Tag: Aging Research

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Aging-US Supports the Future of Aging Research Mixer 2025

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Aging-US proudly sponsored the Future of Aging Research (FAR) Mixer 2025, hosted by the Aging Initiative on November 7 in Cambridge, MA, uniting students, researchers, and biotechnology leaders to advance aging research and shape a healthier, longer-lived future.

Highlights from the FAR Mixer 2025

The 2025 FAR Mixer featured keynote speaker Dr. Kristen Fortney, Co-Founder and CEO of BioAge Labs, who shared insights into how translational research and clinical pipelines have evolved over the past decade. 

Dr. Fortney highlighted how obesity-targeting drugs are opening new avenues for metabolic and aging research. She explained that while obesity and osteoporosis are currently major therapeutic priorities, the next wave of reimbursable diseases will likely focus on muscle loss and chronic inflammation, reflecting their growing recognition as key factors in healthy aging. 

She also emphasized the importance of human databases in target discovery, cross-sector partnerships between pharma and biotech, and the increasing focus on small-molecule interventions to address age-related diseases.

Focus talks showcased the diversity and depth of modern aging research:

  • Dr. Brad Manor (Senior scientist & Director of the Mobility and Falls Program at the Hinda & Arthur Marcus Institute for Aging Research, faculty member in medicine at Harvard Medical School, and  Beth Israel Deaconess Medical Center) explained how balance and fall prevention in older adults are tightly linked to cognitive function, presenting dual-task gait assessments as meaningful biomarkers of brain health. These assessments measure how walking performance changes when combined with a thinking task, such as counting backward or naming words.

Dr. Manor also noted that noninvasive brain stimulation (tDCS) targeting cognitive-motor regions can enhance dual tasking and mobility in older adults, emphasizing the need for more precise and personalized applications in the future.

  • John Bailey (Head of hardware at Until Labs) discussed the challenges of cryopreservation, such as achieving sufficient cooling speed, temperature uniformity, and avoiding toxic concentrations of cryoprotectants. He then described recent innovations in medical hibernation and the development of advanced electromagnets for rewarming large cryopreserved samples; technology that could revolutionize organ donation and long-term tissue preservation.
  • José Luis Ricón (Head of Theory at Retro Biosciences) described how cell and tissue replacement strategies could extend healthy lifespan by targeting core mechanisms of aging. He explained that Retro’s approach focuses on developing interventions capable of stopping or even reversing disease progression, aiming for substantial and measurable improvements in health outcomes.
  • Dr. Martin Borch Jensen (CEO of Gordian Biotechnology) reflected on the challenges and promise of mosaic screening technologies for identifying interventions that could add years of healthy life.

The Biotech Investing & Startups Creation Panel featured Dr. Alex Colville (Co-founder and General Partner at age1 VC), Dr. Nabiha Saklayen (Co-Founder & CEO of Cellino Biotech) and Dr. Matthew Hammond (Partner at RA Capital Management). The discussion was centered around the future of venture investment in longevity, the role of AI in cell therapy manufacturing, and advice for young scientists entering the biotech field, emphasizing focus, resilience, and sustained enthusiasm.

Supporting Emerging Leaders in Aging Research

Nearly a hundred participants were present. Attendees included undergraduate, graduate, and postdoctoral researchers, alongside industry professionals and early-stage entrepreneurs. Many were returning participants from previous events, proof of a growing and dedicated community.

Through its sponsorship, Aging-US reaffirmed its mission to support and connect the next generation of aging researchers. The event extended networking opportunities, enabling attendees to exchange ideas and discuss new research directions.

The Aging Initiative, now officially recognized as a 501(c)(3) organization, continues to strengthen this community through programs such as journal clubs, lectures, and mentorship events. Future plans include participation in Massachusetts’s DRIVE Initiative (Discovery, Research, and Innovation for a Vibrant Economy) and organizing the upcoming NOVA Conference on the Neuroscience of Vitality and Aging in April 2026.

Our Commitment to Advancing Aging Research

Founded in 2008 by visionary scientists—the late Dr. Mikhail (Misha) Blagosklonny, the late Dr. Judith Campisi, and Dr. David Sinclair, Aging-US was created as a journal by scientists, for scientists, to publish innovative ideas and studies in the rapidly developing field of aging research. Since then, it has remained dedicated to advancing the understanding of aging and age-related diseases.

Supporting initiatives such as the Future of Aging Research Mixer 2025 reflects our belief that progress in aging science depends on collaboration, mentorship, and the open exchange of ideas between academia, industry, and young innovators. By investing in the next generation of researchers, we aim to accelerate discoveries that will lead to longer, healthier lives for all.

Sponsoring this initiative is more than an investment, it’s a commitment to the future of aging science and to the vision of a world where longevity and well-being advance hand in hand.

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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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Alpha-Synuclein Overexpression in Rats Reveals Early Clues to Synucleinopathies

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“Synucleinopathies are age-dependent neurodegenerative diseases characterized by alpha-synuclein accumulation with distinct vulnerabilities across brain regions.”

Synucleinopathies are a group of age-related neurological disorders, including Parkinson’s disease, dementia with Lewy bodies, and multiple system atrophy. Most individuals are not diagnosed until these diseases have significantly progressed, as early symptoms, such as a reduced sense of smell, subtle cognitive or motor changes are too vague to serve as reliable indicators. 

To uncover specific biological signs that appear earlier and clearly point to the disease process, researchers from Saarland University developed a study titled “Brain region-specific and systemic transcriptomic alterations in a human alpha-synuclein overexpressing rat model,” featured as the cover of Aging-US, Volume 17, Issue 10.

Understanding Synucleinopathies

Synucleinopathies are characterized by the abnormal buildup of the protein alpha-synuclein in the brain. When this protein misfolds, it accumulates inside neurons and forms toxic clumps that disrupt their normal function and threaten cell survival. Because brain samples from patients are usually obtained only after death, scientists rely on animal models to investigate how these diseases start and progress.

The Study:  Exploring Early Gene Changes Associated with Synucleinopathies

A research team from Saarland University, led by Vivien Hoof and Thomas Hentrich, studied a genetically engineered rat model that overexpresses the human form of alpha-synuclein. Their goal was to examine how this protein affects gene activity in both the brain and the gut at different life stages.

The researchers focused on three brain regions known to be involved in movement and cognition: the striatum, cortex, and cerebellum. They examined gene expression in rats at two ages, at five and twelve months, representing early and mid-adulthood, roughly equivalent to young and middle-aged humans. Gut tissue was also studied to better understand the possible systemic effects of alpha-synuclein accumulation.

The Results: Early and Widespread Gene Changes Across the Brain and Gut

The study revealed that gene activity was more significantly disrupted in younger rats, particularly in the striatum, a key area for motor control. Many of the affected genes were involved in communication between nerve cells, suggesting that vital brain functions start shifting early in the disease process.

In older rats, changes were especially noticeable in the cortex and related to myelination, the process that insulates nerve fibers. Similar patterns have also been observed in patients with synucleinopathies, highlighting the value of the rat model.

Importantly, the team identified a core group of genes that were consistently altered across all three brain regions. Some of these same gene changes were also found in the gut, suggesting that the impact of alpha-synuclein accumulation is not limited to the brain but may influence the entire nervous system, including the enteric (gut) nervous system.

The Breakthrough: Evidence That Synucleinopathies May Begin Long Before Symptoms Appear

This study provides compelling evidence that synucleinopathy-related changes begin early at the molecular level, well before clinical symptoms emerge, challenging the notion that such diseases only manifest in later life. These early alterations are both brain region-specific and systemic. The presence of similar gene changes in the gut supports the growing understanding that synucleinopathies are not just brain disorders, but may affect the entire body. These early molecular signals could serve as biomarkers, helping to detect disease before lasting damage occurs.

The Impact: Opening New Paths for Early Detection and Intervention

These findings could shift research toward diagnosing synucleinopathies in their earliest stages. If similar patterns of gene activity can be identified in humans, potentially through blood or stool samples, it may be possible to detect these diseases years before symptoms arise. Early detection could enable timely and more effective treatment.

The study also sheds light on previously overlooked genes involved in neuroprotection and neural communication, which may become new targets for therapeutic development.

Future Perspectives and Conclusion

While synucleinopathies are often seen as diseases of aging, this study highlights that crucial biological changes may occur far earlier. Mapping these early molecular changes provides a strong foundation for developing new diagnostic tools and early-stage treatments. It also reinforces the need to study not just the brain but the entire nervous system, including the gut, which may serve as an accessible window into early disease processes.

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).

Click here to subscribe to Aging publication updates.

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How Long-Term Social Connection Supports Brain Health and Memory in Aging

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“While environmental enrichment (EE) can protect against cognitive deficits in old age, whether EE with long-term social housing provides greater protection than EE alone, and the underlying neuronal mechanisms, remain unknown.”

As people age, it is common to experience some memory lapses or slower thinking. Although this is often a normal part of aging, it can still affect a person’s quality of life. Scientists have been investigating ways to slow or prevent cognitive decline, and growing evidence points to the potential role of social interaction.

Recently, a study using rats found that long-term social connection may help protect the brain from age-related memory decline. This work, titled “The impact of long-term social housing on biconditional association task performance and neuron ensembles in the anterior cingulate cortex and the hippocampal CA3 region of aged rats,” was recently published in Aging-US (Volume 17, Issue 9).

The Study: How Long-Term Social Connection Influences the Aging Brain 

Previous studies have shown that environmental enrichment, such as physical activity and cognitive challenges, can support brain health. However, it has been less clear whether social living, on its own, provides additional benefits. To address this question, a research team led by Anne M. Dankert from Providence College and the University of North Carolina at Chapel Hill investigated how long-term social housing affects memory and brain activity in aging rats.

The researchers divided the animals into three groups: young rats, aged rats that were housed alone, and aged rats that were housed with companions throughout life. All aged rats had access to physical and cognitive enrichment, but only one group also experienced long-term social interaction.

The study focused on two areas of the brain that are involved in memory and decision-making: the anterior cingulate cortex (ACC), which is associated with attention and behavioral control, and the hippocampal CA3 region, which is essential for forming and distinguishing between similar memories.

The Results: Long-Term Social Connection Supports Memory and Brain Function in Aging Rats

The aged rats that lived in social groups performed significantly better on tasks involving memory and decision-making compared to those that were housed alone. In a challenging task that required the animals to associate specific objects with their correct locations in a maze, only the socially housed aged rats performed at a level similar to that of young rats. The isolated aged rats made more errors and showed signs of cognitive decline.

In addition to behavioral results, the researchers found differences in brain activity. The socially housed aged rats showed stronger activation in the hippocampal CA3 region during testing, which suggests better memory function. At the same time, their ACC was less overactive during simpler tasks, indicating more efficient brain activity. 

The Breakthrough: Social Interaction Promotes Better Brain Function in Rats

This study provides evidence that sustained social interaction may help preserve brain function during the aging process. Unlike previous research that often combined social factors with other types of environmental enrichment, this work isolated the effect of long-term social housing on memory and brain activity. The findings show that even when other enriching elements—such as physical and cognitive stimulation—are present, the addition of social living offers distinct cognitive and neural benefits. 

The Impact: Rethinking the Role of Social Life in Healthy Aging

This study supports the idea that social connection could be an important factor in maintaining brain health. If social interaction alone provides measurable benefits—even when other forms of enrichment are present—it reinforces the value of strong social bonds in later life. Social programs, family engagement, and opportunities for daily interaction may play a key role in protecting cognitive abilities in older adults.

Future Perspectives and Conclusion

Although the study was conducted in rats, the findings are consistent with previous human research suggesting that social engagement supports brain health. Future research can explore how these effects translate to people and whether specific types or durations of social interaction are more effective.

Overall, this work shows that long-term social connection may help preserve memory and support more efficient brain function during aging. Maintaining close relationships may therefore be a valuable and practical approach to supporting cognitive health in older adults.

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).

Click here to subscribe to Aging publication updates.

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New Anti-Aging Combo Boosts Lifespan in Old Male Mice

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“Extending lifespan and healthspan remains a central goal of biomedical research and has been tackled through numerous and diverse approaches.”

As life expectancy increases, there is growing interest not only in extending lifespan but also in improving the quality of those additional years. To address the physical and cognitive decline that often accompanies aging, researchers have explored a variety of strategies. Many of these focus on a single biological factor, such as reducing inflammation or stimulating stem cell activity. However, aging is a complex process involving multiple, interconnected changes in the body.

Recognizing this, researchers at the University of California, Berkeley proposed a more comprehensive approach: targeting multiple aging-related pathways simultaneously. Their study, titled “Sex-specific longitudinal reversal of aging in old frail mice,” was recently featured on the cover of Aging-US (Volume 17, Issue 9).

The Study: A Dual Treatment Using Oxytocin and an Alk5 Inhibitor

In this study, a team led by first author Cameron Kato and corresponding author and Aging-US Editorial Board member Irina M. Conboy tested a combination treatment on very old and frail mice, roughly equivalent in age to 75-year-old humans. The treatment involved two compounds: oxytocin, a hormone that naturally declines with age and is involved in tissue repair and regeneration, and an Alk5 inhibitor, which blocks part of the TGF-β signaling pathway. This pathway often becomes overactive in older individuals, contributing to inflammation and impaired tissue function.

The researchers aimed to determine whether targeting both the declining and overactive systems at the same time would be more effective than addressing just one.

The Results: Distinct Effects in Male and Female Mice

In male mice, the results were notable. Lifespan increased by 14 percent when measured from birth, and by over 70 percent when measured from the start of treatment in old age. These mice also showed improved physical performance, including better endurance, strength, and memory. Even after reaching a certain level of frailty, they continued to live longer than untreated mice, suggesting that the treatment not only prolonged life but also helped maintain function.

In contrast, the same treatment did not improve lifespan or general health in female mice. However, when administered to middle-aged females, the treatment enhanced fertility. This suggests that biological sex and timing may significantly influence how the treatment works.

The Impact: Multi-Target Strategies for Addressing Aging

Although this research was conducted in mice, it adds valuable insight to a growing field focused on coordinated, multi-target approaches to aging. Both oxytocin and Alk5 inhibitors are already being studied or used in clinical settings for other conditions, which means their safety profiles are at least partially understood. This opens the door for future studies exploring whether similar treatments could be applied to human aging.

Future Perspectives and Conclusion

This study presents a promising model for how aging could be addressed through balanced therapeutic strategies. It also highlights the importance of understanding sex-specific responses to treatment. The effectiveness of the therapy in males, and the fertility response in females, point to the need for personalized approaches in future research.

While more studies are necessary to determine whether these findings can be translated to humans, the results suggest that even in later stages of life, it may be possible to improve health and resilience by restoring balance in the body’s signaling systems.

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).

Click here to subscribe to Aging publication updates.

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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).

Click here to subscribe to Aging publication updates.

For media inquiries, please contact [email protected].

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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).

Click here to subscribe to Aging publication updates.

For media inquiries, please contact [email protected].

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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).

Click here to subscribe to Aging publication updates.

For media inquiries, please contact [email protected].

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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).

Click here to subscribe to Aging publication updates.

For media inquiries, please contact [email protected].

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Now Accepting Submissions: Special Collection on Cognitive Aging

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

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

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

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

POTENTIAL TOPICS

Molecular and Cellular Mechanisms

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

 Genetics and Biomarkers

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

Interventions and Lifestyle Factors

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

Environmental and Social Contexts

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

SUBMISSION DETAILS:

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

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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).

Click here to subscribe to Aging publication updates.

For media inquiries, please contact [email protected].

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