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DoliClock: A Lipid-Based Clock for Measuring Brain Aging

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“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 Central, Web 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

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“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 5, Dr. 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 Central, Web 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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Oxygen Deprivation and the Aging Brain: A Hidden Trigger for Cognitive Decline

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“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 Central, Web 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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Study Identifies Foods That May Reverse Biological Age and Promote Healthy Aging in Men

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“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 Central, Web 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.

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

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

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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) Blagosklonny, Dr. Judith Campisi, and Dr. David Sinclair—Aging (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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Breast Cancer Treatment’s Hidden Impact: Accelerated Aging Among Survivors

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“Breast cancer (BC) is the most commonly diagnosed cancer among women in the US and worldwide .”

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.

The Study: Measuring Long-Term Aging in Breast Cancer Patients

Researchers at Vanderbilt University conducted a decade-long study involving 1,264 breast cancer patients and 429 cancer-free women. The research team, led by first author Cong Wang and corresponding author Xiao-Ou Shu, used a tool called Phenotypic Age Acceleration (PAA), which estimates biological age using standard blood test data. Unlike chronological age, biological age reveals how “old” the body functions, offering a clearer picture of a person’s overall health and aging rate. 

The Results: Long-Term Effects of Breast Cancer Treatments on Aging

At diagnosis, breast cancer patients already appeared nearly four years older biologically than their cancer-free counterparts. One year after treatment, they still seemed two years older. Even ten years later, signs of accelerated aging remained.

When it comes to treatments, not all had the same long-term impact on aging. Chemotherapy was linked to the most immediate spike in aging markers, with effects most noticeable in the first year. In contrast, endocrine therapy showed slower, long-term effects, becoming more apparent many years later. Surgery and radiation therapy were associated with lower levels of age acceleration over time, suggesting that localized treatments may carry fewer long-term aging effects than systemic therapies.

Tumor characteristics also influenced aging levels. Women diagnosed with advanced-stage cancer (Stage III or IV) or those with high-grade tumors experienced the most pronounced biological aging. These findings suggest that both the disease itself and the intensity of treatment contribute to how quickly a survivor may age.

The Breakthrough: Simple Blood Tests to Monitor Aging in Breast Cancer Survivors

This study provides valuable insight into how breast cancer and its treatments can impact survivors’ long-term health. One of its most important contributions is highlighting a simple, accessible way to track biological aging, the PAA test. This method is cost-effective, easy to use in regular medical care, and gives clinicians a powerful tool to identify high-risk patients and tailor long-term follow-up strategies.

The Impact: Rethinking Long-Term Breast Cancer Care

The paper offers valuable insights that could reshape how clinicians think about survivorship care. Breast cancer survivors already face increased risks for heart disease, osteoporosis, and cognitive decline. Accelerated aging may be a contributing factor. By identifying these effects early, healthcare providers can develop more personalized support strategies, potentially improving quality of life and long-term health outcomes.

Future Perspectives and Conclusion

The journey does not end with breast cancer remission. This study underscores that cancer and its treatments can leave lasting effects on the body’s aging process. Implementing appropriate strategies—whether medical, lifestyle-based, or a combination of both—may help survivors not only extend their lifespan but also increase their long-term health and quality of life.

Integrating biological age monitoring into routine follow-up care could enable healthcare providers to better understand each survivor’s health trajectory. For all the women navigating life after breast cancer, such information could translate into not just more years, but better years.

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 Central, Web 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.

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Senolytic Compounds Show Promise in Targeted Alzheimer’s Treatments

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“Cellular senescence is a hallmark of aging and the age-related condition, Alzheimer’s disease (AD).”

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.

Led by Dr. Sultan Darvesh, the study tested six compounds: five senolytics—dasatinib, nintedanib, fisetin, quercetin, and GW2580—and one nootropic, meclofenoxate hydrochloride, known for its memory-enhancing potential. The researchers used post-mortem brain tissue from Alzheimer’s patients, enzyme activity assays, and computer modeling to examine how these compounds interact with the enzymes.

The Challenge: Targeting the Right Enzymes

One of the limitations of current Alzheimer’s treatments is that they do not distinguish between the normal and the altered forms of cholinesterases. While these drugs can raise levels of the memory-related chemical acetylcholine and improve cognitive function, they often come with side effects due to their broad activity. A more precise approach—targeting only the versions of AChE and BChE tied to Aβ plaques—could offer better outcomes with fewer drawbacks.

The Results: Senolytics Show Precision in Enzyme Targeting

The results were promising. Some of the senolytics tested, like dasatinib and nintedanib, effectively blocked the cholinesterases attached to Aβ plaques without affecting the normal versions of these enzymes in healthy brain tissue. Meclofenoxate also showed strong activity against the disease-associated forms. Interestingly, this selectivity was linked to how these compounds bind to the enzymes. Instead of locking onto the main active site, many of them attached to alternative regions, known as allosteric sites, which are only altered in the plaque-associated forms. This type of binding allowed the compounds to distinguish between harmful and healthy enzymes.

The Breakthrough: Targeting the Disease, Preserving the Brain

This study is the first to show that certain senolytic and cognitive-enhancing drugs can selectively inhibit the dysfunctional versions of cholinesterases found in Alzheimer’s without affecting their normal forms. This level of precision could mark a major step forward in Alzheimer’s therapy.

The Impact: A Dual-Action Path to Treating Alzheimer’s

By focusing on only the problematic forms of AChE and BChE, this approach could lead to Alzheimer’s treatments that better preserve cognitive function while avoiding side effects. The research also bridges two important areas of study: aging and neurodegeneration. It suggests that drugs developed to slow aging might also be used as targeted treatments for Alzheimer’s, offering a two-in-one therapeutic advantage. 

Future Perspectives and Conclusion

Although more research is needed, especially in living models and clinical trials, the potential of the findings is encouraging. They lead the way for a new generation of Alzheimer’s treatments that are more targeted and safer.

By understanding better how aging and brain disease intersect at the cellular level, scientists may be moving closer to developing more effective and personalized approaches to combat Alzheimer’s.

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 Central, Web 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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How Environmental Chemicals May Accelerate Biological Aging

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“Epigenetic clocks can serve as pivotal biomarkers linking environmental exposures with biological aging.”

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.

The Challenge: Unraveling the Complex Relationship Between Toxins and Aging

For years, scientists suspected that environmental toxins might contribute to aging, but most studies focused on a small set of chemicals. This work took a broader and more systematic approach to analyze a wide range of pollutants that people are commonly exposed to. The goal was to uncover previously unknown connections between chemical exposure and biological aging at the genetic level.

The Results: Environmental Chemicals That Speed Up Aging

The study identified several chemicals that were significantly associated with epigenetic age acceleration. One of the most concerning findings was the impact of cadmium, a toxic heavy metal found in cigarette smoke, industrial pollution, and some foods. Higher levels of cadmium in the blood were linked to faster aging across multiple epigenetic clocks.

Another key finding was the role of cotinine, a biomarker of tobacco exposure. People with higher levels of cotinine in their system showed signs of accelerated DNA aging, reinforcing the long-known link between smoking and premature aging.

The study also found that lead and dioxins, commonly found in industrial pollutants and certain processed foods, might contribute to biological aging. Interestingly, some pollutants, like certain polychlorinated biphenyls (PCBs), were associated with slower aging, though the health effects of these compounds remain unclear.

The Breakthrough: Why Cadmium and Smoking Are Major Aging Accelerators

This research highlights cadmium as a major environmental driver of aging. Since cadmium exposure comes from both smoking and diet, reducing it could be a key anti-aging strategy. The findings also provide further evidence that smoking is one of the most significant factors influencing epigenetic aging.

Reducing exposure to cigarette smoke, polluted air, and contaminated foods could help slow down DNA aging and potentially increase lifespan.

The Impact: How These Findings Can Influence Health Policies and Personal Choices

The results of this study could lead to stronger environmental regulations on heavy metals and toxic pollutants. Policymakers may push for stricter air quality standards, better food safety regulations, and more public health initiatives to reduce exposure to aging-accelerating chemicals.

For individuals, this research reinforces the importance of reducing exposure to toxins. Avoiding cigarette smoke, choosing organic and non-processed foods, and being mindful of products containing chemicals could help protect DNA health and promote longevity. 

Future Perspectives and Conclusion

While this study provides strong evidence that environmental toxins influence aging, further research is needed to determine whether reducing exposure can slow down or even reverse epigenetic aging. Future studies could focus on younger populations and examine how lifestyle changes interact with these environmental exposures.

For now, taking steps to avoid cigarette smoke, limit exposure to heavy metals, and maintain a clean diet could be practical ways to protect long-term health and slow down biological aging.

By understanding how environmental pollutants impact aging, individuals and policymakers can make informed decisions that promote a longer, healthier life.

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

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“These insights underscore the importance of personalized treatment approaches and the need for further research to improve radiotherapy outcomes in cancer patients.”

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.

The Study: Investigating Radiation Therapy’s Impact on Cancer Patients Survival

A 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, studied how radiation therapy affects cancer patient survival. They examined data from The Cancer Genome Atlas (TCGA), which includes 32 types of cancer. When they found that GBM and LGG had very different survival outcomes after radiation, they decided to focus on these two types of brain cancer. To learn more about their differences, gene expression and molecular pathways connected to radiation therapy responses were studied.

The Challenge: Why Radiation Therapy Works Only in Certain Tumors

Radiation therapy is an important cancer treatment, but its success is not the same for everyone. Even patients with the same type of cancer can respond differently, making it difficult to predict who will benefit. Understanding why some tumors are sensitive to radiation while others resist it is key to improving treatment and patient survival.

The Results: Radiation Therapy Works for Glioblastoma but Not for Low-Grade Gliomas

Overall, GBM had the highest percentage of patients receiving radiation therapy (82%), followed by LGG (54%). When researchers compared survival outcomes, they found that while radiation improved survival in breast cancer and GBM patients, it had a negative effect on patients with lung adenocarcinoma and LGG. This led researchers to take a closer look at GBM and LGG, especially since LGG can develop into GBM over time.

A key discovery was how GBM and LGG regulate DNA repair differently. GBM tumors have weak DNA repair activity, making them more vulnerable to radiation-induced damage. LGG tumors, however, activate more DNA repair pathways, allowing cancer cells to survive radiation and potentially making treatment less effective.

The immune response to radiation therapy was also different. In GBM, radiation triggered an immune response, which may help fight the tumor. In LGG, however, immune activation was significantly lower, meaning that radiation therapy did not enhance the body’s ability to attack cancer cells. This fact may contribute to worse survival outcomes for LGG patients after treatment.

Further genetic analysis revealed that ATRX gene mutations made GBM and LGG patients more sensitive to radiation. On the other hand, higher EGFR gene activity was linked to lower survival rates after radiation in LGG patients. Similar findings for GBM tumors indicate treatment resistance.

The Breakthrough: Toward Personalized Treatment

This study offers new insights into why radiation therapy benefits certain brain tumors while being less effective, particularly in GBM and LGG. Finding important biological factors, like DNA repair activity, immune response, and genetic changes that may serve as biomarkers, will help radiation therapy be more precisely tailored to each patient’s unique tumor profile. 

The Impact: Rethinking Glioblastoma and Low-Grade Gliomas Treatment

These findings highlight the importance of precision medicine in brain cancer treatment. Instead of automatically recommending radiation therapy for all LGG patients, oncologists should consider genetic testing to determine whether this treatment will be beneficial or not. If not, alternative treatments may be necessary. Immunotherapy and targeted drugs against EGFR could provide better outcomes for patients who do not respond well to radiation therapy.

For GBM, researchers are investigating ways to enhance radiation’s effectiveness by combining it with DNA repair inhibitors, such as PARP inhibitors. These drugs could increase tumor sensitivity to radiation and improve survival rates. 

Conclusion

Advancing cancer treatment requires a personalized approach. Identifying biomarkers that predict how GBM and LGG tumors respond to radiation therapy can help clinicians make more informed treatment decisions, ensuring that patients receive the most effective and least harmful therapies. By uncovering key genetic and molecular insights, this study moves the field closer to individualized brain cancer treatments, improving survival rates while reducing unnecessary risks for patients.

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 Central, Web 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].

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