Now Accepting Submissions: Special Collection on Cognitive Aging

In this special collection, Aging seeks to bring together cutting-edge research that spans the cellular and molecular underpinnings of cognitive aging with insights into the psychosocial, behavioral, and environmental factors that modulate its course.

BUFFALO, NY — July 8, 2025 — As populations worldwide continue to age, understanding the mechanisms and manifestations of cognitive aging is increasingly urgent for science, medicine, and society. Age-related cognitive decline ranges from mild memory lapses to the onset of dementia, and is shaped by a complex interplay of molecular, cellular, systemic, and social determinants.

In this special collection, Aging (Aging-US) seeks to bring together cutting-edge research that spans the cellular and molecular underpinnings of cognitive aging with insights into the psychosocial, behavioral, and environmental factors that modulate its course. By integrating basic biology with translational and societal dimensions, this collection aims to foster a holistic understanding of how and why cognitive function changes with age—and what can be done to preserve it.

We welcome original research articles, reviews, and perspectives across model systems and human studies, particularly those that promote interdisciplinary insights and translational potential.

POTENTIAL TOPICS

Molecular and Cellular Mechanisms

  • Senescence, inflammation, and neurodegeneration in cognitive decline
  • Mitochondrial dysfunction and oxidative stress in aging neurons
  • Neurovascular aging and blood-brain barrier integrity
  • Single-cell and spatial transcriptomics of the aging brain
  • mTOR, autophagy, and proteostasis in age-related cognitive impairment
  • The role of glial cells (microglia, astrocytes) in brain aging

 Genetics and Biomarkers

  • Genetic risk factors and epigenetic modifications associated with cognitive aging
  • Biomarkers of cognitive resilience and vulnerability
  • Neuroimaging and fluid-based biomarkers in aging populations

Interventions and Lifestyle Factors

  • Cognitive benefits of caloric restriction, exercise, or senolytic therapies
  • Preclinical and clinical trials targeting aging pathways to prevent cognitive decline
  • Impact of sleep, nutrition, and metabolic health on cognition in older adults
  • Use of cognitive strategies and compensatory techniques to maintain or enhance function in aging

Environmental and Social Contexts

  • Impact of social isolation, education, and socioeconomic status on cognitive trajectories
  • Lifelong cognitive reserve and its determinants
  • Cross-cultural and demographic studies on aging and cognition
  • Digital health tools for monitoring or enhancing cognitive function in the elderly

SUBMISSION DETAILS:

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

Click here to subscribe to Aging publication updates.

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DoliClock: A Lipid-Based Clock for Measuring Brain Aging

Aging is a multifaceted process influenced by intrinsic and extrinsic factors, with lipid alterations playing a critical role in brain aging and neurological disorders.”

A new study published recently as the cover of Aging Volume 17, Issue 6, describes a new method to estimate how fast the brain is aging. By analyzing lipids, or fat molecules, in brain tissue, researchers from the National University of Singapore and Hanze University of Applied Sciences created a biological “clock” called DoliClock. This innovation highlights how conditions such as autism, schizophrenia, and Down syndrome are associated with accelerated brain aging.

Understanding Brain Aging

As people grow older, their brains naturally change. However, in many neurological disorders, these changes seem to appear earlier and progress more rapidly. Disorders like autism, schizophrenia, and Down syndrome reduce quality of life and contribute to premature death. Scientists have long searched for better ways to measure biological age in the brain to understand these processes and develop strategies to slow them down.

Most existing methods for estimating biological age rely on genetic markers, such as DNA methylation, which are chemical modifications of DNA. While useful, these approaches may not fully capture the complexity of aging, especially in the brain. Lipids, which are essential components of brain cells and play important roles in energy storage and signaling, offer another perspective.

The Study: Building a Lipid-Based Aging Clock

A team led by first author Djakim Latumalea and corresponding author Brian K. Kennedy introduced DoliClock, a model that predicts brain age using lipid profiles from the prefrontal cortex. This region of the brain, located just behind the forehead, plays a key role in decision-making, memory, and emotional regulation.

The study titled “DoliClock: a lipid-based aging clock reveals accelerated aging in neurological disorders” analyzed post-mortem brain samples from individuals with and without neurological conditions such as autism, schizophrenia, and Down syndrome.

The researchers focused on a class of lipids called dolichols, which are involved in vital cellular processes such as protein transport and glycosylation. These lipids tend to accumulate in brain tissue as people age, making them promising markers for measuring biological aging.

Results: Lipids Reflect the Pace of Aging

The DoliClock model showed that dolichol levels in the brain increased gradually with age. This change became particularly noticeable around the age of 40, suggesting a shift in how the brain regulates lipid metabolism during midlife. In addition to dolichols, the researchers observed an increase in entropy, a measure of disorder in lipid composition, which also intensified around this age.

When applied to brain samples from individuals with neurological disorders, DoliClock revealed significant differences. Samples from people with autism, schizophrenia, and Down syndrome showed higher predicted biological ages compared to their actual ages. This finding indicates that these disorders are associated with accelerated brain aging. The results align with previous studies using other biological clocks but add a new layer of understanding by focusing on lipid metabolism.

The Impact: A New Window into Brain Aging

DoliClock represents an important step in aging research because it demonstrates how lipid profiles can serve as markers of biological age. Unlike genetic markers, which may not fully capture brain-specific changes, lipidomic data directly reflect the brain’s structure and metabolic state. Dolichols, in particular, emerged as strong indicators of aging and may also play a role in the development of neurological disorders. This lipid-based clock could help scientists better understand the brain aging process and identify individuals at risk of premature decline.

Future Perspectives and Conclusion

DoliClock opens new possibilities for studying the molecular basis of brain aging. Although the current study used post-mortem brain tissue, future research could adapt this approach for use with more accessible samples. Similar lipid signatures might eventually be detectable in blood or cerebrospinal fluid, offering a non-invasive way to monitor brain health. Such tools could support early diagnosis and help track the effectiveness of treatments designed to slow brain aging.

Investigating how interventions such as dietary changes or medications affect lipid-based aging markers could also lead to new strategies for promoting healthy brain aging, making DoliClock a promising foundation for further exploration in aging research and brain health.

Click here to read the full research paper published in Aging.

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Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed CentralWeb of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).

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A New Vision for Healthcare: Addressing Aging Before Disease Begins

“This shift in focus from reactive disease management to proactive healthspan extension is transformative.”

Recent discoveries in aging research reveal a powerful insight: the biological changes that lead to chronic diseases begin far earlier than most people realize—often in midlife, well before symptoms appear. This early phase offers a valuable opportunity for prevention. As highlighted in a recent editorial by Marco Demaria, Editor-in-Chief of Aging and a researcher at the European Research Institute for the Biology of Ageing (ERIBA)University Medical Center Groningen, and the University of Groningen (RUG), the aging process itself – not just the diseases it produces – can and should be a primary focus of healthcare. 

The Problem with Traditional Medicine

While modern healthcare has extended lifespan and improved treatment for many diseases, it tends to be insufficient in addressing the complex needs of aging populations. Older individuals frequently experience multiple chronic conditions simultaneously, such as cardiovascular disease, diabetes, cancer, and neurodegenerative disorders. This state of multimorbidity complicates care, increases the use of multiple medications, and reduces quality of life. The dominant traditional healthcare system, which typically begins only after symptoms appear, is costly and insufficient for addressing the interconnected nature of these conditions.

A New Model for Healthcare: Insights from the Editorial

In his recent editorial, Rethinking healthcare through aging biology,” published in Aging Volume 17, Issue 5Dr. Demaria outlines a shift from disease-specific treatment to targeting the biological mechanisms of aging itself, a more integrated and forward-looking approach. He presents three evolving healthcare models.

The first is the traditional reactive model, focused on treating diseases after they develop. The second is a proactive model that intervenes after aging-related damage begins but before major diseases appear. Promising therapies in this category include senolytics, which remove damaged senescent cells, and rapalogs, which regulate aging-related pathways. The third model, and the most progressive, calls attention to prevention, acting before damage starts. This approach includes lifestyle choices, early-life interventions, and the use of emerging technologies to monitor biological aging and guide personalized care.

From Treatment to Prevention: Targeting the Root Causes of Aging

Central to the proactive healthspan extension model is the recognition that aging itself drives many chronic diseases. By addressing biological decline early, healthcare can move beyond managing symptoms to truly preventing disease. The goal is not simply to repair damage but to maintain cellular and systemic balance throughout life—supporting longer, healthier lives and reducing the need for intensive treatments later on.

Impact and Implications

This shift holds significant benefits at both individual and societal levels. Early interventions can improve well-being, decrease reliance on medication, and reduce healthcare costs. Preventive healthcare rooted in aging biology offers a more sustainable and efficient system, delaying illness and lightening the burden on healthcare infrastructure. As research and technologies continue to evolve, this model becomes increasingly achievable.

Future Perspectives and Conclusion

Transforming healthcare along these lines will require systemic changes, not only in research funding and policy but also in how future clinicians are trained. Medical education must include aging biology and promote interdisciplinary collaboration to deliver predictive, preventive, and personalized care. As Dr. Demaria emphasizes, focusing on the biology of aging opens the door to a new era in medicine—one that improves not just longevity, but quality of life at every stage. Rethinking the approach to healthcare in this way is not only timely, it is essential.

Click here to read the full editorial published in Aging.

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Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed CentralWeb of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).

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For media inquiries, please contact [email protected].

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

“As advanced age is associated with increased incidence of hypoxia-associated conditions such as asthma, emphysema, ischemic heart disease, heart failure, and apnea, our findings have important implications for many people.”

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

Understanding Hypoxia in the Brain

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

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

The Study: Exploring Brain Vulnerability to Hypoxia

To investigate how age affects the brain’s response to low oxygen, researchers at the San Diego Biomedical Research Institute studied young and old mice. They exposed the mice to different levels of oxygen—from normal (21%) down to 8%—to see at what point the BBB  begins to fail. The study by Arjun Sapkota, Sebok K. Halder, Richard Milner, also tracked how sensitivity to hypoxia changes across the lifespan, examining mice from 2 to 23 months old.

The Results: Low Oxygen Damages the Blood-Brain Barrier in Older Brains

The results showed that older mice experienced blood-brain barrier disruption at higher oxygen levels—around 15%—compared to younger mice, which only showed damage at more severe hypoxia (13%). The damage in aged mice was also more severe: their BBB was four to six times leakier than in young mice under the same conditions.

Interestingly, the increased brain vulnerability began earlier than expected. Mice showed greater sensitivity to hypoxia between the ages of 2 and 6 months and again between 12 and 15 months. Additionally, microglia—immune cells in the brain—were more reactive in older mice, even at mild oxygen reductions. This suggests that as we age, the brain becomes not only more sensitive to hypoxia but also more prone to inflammation.

The Breakthrough: Understanding the Link Between Hypoxia and Cognitive Decline

This study is the first to clearly define how the threshold for oxygen-related brain damage changes with age. In simple terms, oxygen levels that are safe for young individuals can harm older adults. This discovery helps explain why conditions like sleep apnea, which reduce oxygen during sleep, are linked to higher dementia risk in older populations.

The Impact: A New Approach to Brain Health in Aging Populations

For older adults, keeping oxygen levels within a healthy range could be essential to protecting brain function. The study also has practical implications for people traveling to high altitudes. Oxygen levels similar to 15%, which were enough to cause BBB damage in aged mice, are found at elevations around 8,600 feet.

These findings highlight the importance of monitoring oxygen exposure, especially for those with chronic illnesses. Strategies to strengthen the blood-brain barrier may help reduce the risk of hypoxia-induced cognitive decline in aging individuals.

Future Perspectives and Conclusion

The aging brain is more vulnerable to low oxygen than previously believed. Even mild reductions in oxygen can lead to blood-brain barrier disruption, brain inflammation, and cognitive problems. This study offers valuable insights that can help guide future treatments aimed at protecting the brain in older adults.

For anyone living with respiratory or heart conditions, this research delivers an important message. Preventing hypoxia is just as crucial as treating illness. Monitoring and managing oxygen levels may not only extend lifespan but also help ensure better brain health and quality of life as we age.

Click here to read the full research paper in Aging.

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Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed CentralWeb of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).

Click here to subscribe to Aging publication updates.

For media inquiries, please contact [email protected].

Aging Sponsors Open Access Team in 2025 Ride for Roswell

Impact Journals, the publisher of Aging, is once again proudly sponsoring the Open Access Team in the annual Ride for Roswell.


BUFFALO, NY — June 10, 2025 — The Ride for Roswell, one of the USA’s largest cycling events supporting cancer research, returns to Buffalo on Saturday, June 28, 2025. Hosted annually by Roswell Park Comprehensive Cancer Center, this community-wide event brings together riders, volunteers, and supporters to raise funds for cancer research, celebrate survivors, and honor those lost to the disease. 

Among the returning participants is the Open Access Team, led by team captain Sergei Kurenov. This year, the team is once again proudly sponsored by Impact Journals, the publisher of open access journals AgingOncotargetGenes & Cancer, and Oncoscience.

“For the last 10 years, I have continuously participated in the Ride for Roswell in honor of those who have bravely fought cancer,” said Kurenov. “This journey is deeply personal for me. My father battled cancer, and some of my closest friends have fought through prostate and lung cancer with incredible strength.”

This year, the Open Access Team rides in honor of Dr. Mikhail (Misha) Blagosklonny, a visionary scientist who dedicated his career to advancing cancer and aging research. As the founding Editor-in-Chief of AgingOncotarget and Oncoscience, Dr. Blagosklonny was a pioneer of open-access publishing. His groundbreaking work on mTOR signaling and rapamycin transformed our understanding of cancer biology and healthy lifespan extension.

The 2025 Ride for Roswell features nine route options, ranging from 4 to 100 miles, all beginning at the University at Buffalo North Campus. Riders from across the USA and beyond are invited to participate and make a meaningful impact in the fight against cancer.

This ride is more than just a journey on two wheels—it’s a commitment to building a future where no one has to fear a cancer diagnosis. There is still time to support the Open Access Team in the 2025 Ride for Roswell. Whether by donatingjoining the team, or sharing their story, every action brings us closer to better treatments, deeper understanding, and, ultimately, a cure.

Visit the Open Access Team page to join or donate today.

Click here to learn more about the 2025 Ride for Roswell.

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

Click here to subscribe to Aging publication updates.

For media inquiries, please contact [email protected].

Longevity & Aging Series Wins Silver Award for Excellence in Video/Film at SSP EPIC Awards

The EPIC Awards recognize the achievements of those who are advancing scholarly publishing through creativity, collaboration, and cutting-edge innovation.

Buffalo, NY — June 4, 2025 — The Longevity & Aging Series has been honored with the Silver Award for “Excellence in Video/Film” at the inaugural EPIC Awards celebration on May 29, 2025, during the Society for Scholarly Publishing (SSP) 47th Annual Meeting in Baltimore, Maryland.

The EPIC Awards recognize the achievements of those who are advancing scholarly publishing through creativity, collaboration, and cutting-edge innovation. The Longevity & Aging Series, hosted by Aging (Aging-US) Editorial Board member Dr. Evgeniy Galimov, stood out for its impactful storytelling, production quality, and commitment to advancing understanding in the field of aging research.

The Longevity & Aging Series brings together leading experts to discuss the latest developments in the biology of aging, healthy longevity, and interventions to improve healthspan. Now in its third season, the series is a trusted resource for scientists, clinicians, and the broader public interested in the future of aging research.

For more information about the Aging (Aging-US) Longevity & Aging Series and to view the award-winning videos, please visit our show page or YouTube channel. If you are interested in becoming a guest or would like to know more about the series, please email us at [email protected].

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

Click here to subscribe to Aging publication updates.

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

“At the end of the trial, the intervention group was, on average, 2.04 years younger than their baseline epigenetic age (p = 0.043).”

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

Understanding Epigenetic Aging

While chronological age is simply the number of years we have lived, epigenetic or biological age reflects how fast our bodies are aging at the cellular level. This process is measured by patterns in DNA methylation—chemical changes that can alter gene activity without changing the DNA sequence itself. Over time, shifts in DNA methylation are linked to increased risks for conditions like cancer, heart disease, and dementia. Because lifestyle factors such as diet can influence DNA methylation, researchers are exploring whether healthy eating might actually help us age more slowly.

The Study: How Food Might Influence Epigenetic Aging

In an earlier trial called the Methylation Diet and Lifestyle study, 43 healthy men between the ages of 50 and 72 followed a comprehensive eight-week program involving diet, sleep, exercise, and meditation. Participants in the intervention group became, on average, more than two years “younger” in terms of their epigenetic age. The dietary component of the program emphasized whole, plant-based foods, lean meats, and a group of foods classified as “methyl adaptogens.”

In a follow-up study titled “Dietary associations with reduced epigenetic age: a secondary data analysis of the methylation diet and lifestyle study,” a research team led by Jamie L. Villanueva from the University of Washington and the National University of Natural Medicine, along with Ryan Bradley also from the National University of Natural Medicine and the University of California, San Diego, analyzed participants’ self-reported diets to understand why some experienced greater biological age reversal than others.

The Results:  A Diet That May Slow Epigenetic Aging

The study found that men who consumed more methyl adaptogen foods—such as green tea, turmeric, garlic, berries, rosemary, and oolong tea—showed the most substantial reductions in epigenetic age, up to 8 years. These associations remained strong even after accounting for weight loss, suggesting that the foods themselves played a central role in the observed biological changes.

Methyl adaptogens are rich in polyphenols, plant compounds known to influence DNA methylation by regulating enzymes that control gene expression. These polyphenols interact with cellular systems involved in DNA repair, inflammation, and metabolism—all key players in the aging process. Compounds like EGCG in green tea, curcumin in turmeric, and allicin in garlic are also known to influence the PI3K/AKT/mTOR pathway, a major regulator of cell survival and aging. 

The Impact: A Natural Way to Care for Our Health

These findings support the idea that food can be a powerful tool for promoting healthier aging. Unlike drugs or supplements, this approach is natural, non-invasive, and based on foods that are already accessible to many. The findings could lead the way for personalized nutrition strategies that go beyond disease prevention, aiming to influence the very pace of aging.

Future Perspectives and Conclusion

Although the study was relatively small and limited to middle-aged men, the results are promising. Larger, more diverse studies are needed to confirm these findings and assess their broader applicability, including for women and other age groups. The researchers also note that additional tools for measuring aging more accurately would be valuable in future investigations.

Nevertheless, this research provides a positive reminder: our daily choices, particularly the foods we consume, can significantly influence our aging process. Including foods such as green tea, garlic, berries, and turmeric in our diets may not only promote better health but also slow down the aging process.

Click here to read the full research paper in Aging.

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Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed CentralWeb of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).

Click here to subscribe to Aging publication updates.

For media inquiries, please contact [email protected].

Fighting Premature Aging: How NAD+ Could Help Treat Werner Syndrome

“Werner syndrome (WS), caused by mutations in the RecQ helicase WERNER (WRN) gene, is a classical accelerated aging disease with patients suffering from several metabolic dysfunctions without a cure.”

Werner syndrome is a rare condition marked by accelerated aging. A recent study, featured as the cover paper in Aging (Aging-US), Volume 17, Issue 4, led by researchers at the University of Oslo and international collaborators, suggests that nicotinamide adenine dinucleotide (NAD+), a vital molecule involved in cellular energy production, may be key to understanding this disease and developing future strategies to manage it.

Understanding Werner Syndrome

Werner syndrome (WS) is a rare genetic condition that causes people to age more quickly than normal. By their 20s or 30s, individuals with WS often show signs typically associated with older age, such as cataracts, hair loss, thinning skin, and heart disease. This premature aging is caused by mutations in the WRN gene, which normally helps repair DNA and protect cells from damage. While the WRN gene’s role in maintaining genetic stability is well understood, the reasons behind the rapid decline of cells in WS patients are still not fully clear.

The Study: Investigating NAD+ in Werner Syndrome

Nicotinamide adenine dinucleotide levels naturally decline with age. In the study titled Decreased mitochondrial NAD+ in WRN deficient cells links to dysfunctional proliferation,” researchers investigated whether this decline is more severe in people with WS and whether restoring NAD+ levels could help slow the aging process in these patients.

The research team, led by first author Sofie Lautrup and corresponding author Evandro F. Fang, used human stem and skin cells from WS patients, as well as gene-edited cells that mimic WS by lacking the WRN gene. These were always compared to control cells isolated from healthy individuals.

The researchers tracked how WRN deficiency affected NAD+ levels in mitochondria, the parts of the cell that generate energy. They then tested whether boosting NAD+ using a compound called nicotinamide riboside (NR)—a form of vitamin B3—could help restore normal cellular function. The team also used other strategies to raise mitochondrial NAD+ directly, including overexpressing a transporter protein known as SLC25A51. Their goal was to determine whether these approaches could reverse aging-related damage and restore cell growth affected by WRN mutations.

The Results: NAD+ Can Reduce Aging Signs

The findings confirmed that WRN-deficient cells had lower levels of mitochondrial NAD+ and showed signs of cellular aging, such as increased senescence and reduced proliferation. Treating these cells with NR significantly reduced aging markers and restored some normal functions in both stem and skin cells from WS patients. In healthy control cells, NR had no such effect, suggesting it works specifically in the context of NAD+ deficiency.

However, increasing NAD+ either through NR supplementation or by enhancing mitochondrial transport was not enough to fully restore cell division in lab-grown cells lacking WRN. This result suggests that while NAD+ supplementation is beneficial, the WRN gene itself plays a unique and irreplaceable role in supporting healthy cell growth.

The Breakthrough: Linking Mitochondrial NAD+ to Cell Aging

This study reveals a deeper role for the WRN gene beyond DNA repair. It shows that WRN also helps regulate how NAD+ is produced and used within cells, particularly in mitochondria. Without WRN, this system becomes unbalanced, accelerating cell aging. While boosting NAD+ helped reduce aging features in WS cells, the findings make clear that NAD+ therapy alone cannot replace the broader functions of WRN.

The Impact: A Step Toward Slowing Down Cellular Aging

This is the first study to directly show how low mitochondrial NAD+ contributes to premature aging in WS. Beyond its relevance to WS, the research highlights the broader potential of targeting NAD+ metabolism as a strategy for addressing age-related diseases. By increasing our understanding of how energy production affects aging, this study opens the door to future treatments aimed at promoting healthier aging across a wider population.

Future Perspectives and Conclusion

This study offers promising new insights but also demonstrates the complexity of cellular aging. The WRN gene plays a much broader role than DNA repair alone. It appears to regulate networks of genes linked to metabolism and genome organization. While boosting NAD+ can reduce some signs of cellular damage, it cannot fully compensate for the loss of WRN function.

Looking ahead, further research will be crucial to understanding how NAD+ operates in different parts of the cell and how it might work in combination with other treatments. For individuals with Werner syndrome, and potentially for the wider aging population, these findings bring us closer to future therapies aimed at improving health and longevity. 

Click here to read the full research paper in Aging.

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Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed CentralWeb of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).

Click here to subscribe to Aging publication updates.

For media inquiries, please contact [email protected].

Call for Papers: Commemorative Collection Honoring Dr. Judith Campisi

Dr. Judith Campisi

“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.”

BUFFALO, NY — May 1, 2025 — 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:

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

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.

Next-Generation Therapeutic Approaches

Lada Nuzhna, founder and CEO of Stealth Newco and director at Impetus Grants, shared her vision for advancing muscle health through innovation. With a strong focus on translational impact, she discussed her interest in developing a comprehensive program that combines various exerkines—exercise-induced signaling molecules—to improve muscle function.

Dr. Francisco Leport, co-founder and CEO of Gordian Biotechnology, introduced a new method for studying treatments for osteoarthritis, a common age-related joint condition that causes pain and stiffness. His approach, called in vivo pooled screening, allows scientists to test millions of potential therapies inside a single animal with the disease. This technique speeds up research and reduces the need for using multiple animals, helping to move from discovery to treatment more quickly.

Biotech and Drug Development for Muscle Aging 

This panel brought together leading voices from Lilly (Dr. Andrew Adams), Novartis (Dr. Anne-Ulrike Trendelenburg), Regeneron (David Glass, MD), and Versanis Bio (Ken Attie, MD). Together, they explored therapeutic strategies focused not just on lifespan extension but on preserving mobility, muscle function, and independence as people age.

The discussion emphasized a human-centric approach to drug development, focusing on targeting mechanisms quickly and efficiently in clinical studies, and the importance of early intervention to achieve larger effect sizes and better long-term outcomes. Panelists also stressed that muscle function matters more than mass and highlighted how older individuals often experience a loss of mitochondrial function, leading to fatigue and reduced stamina—underscoring the need for programs that support mitochondrial health.

The panel further noted that nerve decline may precede muscle decline with age. While there is no definitive data linking cognitive and muscle function, improvements in vascular health through exercise were highlighted as a way to reduce inflammation and support overall health. In addition, they addressed the rise of GLP-1-based therapies, including the public health concern of weight regain following treatment.

Exercise Science for Muscle Longevity

This energizing final session featured Dr. Brad Schoenfeld from Lehman College and Dr. Jeff Nippard, a professional bodybuilder, powerlifter, and science communicator. Together they shared research-backed strategies for preserving muscle health at any age, emphasizing that it is never too late to start training and that even minimal, consistent exercise can significantly boost mobility and independence. They also recommended incorporating power and explosive movements into workouts and emphasized the importance of adequate leucine intake to support muscle health.

Driving Scientific Progress in Muscle and Aging Research

The MAST Symposium, like previous Aging Initiative at Harvard University events, showcased the power of interdisciplinary collaboration, mentorship, and early engagement in driving scientific progress. Aging (Aging-US) is proud to support initiatives that highlight the latest breakthroughs while inspiring younger generations to pursue meaningful careers in aging research.

From innovative drug development to accessible exercise interventions, the MAST Symposium emphasized the urgency and opportunity in addressing muscle aging—a key driver of health and independence in older adults.

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Founded in 2008 by visionary scientists—Dr. Mikhail (Misha) BlagosklonnyDr. Judith Campisi, and Dr. David SinclairAging (Aging-US) was created as a platform for publishing innovative and sometimes unconventional ideas in the rapidly evolving field of aging. Supporting events like the MAST Symposium is not just aligned with this mission—it reflects our long-term commitment to advancing aging science and empowering the next generation of researchers.

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