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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).

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

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“Senescent cells accumulate in aging tissues, impairing their ability to undergo repair and regeneration following injury.”

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

Understanding How Aging Affects Skin Healing

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

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

The Study: How Clearing Aging Cells Improves Skin Repair

A team of researchers from Boston University Aram V. Chobanian and Edward Avedisian School of Medicine, led by first author Maria Shvedova and corresponding author Daniel S. Roh, tested whether ABT-263 could enhance wound healing in aging skin. They applied topical ABT-263 to the skin of 24-month-old mice—roughly equivalent to elderly humans—over a five-day period. After the treatment period, the researchers created small skin wounds on the mice and monitored their healing process compared to a control group. They also analyzed molecular changes in the skin to understand how the drug influenced tissue repair.

The Challenge: Why Aging Skin Heals More Slowly

Older skin does not regenerate as well as younger skin due to a combination of factors. One key reason is the accumulation of senescent cells, which interfere with normal repair processes by increasing inflammation and reducing collagen production, a critical component of wound healing.

Even though the body has mechanisms to remove damaged cells, these processes weaken with age. As a result, senescent cells accumulate, contributing to chronic inflammation that delays wound closure.

The Results: Faster Healing and Improved Skin Function

The study found that topical ABT-263 effectively reduced the number of senescent cells in aged skin. Markers of cellular aging were significantly decreased, confirming that the drug successfully eliminated dysfunctional cells.

When wounds were induced after treatment, mice that received ABT-263 healed significantly faster than those in the control group. The researchers also observed an increase in gene activity related to collagen production, cell proliferation, and extracellular matrix organization—all crucial factors for effective wound repair.

Interestingly, the treatment triggered a temporary inflammatory response, with immune cells, particularly macrophages, infiltrating the treated skin at higher levels. This response, while short, appeared to accelerate repair by clearing out damaged tissue and promoting regeneration.

By day 15, the wounds of ABT-263-treated mice had closed significantly faster than those of untreated mice. By day 24, 80% of the treated mice had achieved complete wound closure, compared to only 56% in the control group.

The Breakthrough: A New Approach to Enhancing Skin Regeneration

This study provides strong evidence that removing senescent cells before an injury can prime aging skin for faster healing. The results suggest that topical senolytic drugs like ABT-263 could serve as a pre-treatment for surgeries or individuals prone to slow-healing wounds, providing a safer, more targeted approach than systemic treatments. Additionally, the observed increase in collagen expression suggests that this method not only accelerates healing but also improves the overall strength and quality of repaired skin.

The Impact on Wound Care and Skincare

If similar results can be achieved in humans, ABT-263 or similar senolytic treatments could become valuable tools, particularly for elderly patients undergoing surgery, where slow wound healing increases the risk of complications. It may also help individuals with chronic wounds, such as diabetic ulcers, which often struggle to heal properly. In post-surgical skincare, accelerating recovery could lead to better outcomes and reduced scarring. Additionally, in anti-aging dermatology, this treatment has the potential to reverse some of the cellular effects of aging on the skin.

​​Future Prospects and Conclusion

This study marks an important step toward clinical applications. While the findings are promising, further research is necessary to confirm whether ABT-263 offers similar benefits in humans. Clinical trials will be crucial in assessing its safety, efficacy, and long-term effects, particularly in wound healing and dermatological treatments. If successful, senolytic creams or topical therapies could offer new solutions for age-related skin challenges and slow-healing wounds.

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

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“Brown adipose tissue (BAT), a major subtypes of adipose tissues, is known for thermogenesis and promoting healthful longevity.”

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

Understanding Brown Fat

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

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

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

How Brown Fat Enhances Physical Performance

While most studies focus on how exercise activates BAT, this research perspective suggests that brown fat itself may actively enhance physical performance. The authors, Dorothy E. Vatner, Jie Zhang, and Stephen F. Vatner, base their hypothesis on studies involving genetically modified mice lacking a protein called RGS14. These RGS14 knockout (KO) mice not only live longer but also exhibit improved endurance and better health markers compared to regular mice. These benefits are linked to the more active and efficient brown fat present in these genetically modified mice.

In experimental studies, brown fat from RGS14 knockout (KO) mice was transplanted into normal mice. The results were striking—within just three days, the recipient mice showed significant improvements in exercise performance, whereas mice that received brown fat from regular donors required several weeks to experience similar benefits.

These findings suggest that BAT is more than just a passive energy-burning tissue. It may actively influence strength, cardiovascular function, and overall health, highlighting BAT’s potential in supporting longevity.

The Importance of Brown Fat for Exercise and Aging

Different research studies highlight how BAT influences exercise capacity and aging. Beyond burning calories, BAT improves blood flow, enhances mitochondrial function, and reduces oxidative stress—factors essential for maintaining muscle health and endurance, especially with age.

In mice with active BAT, researchers observed increased blood vessel formation, which improves oxygen and nutrient delivery to muscles during physical activity. Combined with BAT’s support for mitochondrial health, this leads to greater stamina and resilience against age-related decline.

Additionally, BAT seems to offer broader health benefits, helping protect against conditions such as obesity, diabetes, heart disease, and neurodegenerative disorders like Alzheimer’s disease. All these findings highlight BAT’s potential, making it a possible target for therapies aimed at combating age-related conditions​.

Future Directions: Brown Fat as a Potential Therapeutic Target

Various scientific findings about BAT have led researchers to suggest developing therapies that can mimic its effects. For example, a pharmaceutical analog of BAT could help treat age-related conditions, such as reduced physical capacity, metabolic disorders, and chronic diseases.

Beyond weight management, these therapies might enhance fitness, improve metabolic health, and support healthy aging, potentially extending lifespan. This approach could be especially valuable for individuals with limited mobility due to chronic conditions or age-related decline.

As research progresses, BAT-based therapies may transform how we address aging and metabolic diseases, offering new hope for improving quality of life.

Conclusion: Rethinking the Role of Brown Fat

Beyond its role in energy regulation, BAT may contribute to metabolic health, physical performance, and healthy aging. 

Recognizing the potential health benefits of BAT challenges the traditional view of fat as something exclusively to reduce or eliminate. Instead, BAT appears to play an active role in the body’s metabolic processes, with potential implications for longevity and disease prevention. While further research is needed, exploring BAT’s functions may offer new strategies to support human health.

Click here to read the full research perspective 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 Scientists Are Measuring Aging at the Cellular Level

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

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

Understanding Biological Age

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

The Study: Measuring Aging More Precisely

To explore how different cell types age, researchers from the Chinese Academy of Sciences and Monash University analyzed publicly available DNA methylation data from brain and liver tissues using advanced computer models. The samples included healthy individuals and those with diseases like Alzheimer’s and non-alcoholic fatty liver disease. 

In addition to brain and liver samples, the study included data from other tissues such as the prostate, colon, kidney, and skin. This broader dataset ensured that the findings applied to a wide range of conditions.

The Challenge: Understanding Aging at a Cellular Level

One of the biggest challenges in estimating biological age has been the inability to distinguish between different cell types within a tissue. Traditional methods analyze a tissue as a whole, averaging the age of all existing cells. This can hide the fact that some cells age faster than others, making it difficult to identify early signs of disease.

In organs like the brain and liver, different cell types—such as neurons and glial cells in the brain, or hepatocytes in the liver—age at different rates. Without a method to study cell types individually, it has been challenging to identifying which cells are most affected by aging and how they contribute to diseases like Alzheimer’s and liver diseases.

Aging is also influenced by two factors: intrinsic aging, which refers to changes within the cells themselves, and extrinsic aging, which occurs due to changes in cell composition within a tissue. Traditional methods struggle to separate these aspects, limiting their usefulness in developing targeted anti-aging treatments.

The Results: Key Findings in Alzheimer’s and Liver Disease

The study found that different types of cells within the same tissue age at different rates. In Alzheimer’s disease, neurons and glial cells in the brain showed signs of accelerated aging, with glial cells in the temporal lobe being the most affected. This suggests that glial cells could play a crucial role in the progression of neurodegeneration. Similarly, in liver conditions such as fatty liver disease and obesity, hepatocyte-specific clocks detected signs of accelerated aging that were not as easily identified previously.

By applying their approach to brain and liver tissues, the researchers demonstrated that cell-type specific epigenetic clocks can improve tissue-specific estimation of biological age, as well as chronological age.

The Breakthrough: Cell-Type Specific Epigenetic Clocks

Before this study, biological age could only be estimated at the tissue level, providing a general picture but not showing how individual cell types were changing over time. With the development of cell-type specific epigenetic clocks, researchers can now measure aging within specific types of cells, such as neurons in the brain and hepatocytes in the liver. Also, by distinguishing intrinsic aging from changes in cell composition, this new method offers new insights into how diseases develop and progress.

The Impact: What This Means for Healthcare

The implications of this research are significant. Measuring the biological age of individual cell types can lead to earlier diagnosis of age-related diseases, more effective treatments, and personalized healthcare plans. It could also help scientists track the effectiveness of anti-aging therapies and lifestyle changes more accurately, giving individuals better tools to manage their health.

This research also offers valuable insights into age-related conditions like Alzheimer’s and liver diseases, by pinpointing which cells experience the most stress and deterioration, allowing researchers to focus their efforts on the most affected cell types.

​​Future Prospects and Conclusion

Looking ahead, researchers plan to use this method to study other tissues and cell types, further advancing the field of precision medicine. As more data becomes available, cell-type specific epigenetic clocks could become essential tools for tracking aging at an individual level.

This study represents an exciting step forward in the science of aging. By measuring aging at the cellular level, scientists are moving closer to a future where aging can be better understood and managed.

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

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“Blagosklonny’s work remains an enduring inspiration, paving the way toward treating aging as a modifiable condition.”

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

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

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

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

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

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

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

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

Read the full paper: DOI: https://doi.org/10.18632/aging.206189

Corresponding author: David A. Barzilai, [email protected]

Keywords: aging, rapamycin, longevity medicine, healthspan, geroscience, hyperfunction

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

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BUFFALO, NY- January 6, 2025 – We are pleased to announce that Dr. Marco Demaria, a leading expert in aging and cellular senescence, has joined Aging (Aging-US) as Editor-in-Chief, effective January 1, 2025. Dr. Demaria will work alongside an esteemed Editorial Board.

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

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

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

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

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

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

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Accelerated Aging in Young People with Sickle Cell Disease

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“[…] adolescents and adults with SCD still experience higher rates of aging-related morbidity and early mortality.”

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

What Is Sickle Cell Disease?

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

The Study: Link Between Sickle Cell Disease and Aging

To understand the connection between SCD and accelerated aging, researchers from the University of North Carolina at Chapel Hill and their collaborators focused on a protein called p16INK4a, or simply p16. This protein builds up in cells as people age. High levels of p16 indicate that a person’s cells are aging faster than normal.

They measured p16 levels in 18 young people with SCD, aged 15 to 27, and compared them to 27 healthy individuals of the same age. 

The Challenge: More Than a Genetic Disorder

Individuals with SCD often experience chronic inflammation, anemia, and physical stress due to their condition. These factors affect their immediate health but also trigger cellular changes that mimic aging, making it vital to explore potential therapies. 

The Results: Sickle Cell Disease Patients Aged 43 Years Faster

The results were startling. Young people with SCD had significantly higher levels of p16 than their healthy peers, indicating that their bodies were biologically much older. On average, their p16 levels suggested an additional 43 years of biological aging. Even the youngest participant, a 15-year-old with SCD, had more p16 than anyone in the non-SCD group.

The Breakthrough: Targeting Cellular Aging for Better Outcomes

The study reveals why young people with SCD face age-related health problems much earlier than their peers. These findings highlight the urgent need for treatments targeting cellular aging. One promising area of research involves senolytics, drugs designed to remove senescent (“old”) cells from the body. By slowing the aging process, senolytics could significantly improve both the quality and length of life for SCD patients. Additionally, measuring p16 levels may serve as a valuable tool to identify high-risk patients and enable more personalized treatment strategies.

The Impact: Why These Findings Matter

These findings elucidate how SCD accelerates biological aging, significantly impacting quality of life and reducing healthy years. Understanding the role of cellular aging allows to redefine SCD care, moving from symptom management to addressing the causes of accelerated aging. 

The impact of this study also extends to other chronic diseases by emphasizing the importance of targeting cellular aging markers. By focusing on cellular senescence, this research lays the groundwork for therapies that improve both lifespan and healthspan—the years of life spent in good health.

​​Future for Sickle Cell Disease Research

While this study is a crucial first step, further research is needed to confirm these findings and explore potential therapies. Larger studies with more diverse groups of SCD patients, as well as long-term follow-ups, will help deepen our understanding of how aging affects the disease and the effectiveness of new treatments like senolytics. Additionally, researchers are also investigating other markers of aging.

Conclusion

This study highlights the long-term impact of SCD on young patients, shedding light on how accelerated aging contributes to their health challenges. For many, these findings represent a future with better and more efficient treatments. By addressing the causes of accelerated aging, innovative therapies could significantly enhance the lives of individuals with SCD, potentially leading to healthier and longer lives.

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

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“Sleep problems in dementia patients are not only common but also contribute to a faster progression of cognitive decline and increased burden on caregivers.”

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

Dementia and Sleep

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

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

The Study: Update on Sleep and Dementia’s Connection

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

The review emphasized how untreated sleep issues can worsen cognitive decline, demonstrating that sleep health is not just a symptom of dementia but an integral part of its progression.

The Challenge: Why Sleep Problems are Overlooked but Critical

People with dementia often face significant sleep disruptions. They might wake up multiple times during the night, feel excessively sleepy during the day, or move around at night. This lack of restorative sleep worsens memory loss and confusion. For example, untreated sleep apnea reduces oxygen flow to the brain, further harming cognitive function. Meanwhile, caregivers experience immense stress and burnout from managing sleepless nights and restless behavior.

Despite these profound effects, many dementia treatment strategies fail to adequately address sleep issues, treating them as secondary problems rather than main components of care. Understanding the relationship between sleep and dementia is critical for designing effective interventions.

The Breakthrough: How Improving Sleep Can Transform Dementia Care

The study highlighted that sleep problems are deeply linked to the progression of dementia rather than being merely side effects. Conditions like cardiovascular disease and diabetes often worsen these disturbances, creating a cycle where poor health accelerates cognitive decline.

The findings showed that improving sleep quality can bring significant benefits. One solution is addressing sleep apnea, which not only improves sleep quality but also enhances brain function and lowers the risk of related health issues such as heart disease. Non-drug therapies such as structured bedtime routines, light therapy, and anxiety management have shown promise in improving sleep for dementia patients. Cognitive-behavioral therapy for insomnia has been especially effective in managing chronic sleep issues. These interventions not only improve brain health but also reduce caregiver stress, promoting a healthier and more supportive environment for everyone involved.

The Future of Dementia Care

Integrating sleep care into dementia treatment is the way forward. Addressing sleep disturbances together with other health conditions like diabetes and anxiety can have a profound impact. Personalized approaches, such as setting up calming bedtime routines and improving sleep environments, can make a real difference. Future research should focus on refining these strategies and equipping caregivers with better tools to manage sleep challenges. 

Conclusion

Sleep disturbances are more than just a symptom of dementia. They are a major factor driving this condition’s progression and affecting quality of life. By prioritizing sleep health in dementia care, memory loss can be slower, day-to-day well-being can be improved, and burden on caregivers can be reduced. Holistic care approaches that address both sleep and overall health hold the key to improving quality of life for dementia patients and their families.

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

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Future of Aging Research Mixer
Future of Aging Research Mixer

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

Key Highlights from the Future of Aging Research Mixer 2024

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

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

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

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

Empowering Future Aging Science Leaders

A majority of the attendees were students from Boston-area universities including Harvard, MIT, UMass and BU. These future scientists, entrepreneurs, and innovators engaged in meaningful discussions about research, career paths, and publishing in academic journals. Many expressed interest in journals like Aging (Aging-US) and sought advice on how to publish their work.

The “Future of Aging Research Mixer 2024” showcased the passion, collaboration, and innovation within the aging research community. Through its sponsorship, Aging (Aging-US) reaffirmed its commitment to fostering a vibrant network of talent and supporting the voices of young, passionate researchers. Initiatives like this inspire the next generation of scientists and entrepreneurs, driving sustained growth and transformative impact in the field.

Beyond the event, the Aging Initiative at Harvard University strengthens the community through ongoing programs like journal clubs, guest lectures, and informal lunches with professors. These initiatives encourage skill-building, idea-sharing, and mentorship, preparing students for impactful careers in aging science.

Why We Support Aging Research

Aging (Aging-US) was founded in 2008 by visionary scientists—the late Dr. Mikhail (Misha) Blagosklonny, the late Dr. Judith Campisi, and Dr. David Sinclair—with a clear mission: to create a journal by scientists, for scientists, so the researchers can publish their ideas, theories (sometimes unconventional) and studies on the rapidly developing aging field. Since then, we have remained dedicated to advancing the understanding of aging and age-related diseases, including cancer, a leading health challenge in today’s aging world.

Supporting initiatives like the Aging Initiative at Harvard University and events such as the “Future of Aging Research Mixer 2024” is central to our mission. By supporting young researchers, we strive to drive meaningful advancements in the field and ensure it receives the recognition and resources it deserves. We are deeply committed to supporting initiatives that empower scientists and promote collaboration, mentorship, and innovation.

Sponsoring this initiative is more than an investment—it’s a commitment to the future of aging science and a healthier, longer life for all.

As we look to the future, we are inspired by the passion and talent within this growing field. Together, through continued collaboration and investment, we can shape a world where aging research leads to healthier and longer lives.

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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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