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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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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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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).

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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.

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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).

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

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“The integration of artificial intelligence (AI), biomarkers, ageing biology, and longevity medicine stands as a cornerstone for extending human healthy lifespan.”

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

Advancements in Aging Research

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

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

The Study: A New AI-Powered Approach to Aging

The work summarizes insights from the 2023 Aging Research and Drug Discovery Meeting. Researchers from renowned institutions explored how AI, biomarkers, and clinical applications can work together to enhance longevity. This fusion, termed “longevity biotechnology,” promises to transform healthcare from reactive treatments to proactive, preventive measures focused on staying healthy as we age.

The Challenge: Targeting Multiple Health Conditions with Longevity Biotechnology

Traditional aging research often targets single diseases, but most elderly individuals experience multiple chronic conditions. Addressing this complex challenge requires identifying biological markers that indicate aging and predicting health risks before diseases manifest.

The Breakthrough: AI in Biomarker Discovery for Aging

The study highlights how AI can accelerate the discovery of biomarkers, allowing scientists to understand aging at the cellular level. By using machine learning to identify unique patterns, researchers can estimate biological age, discover potential treatments, and evaluate the impact of lifestyle changes on health. This personalized approach enables healthcare providers to create prevention and treatment plans suited to each person’s unique health needs.

The Future of Healthcare: Preventive, AI-Driven Longevity Treatments

Currently, healthcare often focuses on managing diseases as they arise. However, these AI-driven tools could bring about a shift to preventive healthcare. Instead of waiting for age-related illnesses, clinicians could use AI insights to address aging’s root causes, improving health before issues arise.

While the promise of AI in healthcare is significant, the research team emphasizes that further investment is needed to make these AI-driven approaches accessible and accurate. With continued advancements, longevity biotechnology could become a standard part of healthcare, offering a new way to maintain vitality and well-being as we age.

Conclusion

Longevity biotechnology represents a groundbreaking shift, with AI and biomarkers helping us envision a future of healthier, longer lives. This approach brings us closer to understanding and managing the aging process, making extended healthspans a real possibility.

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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Tribute to Dr. Mikhail (Misha) Blagosklonny

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Dr. Mikhail (Misha) Blagosklonny

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

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

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

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

After earning his MD/PhD in cardiology and experimental medicine from Pavlov First State Medical University of St. Petersburg, Dr. Blagosklonny was awarded a prestigious Fogarty Fellowship from the National Institutes of Health (NIH) in Bethesda, MD. During his productive fellowship at the National Cancer Institute (NCI) in Dr. Leonard M. Neckers’s laboratory, he co-authored 18 publications in diverse areas of cancer research and was the last author on a clinical phase I/II trial paper. Then, he held a brief but productive senior research fellowship at the University of Pennsylvania in Dr. Wafik S El-Deiry’s laboratory before returning for several years to the NCI, where he collaborated with Dr. Tito Fojo. During those years, Dr. Blagosklonny co-authored over 30 research articles covering various topics in cancer research, including targeting HSP90, p53, Bcl2, Erb2, and Raf-1.

It was also at that time that, as a sole author, he published several experimental and theoretical papers encompassing the most important themes in his scientific career.

The first key theme focused on the selective protection of normal cells during cancer therapy. Despite the dogma, Dr. Blagosklonny showed that drug resistance provides opportunities for protection of non-resistant normal cells with selective killing of drug-resistant cancer cells. The original concept, titled “Drug-resistance enables selective killing of resistant leukemia cells: exploiting of drug resistance instead of reversal,” was published in Leukemia in 1999. The idea was so unconventional that, at first, it was incorrectly cited as “reversal of resistance” instead of “exploiting of resistance.”

The renowned, world famous scientist Dr. Arthur Pardee was so impressed by Dr. Blagosklonny’s idea that he visited the NCI to meet Mikhail, and in 2001 they co-authored the paper “Exploiting cancer cell cycling for selective protection of normal cells.” Later, when Misha launched Oncotarget, Dr. Pardee became one of the journal’s first Founding Editors.

Dr. Blagosklonny continued to develop the concept of normal cells protection in the following years. These are the most essential publications on this topic: 

The second key theme was Dr. Blagosklonny’s innovative research method to generate new knowledge and ideas by synthesizing facts and observations from seemingly unrelated fields. This concept was published in Nature in 2002, titled “Conceptual biology: Unearthing the gems.”

The most significant outcome of this concept was the development of the hyperfunction (or quasi-programmed) theory of aging and the discovery of rapamycin as a potential anti-aging drug. Dr. Blagosklonny first published this idea in 2006, titled “Aging and immortality: quasi-programmed senescence and its pharmacologic inhibition.” Dr. Michael Hall, who discovered the protein TOR (Target of Rapamycin), credited Dr. Blagosklonny for “connecting dots that others don’t even see” in a Scientific American publication.

Dr. Blagosklonny held several faculty positions before joining Roswell Park Comprehensive Cancer Center as Professor of Oncology in 2009, and most recently served there as an adjunct faculty member. In his later years, Dr. Blagosklonny continued to develop his hyperfunction theory of aging and published extensively on the prevention of cellular senescence by rapamycin and other mTOR inhibitors, on cancer (an age-related disease) prevention by slowing down organismal aging, and on combinations of potential anti-aging drugs for use in humans. 

These are just a few essential publications on those topics from more than 200 papers:

Dr. Blagosklonny has published more than 290 papers in peer-reviewed journals, serving as the first, last, or sole author on nearly all of his papers.

Dr. Blagosklonny was also a very passionate editor. He always dreamed of being an editor. It all began in 2002 when he was invited to become an Editor-in-Chief of the journal Cell Cycle, a position he held for more than 16 years.

Understanding the importance of sharing scientific information without borders, he formulated the idea to launch journals for scientists, by scientists. Since cancer and aging research were always the main focus of his scientific interests, Dr. Blagosklonny, in collaboration with his colleagues, founded Aging in 2009 (co-editors-in-chief: the late Judith Campisi and David Sinclair) and Oncotarget in 2010 (co-editor-in-chief: Andrei Gudkov). Both journals are renowned for their outstanding Editorial Boards, innovative approaches, and significant popularity within the scientific community.

In 2012, Dr. Blagosklonny founded Oncoscience, a unique journal that publishes free of charge for both authors and readers. It can be considered a philanthropic endeavor.

In addition, Dr. Blagosklonny has served as an associate editor or a member of the editorial board of such journals as Cancer Research, International Journal of Cancer, Leukemia, Cell Death Differentiation, Cancer Biology & Therapy, American Journal of Pathology, Autophagy, and others.

Misha was a funny and witty person, who always had very interesting and unconventional opinions about various topics and was always looking for the roots of different matters. Everyone who knew him for a long time felt that they grew as a person because of his influence. He realized himself in this life as a scientist, editor, family man and a friend.

Dr. Blagosklonny envisioned his cancer battle as a mission to explore how metastatic cancer can be treated with curative intent. He published several articles about his battle, sharing original ideas and pushing the boundaries of cancer treatment in collaboration with his doctors. In his own words, Dr. Blagosklonny was near-curing of incurable cancer. He was in remission about two years and stayed active until the last days.

Dr. Blagosklonny passed away at his home in Boston, MA.

A special thank you to his colleagues and friends, who continuously supported Misha during his cancer battle: Dr. Tito Fojo, Dr. Wafik El-Deiry, Dr. Andrei Gudkov, Dr. Vadim Gladyshev and Dennis Mangan, to name a few.

He will be deeply missed.

–The entire staff of Impact Journals, LLC

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Exploring Baseline Variations and Mechanical Loading-Induced Bone Formation in Young-Adult and Aging Mice through Proteomics

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

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

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

THE STUDY

In this study, the tibias of young-adult and old mice were analyzed using proteomics and RNA-seq techniques, while the femurs were examined for age-related changes in bone structure. A total of 1,903 proteins and 16,273 genes were detected through these analyses. Multidimensional scaling demonstrated a clear separation between the young-adult and old samples at both the protein and RNA levels. Furthermore, 93% of the detected proteins were also identifiable by RNA-seq, and the abundance of these shared targets showed a moderately positive correlation. Additionally, differential expression analysis revealed 183 age-related differentially expressed proteins and 2,290 differentially expressed genes between young-adult and old bone samples.

Proteomic and RNA-seq analyses were conducted on paired tibias from young-adult and old mice to study age-related differences and the effects of mechanical loading on bone formation. The results showed distinct differences in protein and gene expression between the two age groups. Many of the significantly upregulated and downregulated proteins and genes in old bone have been associated with bone phenotypes in genome-wide association studies (GWAS). The study also identified age-related differentially expressed proteins and genes involved in bone phenotypes and aging processes. Integrated analysis with GWAS data revealed eight targets that may be relevant to human disease, including Asrgl1 and Timp2. Furthermore, co-expression analysis identified an age-related module indicating baseline differences in TGF-beta and Wnt signaling. Baseline age-related differences in ECM/MMPs and TGF-beta signaling were detected in both the proteome and transcriptome. Following mechanical loading, the proteome showed distinct pathway, protein class, and process enrichments, with temporal differences observed between young-adult and old mice.

Overall, the findings provide valuable insights into the molecular mechanisms underlying age-related changes and the response to mechanical loading in mouse long bones.

DISCUSSION

This study aimed to compare the proteome and transcriptome of tibias from young-adult and old mice under baseline conditions and analyze changes in the bone proteome in response to mechanical loading. The researchers successfully developed a proteomics method to detect protein-level changes in cortical bone and used it to perform proteomic and RNA-seq analyses on tibias from both young-adult and old mice. They observed a moderately positive correlation between the proteome and transcriptome in bone tissue. Age-related differences were detected at both the protein and RNA levels, with altered TGF-beta signaling and changes in extracellular matrix (ECM) and matrix metalloproteinases (MMPs) protein and transcript levels in old bones. The researchers identified Tgfb2 as the most reduced Tgfb transcript in old bone, predominantly expressed by osteocytes. Proteomic analysis of the loading response showed modest changes compared to age-related differences, with fewer protein-level changes in old bones. The findings suggest that proteomics is a valuable tool for studying bone biology and can provide insights into protein-specific changes in aging.

The data obtained from the analysis were subjected to various statistical and data exploration techniques. Differential expression analysis was performed to compare protein abundance between different groups. Total RNA was extracted from the bones using TRIzol, and its integrity and concentration were measured. The bones were also processed for paraffin sectioning and RNA in situ hybridization.

Overall, the study involved the collection and analysis of bone samples from female mice to investigate age-related changes and loading responses in the skeletal system.

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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How Single Housing Impacts Growth and Lifespan in African Turquoise Killifish

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“[…] our results suggest that sharing housing with others in early life might influence whole-life attributes, potentially leading to specific life history traits beyond the typical relationship between the growth rate and lifespan.”

In this research, Chika Takahashi, Emiko Okabe, Masanori Nono, Saya Kishimoto, Hideaki Matsui, Tohru Ishitani, Takuya Yamamoto, Masaharu Uno, and Eisuke Nishida from the RIKEN Center for Biosystems Dynamics Research (BDR) in Hyogo, Japan; Brain Research Institute, Niigata University in Niigata, Japan; Research Institute for Microbial Diseases at Osaka University in Osaka, Japan; Kyoto University in Kyoto, Japan; and RIKEN Center for Advanced Intelligence Project (AIP), explored the effects of housing density during the juvenile stage on whole-life traits, including growth, fecundity, and lifespan, in African turquoise killifish. Their research paper was published on the cover of Aging (listed by MEDLINE/PubMed as Aging (Albany NY) and as Aging-US by Web of Science), Volume 16, Issue 18, entitled, “Single housing of juveniles accelerates early-stage growth but extends adult lifespan in African turquoise killifish.”

THE STUDY

A study on African turquoise killifish examined the impact of housing density on juvenile growth. Newly hatched fish were kept in different densities ranging from 1 to 40 fish per tank. It was found that lower housing densities resulted in faster growth, with fish in single housing growing significantly larger than those in group housing. Additionally, single-housed fish reached sexual maturity earlier compared to group-housed fish at higher densities. Comparisons between group-housed and single-housed fish showed that housing conditions in the juvenile stage did not affect the appearance changes during sexual maturation. 

As the fish progressed to middle-aged adults, the rate of increase in body length slowed down, while body weight continued to increase. Differences in body weight between group-housed and single-housed fish persisted into old age, suggesting potential differences in body composition. Surprisingly, single-housed fish had a longer mean adult lifespan compared to group-housed fish, contradicting the commonly held belief that faster growth leads to shorter lifespan. Lower housing densities during the juvenile stage were also found to extend adult lifespan, further challenging the inverse correlation between growth rate and lifespan. These findings suggest that lower housing densities promote accelerated growth in the juvenile stage of African turquoise killifish.

The study also found that single-housed fish had a longer adult lifespan compared to group-housed fish. This led to the suspicion that the egg-laying period of single-housed fish might also be longer. To investigate this, the researchers conducted weekly monitoring of the number of eggs laid until the old adult stage. In group-housed fish, the number of eggs laid was high for the first two weeks, followed by a medium level for the subsequent five weeks, and then decreased. In contrast, single-housed fish showed a medium level of egg-laying for the first nine weeks, followed by a decrease. The cumulative number of live embryos was found to be lower in single-housed fish compared to group-housed fish. These findings suggest that while the number of eggs laid is not very high, single-housed fish have a longer egg-laying period than group-housed fish.

To investigate the potential reasons behind the reduction in offspring number and longer egg-laying period in single-housed fish, the researchers conducted RNA sequencing analysis of testes or ovaries at four life stages. These stages included the onset of sexual maturity, young adult, mature adult, and middle-aged adult. Interestingly, the analysis revealed that single-housed fish showed higher similarity to group-housed fish at earlier life stages compared to group-housed fish at the same life stage. For instance, in the testes, single-housed fish at stage II exhibited the highest similarity to group-housed fish at stage I. Similarly, in the ovaries, single-housed fish at stage II and III showed higher similarity to group-housed fish at stage I. These findings suggest that the rate of gonadal transcriptional change with life stage progression is slower in single-housed fish compared to group-housed fish.

The researchers identified differentially expressed genes (DEGs) between stage I and stage IV in group- and single-housed fish. In the testes, ribosome-related genes and cilium-related genes were highly enriched in DEGs with higher expression in stage I compared to stage IV, suggesting a link between life stage progression, testes development, and spermatogenesis. In the ovaries, growth-related genes and translation-related genes were highly enriched in DEGs with higher expression in stage I compared to stage IV, indicating a link between life stage progression, ovarian development, oogenesis, and aging. Comparing group-housed and single-housed fish at different stages, there were differences in the PC1 values, suggesting that single-housed fish exhibited slower progression of gametogenesis and gonadal maturation relative to life stage progression compared to group-housed fish.

To further investigate this, the researchers focused on specific genes related to spermatogenic differentiation, oocyte development, oocyte construction, and female gonad development. The expression of these genes showed slower changes with life stage progression in single-housed fish compared to group-housed fish in both the testes and ovaries. This suggests that single-housed fish may have slower rates of gametogenesis and gonadal maturation, leading to a lower proportion of mature sperm and oocytes in their gonads. Overall, the results indicate that, at the transcriptional level, the progression of gonadal maturation and ovarian aging is slower in single-housed fish compared to group-housed fish. This slower progression may explain the medium fecundity and extended egg-laying period observed in single-housed fish.

The liver was chosen for analysis as it plays a central role in organismal metabolic processes. Gene expression profiles of the livers were compared between group- and single-housed fish at two different ages: 7 weeks post-hatching (wph) and 14 wph. Surprisingly, despite the 2-week age difference, the correlation coefficients showed that group- and single-housed fish at 14 wph were highly similar. The researchers identified 1588 age-related differentially expressed genes (DEGs) between the two age groups. Hierarchical clustering based on the expression changes of these age-related genes demonstrated that the expression profiles of group- and single-housed fish were similar at 14 wph.

IN CONCLUSION

In summary, juvenile single housing in African turquoise killifish promotes faster growth, longer egg-laying periods, and extended lifespans compared to group housing. These findings challenge traditional assumptions about the relationship between growth and lifespan and shed light on the impact of early-life environmental conditions on overall life history.

Overall, the experiments involved maintaining and rearing the fish, measuring their body length and weight, analyzing RNA sequencing data, measuring lifespan, and counting the number of eggs laid. Statistical analysis was conducted to assess significant differences between groups.

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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