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AI Tools Reveal How IPF and Aging Are Connected

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“Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive lung disease characterized by the excessive accumulation of extracellular matrix components, leading to declining lung function and ultimately respiratory failure.”

Idiopathic Pulmonary Fibrosis (IPF) is a progressive lung disease that primarily affects people over the age of 60. It causes scarring in the lung tissue, which gradually reduces lung capacity and makes breathing difficult. Despite years of research, the exact causes of IPF remain largely unknown, and current treatments mainly aim to slow its progression rather than reverse or cure the disease.

Because IPF tends to develop later in life, researchers have long suspected a connection with biological aging. This is the focus of a recent study by scientists from Insilico Medicine. Their research, titled “AI-driven toolset for IPF and aging research associates lung fibrosis with accelerated aging,” was published recently in Aging-US, Volume 17, Issue 8.

The Study: Using AI to Explore the Link Between IPF and Aging

To investigate the biological relationship between IPF and aging, researchers Fedor Galkin, Shan Chen, Alex Aliper, Alex Zhavoronkov, and Feng Ren, from Insilico Medicine, developed two artificial intelligence (AI) tools. The first, a proteomic aging clock, estimates a person’s biological age using protein markers found in blood samples. The second, a specialized deep learning model named ipf-P3GPT, was trained to analyze patterns of gene activity in both normal aging and fibrotic lung tissue.

The aim was to explore whether IPF mirrors biological aging or whether it follows a separate disease pathway. While aging and IPF share common features, such as chronic inflammation and tissue damage, it is not yet clear if IPF is simply accelerated aging or a distinct biological process. Distinguishing between the two is essential for developing more targeted and effective treatments.

To train the aging clock, the team used the UK Biobank collection of over 55,000 proteomic Olink NPX profiles, annotated with age and gender. They then applied the model to patients with severe COVID-19, a population known to be at higher risk of developing lung fibrosis. In parallel, the ipf-P3GPT model simulated and analyzed gene expression patterns in lung tissue, allowing the team to directly compare the biological signatures of aging and IPF.

Results: IPF and Aging Are Distinct Biological Entities

The aging clock accurately estimated biological age in healthy individuals. When applied to patients with severe COVID-19, the clock predicted higher biological ages compared to healthy controls. This finding suggests that fibrotic lung conditions may be linked to accelerated biological aging and that such changes leave a detectable molecular signature in the body.

Using the ipf-P3GPT model, the researchers found that while 15 genes were shared between lung tissue affected by normal aging and IPF, more than half of these genes displayed opposite patterns of activity, being upregulated in aging but downregulated in IPF, or vice versa. These results indicate that IPF is not merely a faster version of aging but a distinct biological condition influenced by age-related dysfunction and unique molecular alterations.

The Impact: Toward Better Understanding and Treatment of Fibrotic Diseases

A key insight from this study is that although aging and IPF are biologically related, they follow different molecular pathways. IPF involves changes in gene expression and tissue remodeling that go beyond the patterns typically seen in normal aging. This difference could guide the development of therapies that specifically target fibrosis without interfering with healthy aging processes.

The AI tools developed in this research also have broader potential. The aging clock could be used to identify individuals whose biological age is advancing more quickly due to hidden disease processes, even before symptoms appear. At the same time, ipf-P3GPT provides a framework for studying how aging and disease interact on a molecular level, which could be applied to other age-related or fibrotic conditions such as liver or kidney fibrosis.

By combining AI with large-scale biological data, this approach introduces a powerful toolset that supports more personalized treatment strategies and a better understanding of age-related disease mechanisms.

Future Perspectives and Conclusion

While the results are promising, further validation is needed. Both models should be tested across diverse patient datasets and clinical settings to confirm their reliability and usefulness. Still, this study highlights how AI can support medical research by uncovering subtle biological differences between aging and disease.

Overall, this study establishes novel connections between IPF disease and aging biology while demonstrating the potential of AI-guided approaches in therapeutic development for age-related diseases. By helping scientists better understand where aging ends and disease begins, these AI tools may contribute to earlier diagnosis, more accurate monitoring, and improved treatment strategies for patients facing fibrotic and age-related conditions.

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

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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 Exosomes Spread Aging Signals and Could Support Anti-Aging Research

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“Senescent cells release a senescence-associated secretory phenotype (SASP), including exosomes that may act as signal transducers between distal tissues, and propagate secondary senescence.”

As the global population grows older, understanding what drives the aging process is becoming increasingly important. Diseases like Alzheimer’s, cardiovascular conditions, and cancer are more common with age, yet many current treatments only manage symptoms rather than addressing the underlying biological causes.

One contributor to aging is the buildup of “senescent” cells—cells that have stopped dividing but do not die. These cells can harm nearby tissues by releasing molecular signals, a process known as secondary senescence.

Scientists have found that senescent cells release tiny particles called exosomes. A research team from The Buck Institute for Research on Aging recently discovered that these exosomes carry aging-related messages through the bloodstream. Their study, titled “Exosomes released from senescent cells and circulatory exosomes isolated from human plasma reveal aging-associated proteomic and lipid signatures,” was featured as the cover article in Aging (Aging-US), Volume 17, Issue 8.

The Study: Exosomes and Aging

The team led by Sandip Kumar Patel, Joanna Bons, and Birgit Schilling from The Buck Institute for Research on Aging focused their study on exosomes—tiny, bubble-like structures released by cells that carry proteins, lipids, and genetic material. These particles can move through the bloodstream and influence distant tissues. 

The researchers wanted to know whether exosomes from senescent cells and from the blood of older adults shared common markers of aging. Since aging cells are spread throughout the body and lack a single clear marker, exosomes could provide a new way to detect their presence through a simple blood test.

To explore this, the team analyzed exosomes from two sources: lab-grown human lung cells that had undergone senescence and blood samples from both young (20–26 years old) and older (65–74 years old) adults. They used high-throughput mass spectrometry.

Results: Exosomes Reveal Signs of Aging

In total, the team identified over 1,300 proteins and 247 lipids within the exosomes. Specifically, 52 proteins appeared in both senescent cells and the blood plasma of older adults, many of which are associated with inflammation and tissue damage. Some examples include Prothrombin, Plasminogen, and Reelin—molecules involved in blood clotting, tissue remodeling, and neural development. Their presence in both aged blood and senescent cells suggest a broader impact of aging on multiple biological systems.

The team also observed significant changes in the lipid content of the exosomes. Lipids that help maintain cell membrane structure were more common in samples from older individuals, while lipids involved in energy storage were less abundant.

In addition, the researchers detected changes in microRNAs—small pieces of genetic material that regulate gene expression. Several microRNAs found in the blood of older adults have already been associated with diseases such as Alzheimer’s and osteoarthritis.

The Impact: Potential for Diagnostics and Anti-Aging Therapies

This study is among the first to directly compare exosomes from senescent cells and human plasma, revealing shared aging-related markers across biological systems.

These particles act like messengers, spreading signals that may accelerate aging in other cells. This supports the concept of secondary senescence—where aging-like behavior is transmitted from senescent cells to healthy ones—suggesting that exosomes may help propagate aging throughout tissues over time.

This work could lead to the development of blood tests that measure biological age more accurately than a person’s chronological age. It might also help clinicians monitor the effectiveness of anti-aging treatments.

Future Perspectives and Conclusion

Although the study involved a small number of human samples, it presents a promising new approach to studying aging. If confirmed in larger studies, the findings could lead to improved diagnostic tools and therapies for age-related diseases.

In the long term, researchers may explore ways to block or modify harmful exosome signals to protect healthy cells from premature aging. These molecular signatures could also support personalized medicine approaches or help track the effectiveness of anti-aging interventions in clinical settings.

Click here to read the full research paper published in Aging (Aging-US).

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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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Skin Rejuvenation: How Young Blood and Bone Marrow Influence It

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“Heterochronic parabiosis studies illuminated the potential for rejuvenation through blood-borne factors, yet the specific drivers including underlying mechanisms remain largely unknown and until today insights have not been successfully translated to humans.”

A new study published as the cover of Aging (Aging-US) Volume 17, Issue 7, explores how factors in young human blood may affect the biological age of human skin. Researchers from Beiersdorf AG, Research and Development Hamburg in Germany, used a microphysiological co-culture system—a lab-based model simulating human circulation—to test the effects of young versus old blood serum on skin cells. The findings suggest that bone marrow-derived cells play a key role in converting blood-borne signals into effects that support skin rejuvenation.

Understanding Skin Aging and Systemic Influence

As we age, the skin’s ability to regenerate declines, while its biological age increases. This contributes to visible signs of aging and a weakened barrier function. While cosmetic treatments can improve appearance, they rarely target the cellular processes underlying skin aging.

Animal studies have shown that exposure to young blood can promote tissue repair and rejuvenation, likely due to molecules circulating in the bloodstream. However, reproducing these effects in human skin has proven difficult. Applying young serum directly to skin tissue has not produced significant results, indicating that additional cellular interactions may be required.

The Study: A Two-Step Regenerative Protocol

The research team, led by first author Johanna Ritter and corresponding author Elke Grönniger from Beiersdorf AG, developed an innovative in vitro system combining two engineered human tissue models: full-thickness skin and bone marrow. Using the HUMIMIC Chip3plus platform, they created a miniature circulatory system where these tissues could interact through shared culture media.

The study, titled “Systemic factors in young human serum influence in vitro responses of human skin and bone marrow-derived blood cells in a microphysiological co-culture system,” investigated how human serum from young (<30 years) and older (>60 years) donors influenced markers of skin aging over a 21-day period.

Results: Rejuvenation Dependent on Bone Marrow Interaction

The researchers observed that young serum alone had no effect on skin aging markers in either static or dynamic skin-only cultures. However, when skin tissue was co-cultured with bone marrow-derived cells, significant changes occurred.

Skin in the combined system treated with young serum showed increased cell proliferation, indicating improved regenerative potential, and a reduction in biological age as measured by DNA methylation clocks. Bone marrow cells also exhibited improved mitochondrial function and changes in cell composition, particularly an increase in early progenitor cells.

These findings suggest that bone marrow-derived cells respond to young serum by producing signaling proteins that influence skin behavior. Without these intermediary cells, the rejuvenating effects were not observed.

Further proteomic analysis identified 55 proteins that were differentially expressed in bone marrow cells exposed to young versus old serum. Of these, seven proteins were tested individually on aged skin cells. Several—including CHI3L1, CD55, and MMP-9—improved markers related to skin aging, such as collagen production, mitochondrial activity, and cellular plasticity.

The Impact: Identification of Key Rejuvenating Proteins

This discovery highlights specific proteins that may serve as future targets in skin regeneration research. While the results are promising, they were obtained in controlled lab conditions. These findings are not yet applicable to clinical treatments but offer a potential foundation for developing non-invasive skin therapies that mimic the effects of youthful blood composition.

Future Perspectives and Conclusion

The study underscores the importance of systemic and inter-organ communication in skin aging. By incorporating bone marrow-derived cells into the experimental model, the researchers created a more physiologically accurate system to study how circulating factors influence tissue aging.

Although the evidence supports the idea that bone marrow cells mediate the effects of young serum on skin, additional research is needed. Future studies using aged skin models, extended time frames, and clinical validation will be essential to explore therapeutic possibilities.

As an experimental approach, this research adds valuable knowledge to the biological mechanisms of skin aging and could inform future strategies in regenerative medicine and dermatology.

Click here to read the full research paper published in Aging (Aging-US).

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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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Stem Cell Regenera: A Regenerative Approach to Activating Dormant Ovarian Follicles

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“Women with conditions such as Poor Ovarian Response (POR) and Diminished Ovarian Reserve (DOR) face significant challenges in assisted reproduction.”

A new study published recently in Aging (Aging-US) Volume 17, Issue 6, examines a novel treatment for women with ovarian failure. Researchers from IVI Clinics Alicante in Spain investigated a procedure called Stem Cell Regenera, which uses the body’s own stem cells and platelet-rich plasma to activate dormant follicles in the ovaries. This innovative protocol could expand options for patients with ovarian failure who have not responded to conventional fertility therapies.

Understanding Ovarian Failure

Ovarian failure affects women’s ability to conceive by reducing the quantity and quality of eggs in the ovaries. Conditions like Poor Ovarian Response, Diminished Ovarian Reserve, and Premature Ovarian Insufficiency are key reasons for infertility and make it hard to use assisted reproduction methods like in vitro fertilization (IVF).

Standard fertility treatments often fail to improve outcomes for these patients, leaving donor eggs as the primary alternative. However, recent advances in regenerative medicine have raised the possibility of restoring ovarian function using cellular therapies. Emerging research suggests that the right biological conditions could reactivate dormant follicles within the ovaries, potentially helping patients to use their eggs.

The Study: A Two-Step Regenerative Protocol

Led by first author Amparo Santamaria and co-authors Ana Ballester and Manuel Muñoz, the study titled “Enhancing oocyte activation in women with ovarian failure: clinical outcomes of the Stem Cell Regenera study using G-CSF mobilization of peripheral blood stem cells and intraovarian injection of stem cell factor-enriched platelet rich plasma in real-world-practice,” examined the effectiveness of Stem Cell Regenera in a real-world clinical setting. The protocol combined two key steps. First, patients received granulocyte colony-stimulating factor (G-CSF), a substance that mobilizes hematopoietic stem cells from the bone marrow into the bloodstream. Second, clinicians performed an ultrasound-guided injection of platelet-rich plasma, enriched with stem cell growth factors, directly into the ovaries.

The retrospective observational study carried out from January 2023 to December 2024 analyzed data from 145 women aged 26 to 44 years who had previously exhausted conventional fertility options. Researchers evaluated whether this procedure could stimulate ovarian activity and improve pregnancy outcomes.

Results: Activation of Ovarian Function

The study found that nearly 70% of participants demonstrated ovarian activation, defined as either an increase in developing follicles or a rise in Anti-Müllerian Hormone levels. Among these women, approximately 7% achieved spontaneous pregnancies without further intervention, while 14% became pregnant following IVF treatment.

Importantly, the procedure was well tolerated. No severe adverse effects were reported, and most participants experienced only mild and transient symptoms such as headaches or fatigue. The use of the patient’s own cells minimized the risk of immune reactions and contributed to the overall safety profile.

The Impact: Expanding Fertility Options

The Stem Cell Regenera protocol represents a promising development in reproductive medicine by offering an alternative for women with ovarian failure who prefer to use their own eggs rather than donor eggs. Unlike traditional hormonal therapies, this approach focuses on rejuvenating the ovarian environment itself, which may enable natural follicular development.

While the findings are encouraging, the researchers caution that the study was observational in design and lacked a control group. These factors limit the ability to draw definitive conclusions about efficacy.

Future Perspectives and Conclusion

Stem Cell Regenera adds to a growing body of evidence supporting regenerative therapies in fertility care. However, large randomized controlled trials are needed to confirm its effectiveness, identify the patient populations most likely to benefit, and assess long-term outcomes.

As an experimental approach, it may be considered in select cases where conventional therapies have failed. To learn more about this research, readers can watch an interview with the study’s lead author, Dr. Amparo Santamaria, here.

Click here to read the full research paper published in Aging (Aging-US).

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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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DoliClock: A Lipid-Based Clock for Measuring Brain Aging

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

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

Understanding Brain Aging

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

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

The Study: Building a Lipid-Based Aging Clock

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

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

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

Results: Lipids Reflect the Pace of Aging

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

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

The Impact: A New Window into Brain Aging

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

Future Perspectives and Conclusion

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

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

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

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

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A New Vision for Healthcare: Addressing Aging Before Disease Begins

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

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

The Problem with Traditional Medicine

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

A New Model for Healthcare: Insights from the Editorial

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

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

From Treatment to Prevention: Targeting the Root Causes of Aging

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

Impact and Implications

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

Future Perspectives and Conclusion

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

Click here to read the full editorial published in Aging.

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

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

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

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

Understanding Hypoxia in the Brain

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

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

The Study: Exploring Brain Vulnerability to Hypoxia

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

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

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

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

The Breakthrough: Understanding the Link Between Hypoxia and Cognitive Decline

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

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

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

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

Future Perspectives and Conclusion

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

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

Click here to read the full research paper in Aging.

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

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

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

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

Understanding Epigenetic Aging

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

The Study: How Food Might Influence Epigenetic Aging

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

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

The Results:  A Diet That May Slow Epigenetic Aging

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

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

The Impact: A Natural Way to Care for Our Health

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

Future Perspectives and Conclusion

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

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

Click here to read the full research paper in Aging.

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

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

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

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

Understanding Werner Syndrome

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

The Study: Investigating NAD+ in Werner Syndrome

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

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

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

The Results: NAD+ Can Reduce Aging Signs

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

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

The Breakthrough: Linking Mitochondrial NAD+ to Cell Aging

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

The Impact: A Step Toward Slowing Down Cellular Aging

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

Future Perspectives and Conclusion

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

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

Click here to read the full research paper in Aging.

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

Click here to subscribe to Aging publication updates.

For media inquiries, please contact [email protected].

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

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Aging (Aging-US) was proud to sponsor the Muscle Aging Science & Translation (MAST) Symposium, organized by the Aging Initiative at Harvard University on Friday, April 18, 2025.

This important event brought together 350 participants—chosen from more than 1,300 applicants—including students, researchers, company founders, investors, and industry leaders. Together, they explored the latest research and innovations in muscle health and aging. The symposium reflected the journal’s strong commitment to supporting collaboration across fields and advancing research in aging.

-Key Highlights from the MAST Symposium- 

Clinical Research Perspectives on Frailty  

The symposium opened with a strong clinical session led by experts from top institutions: Dr. Roger Fielding (Tufts University and Boston Claude D. Pepper Older Americans Independence Center) and Drs. Douglas Kiel, Shivani Sahni, and Yi-Hsiang Hsu (Harvard Medical School and Beth Israel Deaconess Medical Center).

The panel discussed key topics such as the biology of frailty, how bone and muscle health are connected, and the influence of genetics, diet, and exercise on staying strong as we age. By blending real-life patient care with the latest research, the speakers shed light on the challenges of sarcopenia—the gradual loss of muscle strength and mass that occurs with age—and the new scientific approaches being developed to improve treatment.

Next-Generation Therapeutic Approaches

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

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

Biotech and Drug Development for Muscle Aging 

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

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

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

Exercise Science for Muscle Longevity

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

Driving Scientific Progress in Muscle and Aging Research

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

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

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

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