making vaccines more effective. Other studies suggest rapamycin may help protect the heart, reduce harmful brain inflammation, and prevent the buildup of proteins linked to Alzheimer’s disease. Dr. Blagosklonny also proposed that rapamycin could reduce cancer risk by preventing excessive growth signals that contribute to tumor development.

Believing in rapamycin’s potential as a “longevity drug," Dr. Blagosklonny advocated for its careful use with medical supervision and precise dosing. He called for further research and even envisioned “longevity clinics” where personalized anti-aging treatments could be provided. The review also highlights ongoing scientific efforts to refine rapamycin therapies and explore new options with fewer side effects.

In conclusion, Dr. Blagosklonny has inspired a global shift toward viewing aging as a condition that can be managed rather than an inevitable decline. His research has left a legacy in the fields of geroscience, aging, and cancer prevention.

“This contribution will undoubtedly be remembered in the coming decades and beyond as an innovative contribution to our theoretical grasp of the aging process and a foundation for exploring effective therapeutic approaches.”

DOI - https://doi.org/10.18632/aging.206189

Corresponding author - David A. Barzilai - david.longevity@gmail.com

Video short - https://www.youtube.com/watch?v=3iOcIqfQdyI

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About Aging-US

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:

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Dr. Mikhail Blagosklonny’s Legacy: Hyperfunction Theory & Rapamycin

“We illustrate our strategy in brain and liver tissue, demonstrating how cell-type specific epigenetic clocks from these tissues can improve tissue-specific estimation of chronological and biological age.”

Aging affects everyone differently. There are two types of aging: chronological aging, which refers to the number of years a person has lived, and biological aging, which reflects how well the body is functioning based on cellular changes. A recent study published as the cover for Volume 16, Issue 22 of Aging reports a new discovery that could revolutionize the way we understand aging and its impact on health. 

Understanding Biological Age

Biological age reflects how well the body is aging and can vary based on lifestyle, genetics, and environmental factors. Traditionally, scientists estimate it using epigenetic clocks, which measure DNA methylation, chemical changes that occur over time. Until recently, these clocks could only provide general estimates by analyzing entire tissues, meaning they could not distinguish how different cell types aged within those tissues. A recent study titled “Cell-type Specific Epigenetic Clocks to Quantify Biological Age at Cell-Type Resolution” aims to change that.

Full blog - https://aging-us.org/2025/01/how-scientists-are-measuring-aging-at-the-cellular-level/

Paper DOI - https://doi.org/10.18632/aging.206184

Corresponding author - Andrew E. Teschendorff - andrew@sinh.ac.cn

Video short - https://www.youtube.com/watch?v=FjJa5U2-AqQ

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Keywords - aging, DNA methylation, epigenetic clocks, cell-type deconvolution, biological aging, Alzheimer’s disease, obesity

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:

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How Scientists Are Measuring Aging at the Cellular Level

Emerging research suggests that a specific type of body fat may play an important role in healthy aging and physical performance. Researchers from Rutgers New Jersey Medical School explore this topic in a recent research perspective published in Aging (Aging-US). Their work discusses new findings and emerging ideas about the role of brown adipose tissue (BAT), commonly known as brown fat.

Understanding Brown Fat

The human body contains different types of fat. The most common is white adipose tissue (WAT), which primarily stores excess calories. When present in large amounts, WAT contributes to health problems like obesity, type 2 diabetes, and cardiovascular disease as a result of its role in metabolic imbalance.

In contrast, BAT serves a more dynamic role. Instead of storing energy, BAT burns calories to generate heat through a process called thermogenesis, powered by its high concentration of mitochondria—the energy-producing structures in cells. While BAT is abundant in newborns to help regulate body temperature, it persists in smaller amounts in adults, particularly around the neck, shoulders, and spine. 

According to the research perspective, titled “Brown Adipose Tissue Enhances Exercise Performance and Healthful Longevity” brown fat’s role extends beyond thermoregulation. The authors suggest that BAT can significantly improve metabolic health, enhance physical performance, and promote healthful longevity.

Full blog - https://aging-us.org/2025/02/the-hidden-power-of-brown-fat-a-new-ally-in-healthy-aging/

Paper DOI - https://doi.org/10.18632/aging.206179

Corresponding author - Stephen F. Vatner - vatnersf@njms.rutgers.edu

Video short - https://www.youtube.com/watch?v=n1DvuR7owJQ

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Keywords - aging, brown adipose tissue, white adipose tissue, healthful longevity, exercise, regulator of G protein signaling 14

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:

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The Hidden Power of Brown Fat: A New Ally in Healthy Aging

BUFFALO, NY—February 11, 2025 — A new #research paper was #published in Aging (Aging-US) on January 15, 2025, in Volume 17, Issue 1, titled “Association between physical activity practice and sleep quality of older people in social isolation during the COVID-19 pandemic and Health Guidelines and future studies for the post-COVID period: a systematic review.”

Researchers Alexandro Andrade, Ana Cecília Rosatelli de Freitas Bastos, Anderson D’Oliveira, and Guilherme Torres Vilarino from the Santa Catarina State University (UDESC) in Brazil, conducted a systematic review to examine the relationship between physical activity (PA) and sleep quality in older adults who experienced social isolation during the COVID-19 pandemic. Their findings reveal that a decline in PA levels during social isolation negatively impacted sleep health, emphasizing the need for regular movement in aging populations.

The study reviewed nine studies involving over 11,500 older adults of both sexes from China, Japan, Brazil, Scotland, Canada, Italy, and Spain. The results showed that reduced PA during the pandemic was linked to poorer sleep quality in four studies, while one study found that those who remained active had better sleep patterns. The four other studies showed no significant association.

Getting enough quality sleep is essential for healthy aging, as sleep disorders have been linked to cognitive decline, depression, and reduced mental well-being. The COVID-19 pandemic worsened sleep health due to increased stress, isolation, and anxiety. Researchers suggest that staying active through walking, stretching, and structured exercise routines may help improve sleep quality and overall mental health.

The researchers point out the importance of PA as an accessible way to enhance sleep quality in older adults, particularly during times of crisis. Encouraging regular exercise and movement may help prevent sleep disorders and improve overall well-being in aging populations.

“PA can be considered a safe and effective practice to improve sleep quality in older adults due to its well-documented benefits in the literature.”

As the world moves past the pandemic, the researchers call for public health policies that promote PA for seniors. Health professionals and caregivers should advocate for regular movement as a preventive measure against insomnia, poor sleep, and mental health issues while emphasizing the long-term consequences of physical inactivity. The study also highlights the need for further research on the most effective types and intensities of PA for improving sleep quality in older adults.

“The practice of exercise and PA, individually and in groups, is recommended for this post-COVID scenario, as a measure to reduce social isolation and its negative effects and improve the quality of sleep in older adults.”

Future studies should explore how different exercise routines impact sleep health, especially for older adults recovering from COVID-19 or facing ongoing sleep challenges.

DOI - https://doi.org/10.18632/aging.206180

Corresponding author - Alexandro Andrade - alexandro.andrade.phd@gmail.com

Video short - https://www.youtube.com/watch?v=uV4WXq7I_J0

About Aging-US

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Study Reveals How Physical Activity Impacts Sleep Quality in Older Adults During COVID-19 Pandemic

BUFFALO, NY—February 12, 2025 — A new #research paper was #published in Aging (Aging-US) on January 3, 2025, in Volume 17, Issue 1, titled “Characterization of DNA methylation clock algorithms applied to diverse tissue types.”

Researchers Mark Richardson, Courtney Brandt, Niyati Jain, James L. Li, Kathryn Demanelis, Farzana Jasmine, Muhammad G. Kibriya, Lin Tong, and Brandon L. Pierce from the University of Chicago and University of Pittsburgh, studied how biological aging is measured using DNA. Their study found that while commonly used “DNA methylation clocks” work well for blood samples, they may be less reliable for other tissues like the lungs, colon, and kidneys.

DNA methylation clocks are widely used in forensic science, epigenetics and longevity research to estimate a person’s biological age based on chemical changes in DNA. These epigenetic clocks help scientists predict age-related diseases and assess how lifestyle factors, such as smoking, impact aging. Most were originally developed using blood samples, and their effectiveness in other tissues remains unclear. This study tested eight different DNA methylation clocks across nine human tissue types, including the lungs, prostate, ovaries, skeletal muscle, and kidneys. The researchers analyzed data from 973 tissue samples collected through the Genotype-Tissue Expression (GTEx) project.

Their analysis revealed significant differences in biological age estimates across tissues. While blood samples provided the most reliable results, other tissues showed noticeable variations. For example, testis and ovary tissues appeared younger than expected, while lung and colon tissues appeared older. 

“These differences across tissue types were most apparent for clocks trained using DNAm from blood only (e.g., Hannum), but also present for clocks trained on multiple tissue types (e.g., Horvath, a clock designed for pan-tissue age prediction.”
 
These findings suggest that aging may not occur at the same rate in every organ, and that standard DNA methylation clocks may not always give accurate biological age estimates outside of blood samples. The authors suggest that new, organ-specific epigenetic clocks may be needed to improve biological age prediction. Creating tissue-specific aging clocks could also improve medical diagnostics, age-related disease prevention, and health monitoring.

The researchers emphasize that larger studies with more tissue-specific DNA methylation data are needed to refine these aging clocks. By improving these tools, scientists can better understand how aging affects different organs and develop more reliable methods for measuring biological age. These advancements could lead to better predictions of age-related diseases and new strategies for healthy aging.

DOI - https://doi.org/10.18632/aging.206182

Corresponding author - Brandon L. Pierce - brandonpierce@uchicago.edu

Video short - https://www.youtube.com/watch?v=Jz-daRsZO2o

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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.)

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DNA Methylation Clocks May Require Tissue-Specific Adjustments for Accurate Aging Estimates

BUFFALO, NY—February 18, 2025 — A new #research paper was #published by Aging (Aging-US) on January 8, 2025, in Volume 17, Issue 1, titled “Senolytic agent ABT-263 mitigates low- and high-LET radiation-induced gastrointestinal cancer development in Apc1638N/+ mice.”

Researchers Kamendra Kumar, Bo-Hyun Moon, Santosh Kumar, Jerry Angdisen, Bhaskar V.S. Kallakury, Albert J. Fornace Jr., and Shubhankar Suman from Georgetown University Medical Center explored whether a drug called ABT-263 could help reduce the risk of gastrointestinal (GI) cancer caused by radiation exposure. Their findings suggest that ABT-263, a senolytic agent, helps eliminate harmful aging cells in the gut, reducing inflammation and lowering cancer risk in mice. These results could lead to potential treatments for people exposed to radiation, including cancer patients and astronauts.

Radiation exposure, whether from medical treatments, environmental sources, or space travel, can damage cells and increase the risk of GI cancer. One key factor in this process is cellular senescence, where damaged cells stop dividing but continue to release harmful molecules that promotes tumor growth. This study tested whether ABT-263, a drug designed to remove these aged cells, could lower cancer risk in a mouse model of GI cancer.

In this study, researchers exposed mice to radiation and found that it increased the number of damaged cells in their intestines, leading to more tumors. However, when the mice were given ABT-263, the number of harmful cells decreased, and they developed fewer tumors. The drug also reduced inflammation and blocked signals that promote cancer growth.

“Oral administration of ABT-263 in Apc1638N/+ mice resulted in a significant reduction in low-LET IR-induced intestinal tumor burden at 5 months post-exposure."

These findings highlight the potential of senolytic drugs like ABT-263 as a preventive treatment for radiation-induced cancers. This approach could be especially beneficial for cancer patients undergoing radiation therapy, astronauts exposed to cosmic radiation, and individuals at risk from environmental sources such as radon gas.

However, while ABT-263 showed promise, it also has known side effects, including reduced platelet counts, which can impact blood clotting. Future research will focus on optimizing senolytic treatments to ensure they are both safe and effective for human use. Scientists are also exploring alternative drugs and combination therapies that might offer the same benefits with fewer risks.

This study provides strong evidence that removing senescent cells could help prevent radiation-related GI cancer. With further research, senolytic drugs may become an important tool in protecting at-risk populations from the long-term effects of radiation exposure.

DOI - https://doi.org/10.18632/aging.206183

Corresponding author - Shubhankar Suman - ss2286@georgetown.edu

Video short - https://www.youtube.com/watch?v=M_WEht4vy4w

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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.)

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Senolytic ABT-263 Reduces Radiation-Induced Gastrointestinal Cancer

BUFFALO, NY — February 19, 2025 — A new #research paper was #published by Aging (Aging-US) on January 6, 2025, in Volume 17, Issue 1, titled “The profile of oxidative stress markers (arachidonic and linoleic acid derivatives) in patients with benign prostatic hyperplasia in relation to metabolic syndrome.”

A team of researchers, led by first author Weronika Ratajczak and corresponding author Olimpia Sipak from Pomeranian Medical University, examined how inflammation and metabolic health contribute to benign prostatic hyperplasia (BPH), a common condition that causes prostate enlargement in aging men, leading to urinary problems. Their findings suggest that inflammatory-related molecules in the blood may play a key role in BPH development, especially in men with metabolic syndrome—a group of conditions including obesity, high blood sugar, and high cholesterol.

BPH affects millions of men as they age, making urination more difficult and sometimes painful. While age and hormonal changes are known factors, the precise causes of prostate enlargement remain unclear. This study provides new evidence that inflammation, especially lipid-derived inflammatory markers, may be a driving factor behind BPH, particularly in those with poor metabolic health.

The research team analyzed blood samples from 219 men, including 144 with BPH and 75 without, measuring markers related to inflammation and oxidative stress. The results showed that men with BPH had significantly higher levels of pro-inflammatory molecules such as 12S-HETE and 5-HETE while having lower levels of anti-inflammatory substances like lipoxin A4. The imbalance was even more pronounced in men with both BPH and metabolic syndrome, indicating a possible link between poor metabolic health and worsening prostate conditions​.

“Furthermore, there is mounting evidence that links the onset of inflammation with the development of prostate diseases, including benign prostatic hyperplasia and prostate cancer.”

Metabolic dysfunction and chronic inflammation may not only contribute to BPH development but also exacerbate its severity. Monitoring metabolic health could play a role in reducing the risk of prostate enlargement.

Future research is needed and may focus on whether anti-inflammatory treatments or lifestyle changes—such as improved diet, weight management, and exercise—could help slow the progression of BPH or reduce its symptoms​.

DOI - https://doi.org/10.18632/aging.206187

Corresponding author - Olimpia Sipak - olimpiasipak-szmigiel@wp.pl

Video short - https://www.youtube.com/watch?v=O0VMvqaVsUs

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Keywords - aging, benign prostatic hyperplasia (BPH), metabolic syndrome (MetS), lipid markers, inflammation, fatty acids derivatives

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.

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Inflammation and Metabolic Syndrome Linked to Benign Prostatic Hyperplasia

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

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

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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.

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

Dr. Moshe Szyf from EpiMedTech Global in Singapore  discusses a research paper he co-authored that was published in Volume 17, Issue 1 of Aging (Aging-US), entitled “EpiAge: a next-generation sequencing-based ELOVL2 epigenetic clock for biological age assessment in saliva and blood across health and disease.”

DOI - https://doi.org/10.18632/aging.206188

Corresponding author - Moshe Szyf - moshe.szyf@epimedtech.com

Video interview - https://www.youtube.com/watch?v=NA8Vctks0gY

Video transcript - https://www.aging-us.com/interviews/epiage-ngs-based-elovl2-epigenetic-clock-for-biological-age-assessment

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Keywords - aging, epigenetic clock, elovl2, next-generation sequencing, EpiAge, Alzheimer's disease

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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.

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Behind the Study: EpiAge: NGS-Based ELOVL2 Epigenetic Clock for Biological Age Assessment

BUFFALO, NY — February 24, 2025 — A new #researchpaper was #published in Aging (Aging-US) on January 22, 2025, in Volume 17, Issue 1, titled “EpiAge: a next-generation sequencing-based ELOVL2 epigenetic clock for biological age assessment in saliva and blood across health and disease.”

The research team, experts from both industry (EpiMedTech Global, HKG Epitherapeutics Ltd) and academic institutions (McGill University, Oxford University, University of Catania, and the Research Institute-IRCCS), led by first author David Cheishvili and corresponding author Moshe Szyf, have developed EpiAgePublic, a new method to estimate biological age using only three key DNA sites in the ELOVL2 gene, a well-known marker of aging. Unlike traditional methods that require analyzing thousands of DNA regions, this approach simplifies the process while maintaining accuracy. Their findings show that EpiAgePublic performs as well as, or even better than, more complex models in predicting biological age in diverse populations.

Biological age measures how fast or slow a person’s body is aging. It can be different from chronological age and is influenced by genetics, lifestyle, and health conditions. Understanding biological aging can help researchers and clinicians identify age-related diseases like Alzheimer’s disease and develop anti-aging treatments. However, many existing biological age tests rely on expensive and complicated processes. The EpiAgePublic model overcomes these challenges with a simple yet powerful approach.

The study analyzed data from over 4,600 individuals across different health conditions, including Alzheimer’s disease and HIV. It confirmed that EpiAgePublic accurately tracks aging patterns and can identify factors such as chronic illness or stress that accelerate the aging process. Importantly, the researchers demonstrated that the test works well using saliva samples, offering a convenient and non-invasive alternative to blood-based tests. This makes it easier to conduct epigenetic age testing in both clinical and research settings.

“The simplicity and precision of epiAgePublic, designed for compatibility with next-generation sequencing (NGS) technologies, mark a significant step forward in the field of epigenetic research.”

The ability to measure epigenetic aging with a quick and cost-effective test has significant implications for healthcare, longevity research, and personalized medicine. This method could be used in hospitals, wellness clinics, and longevity studies to track aging and evaluate the effectiveness of anti-aging interventions. It may also help clinicians detect early signs of aging-related diseases, allowing for better preventive care.

Finally, the study’s findings highlight the advantages of next-generation sequencing in epigenetic research, leading the way for more precise and accessible aging diagnostics. Future research will explore how this model can be expanded to other health conditions and used in routine medical practice.

DOI - https://doi.org/10.18632/aging.206188

Corresponding author - Moshe Szyf - moshe.szyf@epimedtech.com

Author interview - https://www.youtube.com/watch?v=NA8Vctks0gY

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EpiAge: A New Test to Measure Biological Age Using Saliva or Blood

In the Season 3 premiere of the Longevity & Aging Series, Dr. Yu-Xuan Lyu from Southern University of Science and Technology (Shenzhen, China) joins host Dr. Evgeniy Galimov to discuss his co-authored research paper, featured as the cover for Aging (Aging-US) Volume 16, Issue 20, titled “Longevity biotechnology: bridging AI, biomarkers, geroscience, and clinical applications for healthy longevity.”
#aging #author #interview #series #biotechnology #ai #artificialintelligence #longevity #healthspan #lifespan #oa #openscience #peerreview #journal #publication #publishing #meded #agingshort #video

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

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Abstract

The recent unprecedented progress in ageing research and drug discovery brings together fundamental research and clinical applications to advance the goal of promoting healthy longevity in the human population. We, from the gathering at the Aging Research and Drug Discovery Meeting in 2023, summarised the latest developments in healthspan biotechnology, with a particular emphasis on artificial intelligence (AI), biomarkers and clocks, geroscience, and clinical trials and interventions for healthy longevity. Moreover, we provide an overview of academic research and the biotech industry focused on targeting ageing as the root of age-related diseases to combat multimorbidity and extend healthspan. We propose that the integration of generative AI, cutting-edge biological technology, and longevity medicine is essential for extending the productive and healthy human lifespan.

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Keywords - aging, biotechnology, artificial intelligence, healthy longevity

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Longevity & Aging Series (S3, E1): Dr. Yu-Xuan Lyu

BUFFALO, NY — March 3, 2025 — A new #research paper was #published in Aging (Aging-US) on February 27, 2025, as the #cover of Volume 17, Issue 2, titled “Variability in radiotherapy outcomes across cancer types: a comparative study of glioblastoma multiforme and low-grade gliomas.” 

An international research team, led by first author Alexander Veviorskiy from Insilico Medicine AI Limited, Abu Dhabi, UAE, and corresponding author Morten Scheibye-Knudsen from the Center for Healthy Aging, University of Copenhagen, investigated how radiotherapy affects survival in different types of cancer, with a special focus on glioblastoma multiforme (GBM) and low-grade gliomas (LGG). Their findings reveal that radiotherapy has opposite effects in GBM and LGG patients. The study highlights key biological differences between these brain cancer types, emphasizing the need for personalized treatment strategies.

Radiotherapy is a standard treatment for many tumors, but its effectiveness varies widely depending on the type of cancer. The researchers began by analyzing data from 32 cancer types using information from The Cancer Genome Atlas (TCGA). They then focused on glioblastoma multiforme (GBM) and low-grade gliomas (LGG), two types of brain cancer with distinct biological behaviors. GBM is an aggressive cancer with poor survival rates, whereas LGG progresses more slowly and often has a better prognosis.

“GBM and LGG are particularly interesting to study together because GBM often originates from a preexisting LGG, representing a progression from a lower-grade to a higher-grade malignancy.”

The results revealed a striking contrast: patients with GBM who received radiotherapy lived longer, whereas those with LGG had shorter survival times after treatment. To understand the reasons behind this, the researchers analyzed gene expression and signaling pathways. They identify several biological processes that may influence radiotherapy outcomes.

For example, GBM tumors have weaker DNA repair mechanisms, making them more vulnerable to radiation-induced damage, which allows radiotherapy to effectively kill cancer cells. In contrast, LGG tumors have stronger DNA repair systems, helping cells survive radiation better and potentially reducing the treatment’s effectiveness. Additionally, differences in immune system activity and genetic mutations—such as EGFR alterations—were linked to worse survival in LGG patients who received radiotherapy.

These findings highlight the need for a more personalized approach to treating brain cancer. The study proposes that a universal approach to radiotherapy is not appropriate, particularly for patients with LGG. Instead, personalized treatment strategies based on genetic and molecular characteristics could improve patient survival outcomes. The research also raises the possibility of combining radiotherapy with targeted therapies, such as immune-boosting therapies or DNA repair inhibitors, to enhance its effectiveness.

In conclusion, this study highlights the complexity of brain cancer treatment and the need for further research to refine therapeutic strategies. By understanding the molecular and genetic differences between the different types of cancers, more effective and personalized approaches can be developed to improve survival and quality of life for brain cancer patients.

DOI - https://doi.org/10.18632/aging.206212

Corresponding author - Morten Scheibye-Knudsen - mscheibye@sund.ku.dk

Video short - https://www.youtube.com/watch?v=j91rzDJHXTE

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Radiotherapy Impacts Survival Differently in Glioblastoma and Low-Grade Glioma

BUFFALO, NY — March 5, 2025 — A new #research paper was #published in Aging (Aging-US) on February 11, 2025, Volume 17, Issue 2, titled “Exposome-wide association study of environmental chemical exposures and epigenetic aging in the national health and nutrition examination survey.” 

First author Dennis Khodasevich and corresponding author Andres Cardenas from Stanford University, and colleagues from other U.S. institutions, studied how exposure to harmful chemicals in the environment affects aging. Using data from the National Health and Nutrition Examination Survey (NHANES), they discovered that cadmium, lead, and cotinine are linked to faster biological aging, a process that can increase the risk of age-related diseases.

The study analyzed data from 2,346 U.S. adults aged 50 to 84 who participated in a national health survey. Researchers tested their blood and urine for 64 different chemicals, including metals, pesticides, and industrial pollutants. They assessed how these exposures influenced eight different epigenetic aging markers—biological clocks that measure how fast a person’s body is aging at the DNA level.

"We harnessed data from the National Health and Nutrition Examination Survey 1999-2000 and 2001-2002 cycles to examine exposome-wide associations between environmental exposures and epigenetic aging."

The strongest effects were linked to cadmium, a toxic metal found in cigarette smoke and some foods. People with higher levels of cadmium in their blood showed signs of accelerated aging. Higher levels of cotinine, a chemical related to tobacco exposure, were also linked to increased biological age, reinforcing the harmful effects of smoking. Additionally, lead exposure, a heavy metal found in old paint and contaminated water, was also associated with faster aging. 

The researchers also found that some pollutants, including a type of PCB (PCB118) and a type of dioxin (HpCDD), were linked to slower biological aging. However, it is unclear if this fact is beneficial, as past research shows that slower aging in some cases can still be linked to health risks.

This study is one of the largest to investigate how pollution affects the aging process. Unlike previous research that focused on only a few chemicals, it examined a wide range of pollutants in a diverse group of people. The findings suggest that everyday exposure to toxic substances can speed up aging at the cellular level, increasing the risk of age-related diseases.

In summary, these findings raise concerns about how widespread environmental contaminants may accelerate aging and contribute to chronic diseases such as heart disease, cancer, and cognitive decline. Reducing exposure to toxic substances like cadmium and lead—found in cigarettes, polluted air, and contaminated food—could help slow biological aging and improve long-term health. These insights highlight the need for stronger environmental health policies to protect individuals from premature aging and disease.

DOI - https://doi.org/10.18632/aging.206201

Corresponding author - Andres Cardenas - andresca@stanford.edu

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Toxic Environmental Pollutants Linked to Faster Aging and Health Risks in U.S. Adults

Radiation therapy or radiotherapy, is a common treatment for cancer, but its effectiveness differs across patients. A recent study published as the cover for Volume 17, Issue 2 of Aging explored why this happens. The findings provide valuable insights, particularly for brain cancers like glioblastoma (GBM) and low-grade gliomas (LGG).

Understanding Glioblastoma and Low-Grade Gliomas

Glioblastoma and LGG are both brain tumors, but they behave in very different ways. GBM is highly aggressive, with most patients surviving only 12 to 18 months, even with surgery, chemotherapy, and radiation therapy. LGG, on the other hand, grows more slowly, and many patients live for decades with proper care.

Despite their differences, LGG and GBM are biologically linked. Some LGG tumors eventually transform into GBM, making early treatment decisions critical. Given radiation therapy’s effectiveness in GBM, it has often been assumed that LGG patients would also benefit from it. However, a new study titled “Variability in radiotherapy outcomes across cancer types: a comparative study of glioblastoma multiforme and low-grade gliomas” challenges this assumption.

Full blog - https://aging-us.org/2025/03/how-radiation-therapy-affects-tumors-glioblastoma-vs-low-grade-gliomas/

Paper DOI - https://doi.org/10.18632/aging.206212

Corresponding author - Morten Scheibye-Knudsen - mscheibye@sund.ku.dk

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Keywords - aging, cancer, biomarkers, radiotherapy, GBM, LGG, survival

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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.

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How Radiation Therapy Affects Tumors: Glioblastoma vs. Low-Grade Gliomas

BUFFALO, NY — March 12, 2025 — A new #research paper was #published in Aging (Aging-US) on February 25, 2025, Volume 17, Issue 2, titled “Epidemiology and genetic determination of measures of peripheral vascular health in the Long Life Family Study.”

Researchers from multiple institutions, led by first author and corresponding author Deidra R. Fricke from the University of Pittsburgh, studied the genetic and lifestyle factors that influence peripheral artery disease (PAD), a condition that restricts blood flow to the legs. Their findings suggest that people from families with exceptional longevity have a lower risk of PAD, possibly due to inherited genetic traits or healthier lifestyle habits.

Peripheral artery disease is a common but often undiagnosed condition that affects millions worldwide. It increases the risk of heart disease, stroke, and mobility issues. This study conducted using data from the Long Life Family Study (LLFS), found that individuals from long-lived families have significantly better vascular health than the general population.

“Peripheral artery disease (PAD) is a major contributor to morbidity in older adults.”

The researchers analyzed over 3,000 participants, including 1,090 long-lived individuals, their 1,554 children, and 362 spouses. Among the oldest participants (average age 89), about 18% had PAD. However, among their children (average age 60), only 1% had PAD—far lower than the expected 12% found in other studies. This finding suggests that certain protective factors, whether genetic or lifestyle-related, help maintain healthier arteries in these families.

In the study, key risk factors for PAD were identified, including aging, high blood pressure, smoking, and hypertension medication use. Interestingly, unlike in other studies, high cholesterol and diabetes were not major risk factors in this group. This data further supports the idea that long-lived families may have genetic protective factors that contribute to better vascular health.

In addition to lifestyle factors, the study found four genomic regions linked to PAD risk. Three of these were new discoveries, while the fourth was similar but not identical to previously published findings. These genetic markers may help scientists better understand why some individuals are more likely to develop PAD and how to prevent it.

“We identified four genomic sites that may harbor variants associated with protection from PAD.”

This research highlights the value of studying long-lived families to unlock the secrets of healthy aging and vascular health. Understanding what helps them maintain better artery function could lead to new strategies for preventing PAD, heart disease, and other age-related conditions.

Paper DOI: https://doi.org/10.18632/aging.206204

Corresponding author: Deidra R. Fricke — der94@pitt.edu

Keywords: aging, ankle-brachial index, peripheral arterial disease, heritability, genomewide linkage analysis, genomewide association study

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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.

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Long-Lived Families Show Lower Risk for Peripheral Artery Disease

Could the air we breathe, the food we eat, or the chemicals in our everyday environment be accelerating our aging process? A recent study published in Aging suggests that exposure to certain environmental chemicals may be linked to faster biological aging through changes in DNA. These findings could have major implications for public health and longevity.

Understanding How Scientists Measure Aging at the DNA Level
Aging is not just about wrinkles and gray hair—it happens at the molecular level too. Scientists use epigenetic clocks to measure biological aging, which can differ from a person’s actual chronological age. These clocks track DNA methylation, a type of chemical modification that can change over time due to environmental factors like diet, pollution, and chemical exposure. Until now, there has been little research into how widespread environmental chemicals impact these aging markers. 

The Study: Investigating the Impact of Environmental Pollutants on Aging
A research team led by first author Dennis Khodasevich and corresponding author Andres Cardenas from Stanford University, conducted an exposome-wide association study to examine how different environmental pollutants affect epigenetic aging. Using data from the National Health and Nutrition Examination Survey (NHANES), they analyzed blood and urine samples from 2,346 adults aged 50 to 84. The study measured 64 environmental chemicals, including heavy metals, pesticides, plastics, and tobacco-related compounds, to identify potential links to accelerated aging. The study titled “Exposome-wide association study of environmental chemical exposures and epigenetic aging in the national health and nutrition examination survey,” was published in Aging on February 11, 2025.

Full blog - https://aging-us.org/2025/03/how-environmental-chemicals-may-accelerate-biological-aging/

Paper DOI - https://doi.org/10.18632/aging.206201

Corresponding author - Andres Cardenas - andresca@stanford.edu

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Keywords - aging, epigenetic aging, environmental exposures, exposome, epigenetics

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How Environmental Chemicals May Accelerate Biological Aging

Could a class of drugs that clear aging cells also help treat Alzheimer’s disease? A recent study, featured as the cover for Aging (Volume 17, Issue 3), titled “Differential senolytic inhibition of normal versus Aβ-associated cholinesterases: implications in aging and Alzheimer’s disease,” suggests they might—and with remarkable precision.

Understanding Alzheimer’s Disease

Alzheimer’s disease is a progressive neurological disorder that gradually steals memory, independence, and a person’s sense of identity. A defining feature of Alzheimer’s is the buildup of amyloid-β (Aβ) plaques—sticky protein clumps that interfere with communication between brain cells. This disruption is closely linked to changes in a group of enzymes called cholinesterases, especially acetylcholinesterase (AChE) and butyrylcholinesterase (BChE). These enzymes normally play a vital role in regulating neurotransmitters critical for memory, learning, and cognitive function. In Alzheimer’s, however, their behavior changes significantly, particularly when they interact with Aβ plaques.

The Study: Exploring Senolytics for Alzheimer’s Enzyme Inhibition

A research team from Dalhousie University in Canada looked into whether senolytic compounds—a class of drugs that eliminate damaged, aging cells often referred to as “zombie” cells—could also target the harmful forms of cholinesterase enzymes found in Alzheimer’s disease. Their goal was to see if these compounds could selectively inhibit the disease-associated versions of AChE and BChE, without affecting the healthy forms that are essential for normal brain function.

Full blog - https://aging-us.org/2025/04/senolytic-compounds-show-promise-in-targeted-alzheimers-treatments/

DOI - https://doi.org/10.18632/aging.206227

Corresponding author - Sultan Darvesh - sultan.darvesh@dal.ca

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Keywords - aging, cellular senescence, β-amyloid, acetylcholinesterase, butyrylcholinesterase, cholinesterase inhibitors

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.

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Senolytic Compounds Show Promise in Targeted Alzheimer’s Treatments

BUFFALO, NY — April 3, 2025 — Aging (Aging-US) is pleased to announce a special Call for Papers for a commemorative collection honoring the legacy of Dr. Mikhail (Misha) Blagosklonny, the founding editor of the journal and a pioneer in aging biology. His groundbreaking work shaped fundamental concepts in the field, particularly regarding the role of mTOR in aging and cancer, the use of rapamycin, bypassing senescence during the process of transformation, personalized medicine, and theories on why we age.

This special collection will explore key themes central to Dr. Blagosklonny’s scientific contributions, with a focus on mechanistic insights, translational approaches, and theoretical perspectives. We invite original research, reviews, and perspective articles covering topics such as:

The role of mTOR in aging and age-related diseases

Rapamycin and other pharmacological strategies to extend lifespan

Senescence bypass and its implications for cancer and regenerative medicine

Personalized medicine approaches in aging and longevity research

Theoretical models and evolutionary perspectives on aging

The special issue will be guest-edited by leading scientist in the field, David Gems, who will oversee the selection of high-quality contributions that reflect the depth and impact of Dr. Blagosklonny’s work.

We encourage researchers working on these topics to submit their manuscripts and contribute to this tribute to one of the most influential figures in aging research.

SUBMISSION DETAILS:

Submission Deadline: December 1, 2025

Manuscript Format: Please follow the journal’s submission guidelines

Peer Review: All submissions will undergo a rigorous peer-review process

Submission Link: https://aging.msubmit.net/cgi-bin/main.plex

We look forward to your contributions to this special issue and to honoring Dr. Blagosklonny’s enduring impact on the field of aging research.

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Call for Papers: Special Collection Honoring Dr. Mikhail (Misha) Blagosklonny

BUFFALO, NY — April 16, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 3, on March 12, 2025, titled “DNA methylation entropy is a biomarker for aging.”

Researchers Jonathan Chan, Liudmilla Rubbi, and Matteo Pellegrini from the University of California, Los Angeles, led a study that discovered a new way to measure changes in DNA that can help predict a person’s age. This method focuses on how random certain chemical tags on DNA become over time. The team compared this new measurement, called methylation entropy, to existing methods and found it performed just as well—or even better. These findings support the idea that changes in our epigenetic information are closely linked to aging and could offer new tools for studying age-related diseases.

The study focused on DNA methylation, a process where chemical marks are added to DNA and help control which genes are turned on or off. Scientists have traditionally measured average methylation levels to estimate biological age using “epigenetic clocks.” This study, however, takes a different approach. The researchers used buccal swabs (cells from inside the cheek) from 100 individuals between ages 7 and 84 and applied targeted bisulfite sequencing techniques to measure methylation entropy across 3,000 regions of the genome.

Entropy in this context reflects how disordered or varied the methylation patterns are at certain sites on the DNA. The researchers discovered that as people age, the entropy of methylation at many locations changes in a reproducible way. Sometimes it increases, reflecting more random patterns, and sometimes it decreases, showing more uniformity. These shifts are not always tied to how much methylation is happening, which suggests entropy provides new information beyond what traditional methods can offer.

To test how well this new metric could predict age, the team used both statistical and machine learning models. They found that methylation entropy predicted age as accurately as traditional methods, and the best results came from combining entropy with other measurements like average methylation and a method called CHALM. These combined models were able to estimate age with an average error of just five years.

"[...] methylation entropy is measuring different properties of a locus compared to mean methylation and CHALM, and that loci can become both more or less disordered with age, independently of whether the methylation is increasing or decreasing with age."

This research supports the growing theory that aging is partly caused by a gradual loss of epigenetic information—the biological “instructions” that help keep our cells working properly. This insight also connects with recent studies suggesting that restoring this lost information might reverse some signs of aging. While more research is needed to study methylation entropy in other tissues, this work points to a more precise and powerful way to measure biological aging, which could influence the future of aging-related treatments and therapies.

Read the full paper: DOI: https://doi.org/10.18632/aging.206220

Corresponding author: Matteo Pellegrini - matteope@gmail.com

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Keywords: entropy, DNA methylation, aging, epigenetics, epigenetic clocks

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DNA Methylation Entropy: A New Way to Track and Predict Aging

Breast cancer survivors are living longer than ever, thanks to research and medical advances, but new studies suggest that some treatments may come with a hidden cost: accelerated aging. A recent study, titled “Accelerated aging associated with cancer characteristics and treatments among breast cancer survivors,” published in Aging (Aging-US), reveals that breast cancer and its treatments may speed up biological aging, with effects lasting up to a decade post-diagnosis.

Breast Cancer and Aging

Breast cancer is one of the most common cancers among women worldwide. Medical advancements have dramatically improved survival rates, making it one of the most treatable forms of cancer. Yet, many survivors report lasting symptoms like fatigue, memory issues, and reduced vitality that resemble accelerated aging. This pattern has led scientists to investigate whether treatments for breast cancer might be contributing to biological age acceleration.

Full blog - https://aging-us.org/2025/04/breast-cancer-treatments-hidden-impact-accelerated-aging-among-survivors/

Paper DOI - https://doi.org/10.18632/aging.206218

Corresponding author - Xiao-Ou Shu - xiao-ou.shu@vumc.org

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Keywords - aging, accelerated aging, PhenoAge, breast cancer, survivors

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Breast Cancer Treatment’s Hidden Impact: Accelerated Aging Among Survivors

BUFFALO, NY — April 21, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 3, on March 14, 2025, titled “Effects of a natural ingredients-based intervention targeting the hallmarks of aging on epigenetic clocks, physical function, and body composition: a single-arm clinical trial.”

A team of researchers, led by first authors Natalia Carreras-Gallo and Rita Dargham, and corresponding author Varun B. Dwaraka from TruDiagnostic, studied how a natural anti-aging supplement called the Cel System might influence the aging process. They found that participants who took the supplement for one year showed a reduction in biological age, along with improved muscle strength and body composition. The study highlights the potential of lifestyle and nutritional supplements to support healthy aging.

“The Cel System supplement range was formulated to target pathways associated with the Hallmarks of Aging when combining Cel1, Cel2, and Cel3 formulas.”

Cel System is a natural supplement made from a mix of plant compounds, vitamins, and antioxidants designed to target the biological mechanisms associated with aging. Over the course of a year, 51 adults between the ages of 54 and 84 participated in the clinical trial. The group included 26 men and 25 women. Researchers tracked changes in biological age using DNA-based tests known as epigenetic clocks, along with physical performance and body composition metrics. Participants were also encouraged to walk for 10 minutes and practice mindfulness for five minutes daily.

Results showed that participants experienced improvements in grip strength, lower body mobility, and reductions in body weight, waist circumference, and body mass index. These physical gains were supported by slower biological aging, as measured by multiple epigenetic clocks. In addition, the supplement appeared to reduce stem cell turnover, a key marker of aging at the cellular level.

The study also reported changes in immune cell composition, suggesting that the supplement may help regulate immune function as people age. Biomarkers associated with liver function also shifted, pointing to potential improvements in organ health. However, levels of inflammation markers did not significantly change.

Analysis of methylation chemical marks on DNA revealed that the supplement influenced gene activity related to stress response, brain function, and cell communication. These molecular-level changes may help explain the broader benefits seen in physical and biological aging measures.

Although this was a pilot study without a control group, the findings suggest that the Cel System supplement shows potential for reducing signs of aging and improving overall health. The authors suggest future randomized controlled trials with larger sample sizes to confirm these results and explore the supplement’s long-term effects on longevity.

This study adds to growing evidence that targeted natural supplements may slow biological aging and extend healthspan. By combining epigenetic analysis with real-world health data, the findings offer new insight into how nutraceuticals, like Cel System, could promote long-term health and resilience.

Paper: DOI: https://doi.org/10.18632/aging.206221

Corresponding author: Varun B. Dwaraka – varun.dwaraka@trudiagnostic.com

Keywords: aging, epigenetic age change, physiological age change, epigenetic biomarker proxies, hallmarks of aging, nutraceutical longevity interventions

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Natural Supplement May Decrease Biological Aging and Improve Muscle Strength

BUFFALO, NY — April 23, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 3, on March 18, 2025, titled “Epigenetic and accelerated age in captive olive baboons (Papio anubis), and relationships with walking speed and fine motor performance.”

In this study, led by Sarah J. Neal from The University of Texas MD Anderson Cancer Center, researchers examined how the epigenetic age of baboons—a measure of biological aging based on DNA methylation—compared to their actual age (chronological age) and whether it related to signs of aging like slower walking or reduced hand coordination. While many baboons showed a mismatch between their epigenetic and chronological ages, these differences did not consistently align with physical performance measures.

Researchers analyzed blood samples from 140 captive olive baboons (Papio anubis) to determine whether these primates, like humans, show signs of “age acceleration”—a condition where epigenetic age surpasses chronological age. The results revealed that about a quarter of the baboons exhibited accelerated aging, while another quarter showed signs of slower aging, known as “age deceleration.” 

“We found that epigenetic age was strongly correlated with chronological age, and that approximately 27% of the sample showed age acceleration and 28% showed age deceleration."

The scientists then investigated whether these differences were reflected in physical indicators such as walking speed or fine motor skills. To do this, researchers measured walking speed by tracking how quickly baboons moved between points in their enclosures and assessed fine motor skills using a simple task that involved picking up small objects.

Older baboons did tend to walk more slowly and perform worse on tasks requiring dexterity, patterns also seen in aging humans. However, these changes were more closely related to chronological age than epigenetic age. Two different methods were used to measure the gap between epigenetic and chronological age. Each method produced slightly different outcomes, highlighting the complexity of defining age acceleration. In one analysis, the oldest baboons appeared to age more slowly epigenetically, possibly reflecting selective survival, where only the healthiest individuals live into old age.

This research is among the first to classify baboons based on their epigenetic aging rate and investigate how this links to real-world signs of aging. Although the findings did not provide clear evidence that epigenetic age acceleration leads to physical decline, they point to the importance of DNA methylation as a biomarker in aging research. Because baboons share many biological similarities with humans, these findings help refine how researchers measure aging and assess potential early warning signs of decline. Continued studies in baboons and other primates may improve our understanding of how epigenetic aging influences health and longevity—and could help develop better tools for predicting age-related decline in humans.

DOI - https://doi.org/10.18632/aging.206223

Corresponding author - Sarah Neal - SJNeal@MDAnderson.org

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Epigenetic Aging Detected in Baboons, But Physical Decline Not Clearly Linked

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/

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

Sponsoring the Muscle Aging Science & Translation Symposium

In this #episode of the Longevity & Aging Series, Dr. Stephen Vatner from the Department of Cell Biology and Molecular Medicine at Rutgers New Jersey Medical School, joins host Dr. Evgeniy Galimov to discuss a #research perspective he co-authored in Volume 16, Issue 22 of Aging (Aging-US), titled “Brown adipose tissue enhances exercise performance and healthful longevity.”

DOI - https://doi.org/10.18632/aging.206179

Corresponding author - Stephen F. Vatner - vatnersf@njms.rutgers.edu

Author interview - https://www.youtube.com/watch?v=-DE4H2DtSZg

Video short - https://www.youtube.com/watch?v=n1DvuR7owJQ

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Keywords - aging, brown adipose tissue, white adipose tissue, healthful longevity, exercise, regulator of G protein signaling 14

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Longevity & Aging Series (S3, E3): Dr. Stephen Vatner

BUFFALO, NY — April 29, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 3, on March 20, 2025, titled “Inhibition of the metalloprotease ADAM19 as a novel senomorphic strategy to ameliorate gut permeability and senescence markers by modulating senescence-associated secretory phenotype (SASP).”

Researchers, led by first author Sudipta Bar and corresponding authors Amit Sharma and Pankaj Kapahi from the Buck Institute for Research on Aging, have found that the enzyme ADAM19 plays an important role in regulating aging in cells and inflammation in the gut. Their study shows that blocking ADAM19 reduced gut damage and inflammation in fruit flies, mice, and human cells. This discovery points to a new possible way to treat gut disorders related to aging by reducing the harmful signals from senescent (aging) cells.

As individuals age, DNA damage can lead to the accumulation of senescent cells, contributing to tissue damage. These are cells that stop dividing and release harmful inflammatory substances called the senescence-associated secretory phenotype (SASP). In this study, researchers used fruit flies to search for genes involved in radiation-related gut damage. They identified a gene called meltrin, which is similar to human ADAM19. When meltrin was turned off, the flies had less gut leakage, less inflammation, and fewer signs of cellular aging.

“Through an unbiased genome-wide association study (GWAS) utilizing 156 strains from the Drosophila Genetic Reference Panel (DGRP), we identified meltrin (the drosophila orthologue of mammalian ADAM19) as a potential modulator of the senescence-associated secretory phenotype (SASP).”

To test if these results applied beyond flies, the team inhibited ADAM19 in mice using a drug called batimastat. Mice treated with the drug after chemotherapy exposure had stronger gut barriers and lower levels of inflammatory markers. The findings extended to human cell cultures, where ADAM19 inhibition reduced signs of cellular aging, including the expression of SASP proteins and β-galactosidase, a classic aging marker. 

Importantly, this approach does not kill aging cells like many 'senolytic' therapies but instead reduces the harmful substances they release, making it a potential "senomorphic" strategy. The study also showed that ADAM19 helps release certain SASP proteins by cutting them at the cell surface, suggesting a direct role in regulating inflammatory signals.

Through proteomic analysis, the team identified 12 SASP proteins that were significantly reduced when ADAM19 was blocked. Many of these proteins are linked to inflammation, immune response, and tissue remodeling in diseases such as inflammatory bowel disease and Crohn’s disease. This connection underlines the relevance of the findings for treating chronic gut disorders in aging populations.

By targeting ADAM19, researchers may have found a new way to protect gut health and lower inflammation caused by aging cells. This study offers a promising path for creating treatments that maintain healthy tissues without having to destroy aging cells, which could benefit people with gut damage related to aging or medical treatments.

DOI - https://doi.org/10.18632/aging.206224

Corresponding authors - Amit Sharma - amit.sharma@sens.org, and Pankaj Kapahi - pkapahi@buckinstitute.org

Video short - https://www.youtube.com/watch?v=dRfxQ20O2fQ

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Inhibiting ADAM19 Reduces Gut Inflammation and Cell Aging Markers Across Species

BUFFALO, NY — May 1, 2025 — A new #research paper was #published in Aging (Aging-US) on April 2, 2025, as the #cover of Volume 17, Issue 4, titled “Decreased mitochondrial NAD+ in WRN deficient cells links to dysfunctional proliferation.”

In this study, the team led by first author Sofie Lautrup and corresponding author Evandro F. Fang, from the University of Oslo and Akershus University Hospital in Norway, discovered that cells from people with Werner syndrome (WS)—a rare genetic disorder that causes  premature aging—have low levels of a molecule called NAD+ in their mitochondria. This molecule is essential for energy production, cellular metabolism, and maintaining cell health. The researchers also found a potential way to improve cell function in WS patients, pointing to new directions for treating age-related decline and other premature aging disorders.

Werner syndrome leads to signs of aging much earlier than normal, including problems such as cataracts, hair loss, and atherosclerosis by age 20 to 30. The team found that when the WRN gene is missing or damaged, cells cannot maintain healthy NAD+ levels in their mitochondria. As a result, the cells age more quickly and stop growing properly. When the researchers boosted NAD+ levels using nicotinamide riboside (a vitamin B3 compound) the affected stem cells and skin cells from patients showed less aging and improved mitochondrial activity.

“Interestingly, only 24 h treatment with 1 mM nicotinamide riboside (NR), an NAD+ precursor, rescued multiple pathways in the WRN−/− cells, including increased expression of genes driving mitochondrial and metabolism-related pathways, as well as proliferation-related pathways.”

The study also found that the WRN gene helps regulate other important genes that control how NAD+ is made in the body. Without WRN, this system becomes unbalanced, which affects how cells function, grow, and respond to stress. Although adding more NAD+ helped some cells look healthier, it could not completely fix the growth problems in other types of lab-grown cells. This suggests that while NAD+ supplementation is beneficial, it cannot fully replace the essential functions of the WRN gene.

These findings offer new insights into the biological mechanisms of aging and reinforce the therapeutic potential of targeting NAD+ metabolism in age-related and genetic diseases. Future studies will aim to better understand how subcellular NAD+ regulation interacts with mutations like those seen in WS. Finally, this research supports ongoing efforts to develop NAD+-based treatments that could slow cellular aging and improve quality of life for patients with premature aging conditions.

DOI - https://doi.org/10.18632/aging.206236

Corresponding author - Evandro F. Fang - e.f.fang@medisin.uio.no

Video short - https://www.youtube.com/watch?v=WpRpi8TYPfU

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Keywords - aging, Werner syndrome, premature aging, NAD+, mitochondria, proliferation

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Boosting NAD+ Levels Slows Aging in Cells from Werner Syndrome Patients

Aging (Aging-US) invites #submissions for a Special Collection dedicated to the theme of cellular #senescence, spanning its basic mechanisms, physiological and pathological functions, and clinical applications.

This collection is published in memory of Professor Judith Campisi, a pioneering force in the field of cellular senescence whose groundbreaking work shaped the understanding of senescence in aging, cancer, and tissue homeostasis. Her legacy continues to inspire generations of scientists working to decode the complex biology of senescent cells and their impact on health and disease.

We welcome original research articles, reviews, and perspectives on topics including:

-Fundamental mechanisms of senescence induction and maintenance

-Regulation and context-specific roles of the senescence-associated secretory phenotype (SASP)

-Beneficial and detrimental effects of senescent cells in vivo

-Senescence in development, aging, regeneration, and age-related diseases

-Biomarkers, imaging, and tools for senescence detection and quantification

-Therapeutic targeting of senescent cells: senolytics, senomorphics, and clinical translation

This Special Collection is guest edited by Han Li and Irina Conboy, both internationally recognized leaders in the study of senescence and aging.

Submission Details:

-Submission Deadline: January 15, 2026
-Manuscript Format: Please follow the journal’s submission guidelines
-Peer Review: All submissions will undergo a rigorous peer-review process
-Submission Link: https://aging.msubmit.net/cgi-bin/main.plex

Call for Papers: Commemorative Collection Honoring Dr. Judith Campisi

BUFFALO, NY – May 5, 2025 – Aging (Aging-US), #published by Impact Journals, is pleased to #announce its participation at the upcoming Society for Scholarly Publishing (SSP) 47th Annual Meeting. The #event will take place from May 28-30, 2025, in Baltimore, Maryland.

Attendees are invited to visit Booth No. 209 to meet members of the Aging (Aging-US) team. The 2025 meeting theme, “Reimagining the Future of Scholarly Publishing at the Intersection of Value and Values,” underscores the urgency of adapting to rapid technological change, including AI, and addressing growing concerns around research integrity and trust. These priorities align closely with our mission to foster open, reliable, and impactful scientific communication in the field of aging and age-related diseases.

In addition, the Longevity & Aging Series - hosted by Dr. Evgeniy Galimov and presented by Aging (Aging-US) - is a Finalist for a Society for Scholarly Publishing (SSP) 2025 EPIC Award in the Video/Film category. Winners will be announced at the EPIC Awards Celebration on May 29.

We look forward to connecting with SSP 2025 attendees to share more about Aging (Aging-US) and our publishing initiatives.

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Aging (Aging-US) to be Featured at SSP 47th Annual Meeting in Baltimore

BUFFALO, NY — May 6, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 4, on April 2, 2025, titled “Fisetin ameliorates vascular smooth muscle cell calcification via DUSP1-dependent p38 MAPK inhibition.”

In this study, researchers at Johannes Kepler University Linz found that fisetin, a natural substance found in fruits and vegetables, helps protect blood vessels from hardening, which is a common problem in older adults and people with kidney disease. This discovery highlights fisetin’s potential to prevent vascular calcification and reduce cardiovascular damage caused by aging and chronic kidney disease.

The research, led by first author Mehdi Razazian and corresponding author Ioana Alesutan, focused on vascular calcification—a condition in which blood vessels stiffen due to calcium deposits. This process is common in aging and chronic kidney disease and increases the risk of heart attacks and strokes. Using human and mouse study models, the researchers tested fisetin’s ability to prevent this calcification in vascular smooth muscle cells (VSMC), which play a key role in maintaining vessel health. Fisetin, known for its anti-inflammatory and antioxidant properties, significantly reduced calcium buildup and calcification markers under stress conditions that mimic disease.

The team also discovered that fisetin suppresses activity in a signaling pathway called p38 MAPK, which is known to promote calcification. This effect depends on a protein called DUSP1. When DUSP1 was blocked, fisetin could no longer protect the cells, showing that this protein is essential for its anti-calcification activity. The researchers confirmed fisetin’s protective effects in isolated mouse arteries and in living mice treated with high doses of vitamin D, which typically increases arterial calcification.

“Mechanistically, fisetin requires the phosphatase DUSP1 to inhibit p38 MAPK in order to mediate its protective effect on VSMC calcification.”

Importantly, the researchers tested fisetin under conditions similar to human disease. When VSMCs were exposed to blood serum from kidney dialysis patients—a condition known to trigger vascular calcification—fisetin again reduced calcium buildup and protected the cells. These findings suggest fisetin could be useful in countering the harmful vascular effects seen in chronic kidney disease.

This study adds to growing evidence that fisetin may protect blood vessels from aging-related damage. While more research is needed before it can be used in clinical treatments, the study highlights fisetin as a promising candidate for slowing or preventing vascular calcification. The findings could have broad implications for aging populations and individuals with kidney disease, who are at greater risk for heart problems due to vascular stiffening.

Read the full paper: DOI: https://doi.org/10.18632/aging.206233

Corresponding author: Ioana Alesutan – ioana.alesutan@jku.at

Keywords: aging, vascular calcification, vascular smooth muscle cells, fisetin, dual-specificity phosphatase 1, p38 MAPK

______

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Fisetin, a Natural Compound, Helps Prevent Artery Hardening from Aging and Kidney Disease

BUFFALO, NY — May 7, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 4, on April 4, 2025, titled “Influence of rapamycin on safety and healthspan metrics after one year: PEARL trial results.”

A research team led by first author Mauricio Moel and corresponding author Stefanie L. Morgan from AgelessRx conducted a clinical trial to determine whether low-dose, intermittent rapamycin could safely improve healthspan in older adults. The findings suggest rapamycin may offer measurable benefits for physical function and overall well-being, reinforcing its potential as a safe intervention to support healthy aging.

Aging remains the leading cause of chronic conditions such as heart disease, diabetes, and dementia. While medical advances have extended lifespan, many people still experience declining health and reduced mobility in later years. This growing gap between lifespan and healthspan has driven interest in therapies that target aging itself. Rapamycin, an FDA-approved drug originally used in transplant medicine, has drawn attention for its ability to influence aging-related pathways in animal studies. Until recently, its safety and benefits in healthy human populations were largely unknown.

The PEARL trial is the longest study so far to explore rapamycin’s use for longevity in healthy aging adults. Researchers followed 114 participants aged 50 to 85 over 48 weeks in a randomized, double-blind, placebo-controlled design. Participants received either a placebo or 5 mg or 10 mg of compounded rapamycin once per week. The study’s primary goal was to measure changes in visceral fat, while secondary outcomes included lean muscle mass, blood markers, and quality-of-life assessments.

The trial found that low-dose rapamycin was safe and well-tolerated, with serious side effects reported at similar rates across all groups. The most frequent minor issue among rapamycin users was mild gastrointestinal discomfort. While no significant reductions in visceral fat were observed, women taking 10 mg of rapamycin showed significant gains in lean muscle and reported reduced pain. In addition, participants taking 5 mg weekly reported improvements in emotional well-being and general health, as measured by validated surveys.

“Our findings provide evidence that these rapamycin regimens are well tolerated with minimal adverse effects when administered for at least one year within normative aging individuals.”

Researchers noted some limitations, including the relatively small and health-conscious participant group, which may have limited the ability to detect larger effects. The compounded form of rapamycin used also had lower absorption than commercial versions, possibly reducing its impact.

Overall, the PEARL trial provides early clinical evidence that low-dose rapamycin may help support physical and emotional well-being in older adults. Further studies with larger and more diverse populations will be essential to confirm the study results and refine dosing strategies for broader application.

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

Corresponding author: Stefanie L. Morgan – stefanie@agelessrx.com

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Keywords: rapamycin, aging, healthspan, longevity, geroscience

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Low-Dose Rapamycin Improves Muscle Mass and Well-Being in Aging Adults

Cancer and aging are two sides of age-related tumorigenesis.

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.)

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

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