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Aging-US Supports the NOVA Conference 2026

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Aging-US proudly sponsored the NOVA (Neuroscience of Vitality and Aging) Conference, hosted by the Aging Initiative on Saturday, April 25 in Boston, MA.

Highlights from the NOVA (Neuroscience of Vitality and Aging) Conference

On April 25, 2026, the NOVA (Neuroscience of Vitality and Aging) Conference brought together a dynamic and interdisciplinary audience in Boston, MA. With over 600 attendees spanning students, researchers, clinicians, investors, and patient advocates, the event highlighted both the complexity of brain aging and the growing momentum behind efforts to better understand and treat neurodegenerative diseases.

In the opening keynote, Dr. Joanne Smikle of the American Brain Foundation emphasized the need to remember the “why” behind this research. She highlighted the power of intentional collaboration and the belief that breakthroughs in one neurological disease may translate to others. Even small monthly contributions as little as $10.00 can collectively drive meaningful progress.

Clinical Progress in Neurodegeneration

Dr. John Sims of Eli Lilly & Company, noted that traditional measures, such as clinical dementia ratings, may be too blunt to capture early cognitive decline. Emerging approaches, such as learning-based assessments and digital cognitive tools, aim to detect subtle changes sooner and more accurately.

Studying the Biology of Brain Aging with New Tools

This breakout session showcased cutting-edge tools transforming how scientists study the aging brain.  Researchers included Dr. Stuart Lipton from Scripps Research, Dr. Eric Sun from MIT, Dr. Jiang He from Vizgen, Dr. Ed Boyden from the McGovern Institute at MIT, and Dr. David Salat from Harvard Medical School. Overall, the researchers are focused on causal models, the importance of needing more high-quality data, and spatial mapping technologies to better understand cellular interactions and disease mechanisms. Additionally, continued advances in molecular imaging, organoid development, and neuroimaging enable more detailed insights into how the brain changes over time. The speakers did stress the importance of rigor (particularly in validating experimental models and ensuring data quality) to draw any meaningful conclusions.

Mainstage Presentations

These presentations highlighted both the promise and challenges of advancing longevity science. Raiany Romanni-Klein of Amaranth emphasized a critical paradox: while human lifespan continues to increase, many individuals spend more years in declining health. From an investment perspective, Michael Reisman of Centerview Partners and Second Century Foundation noted that longevity science is increasingly attracting attention from the financial sector. While past biotech ventures in aging have seen mixed outcomes, the field continues to evolve, with increasing focus on translating biological insights into real-world interventions.

Neurotechnology and Brain-Computer Interfaces

One of the most forward-looking discussions centered on neurotechnology and brain-computer interfaces (BCIs), panelists included Christian Howell of Cognito Therapeutics, Dr. Oliver Armitage from Axoft, Dr. Daniel Rizzuto of Nia Therapeutics, Dr. Alan Mardinly from Science Corp., and Dr. Leigh Hochberg from BrainGate and Massachusetts General Hospital.

The speakers described emerging approaches that use sensory stimulation or implantable devices to preserve or restore brain function. Innovations in this space are already demonstrating tangible benefits. Early studies suggest that closed-loop neurostimulation systems may significantly improve memory performance, while implantable BCIs are enabling patients with severe impairments to communicate and interact with their environment. Despite these advances, challenges remain, including regulatory pathways, reimbursement models, the need for scalable and  patient-centered deployment, and collaboration in terms of sharing ideas between industries and regulators, in technology, and throughout our community.

Still, the outlook is promising. As Dr. Hochberg noted, the field is moving quickly, envisioning a future where, in just ten years, patients with conditions such as ALS may retain the ability to communicate through advanced neurotechnologies.

Investment Landscape

The conference also explored the evolving investment landscape in aging and longevity science. Speakers of this panel included Dr. Alex Colville of age1, Dr. Daniel Carbonero from PsyMed Ventures, Dr. Jarod Rutledge from Starbloom Capital, and Karen Harris from the Alzheimer’s Drug Discovery Foundation.

Although previous biotech efforts have yielded mixed results, confidence is growing that targeting the biology of aging is both scientifically feasible and financially promising. Investors emphasized the importance of strong founding teams and highlighted areas of interest such as neuroinflammation, genetic medicine, and biomarker development. Blood-based biomarkers, in particular, were identified as critical tools for improving clinical trial design and patient stratification.

Repair and Regeneration

Panelists of this important discussion included Dr. Mark Tomishima of BlueRock Therapeutics, Dr. Jean Hebert from ARPA-H, Dr. Nabiha Saklayen of Cellino, Dr. Parastoo Khoshakhlagh of GC Therapeutics, and Dr. Abdulkader Rahmo from SMS Biotech, Inc.

Speakers on repair and regeneration highlighted the potential of cell and tissue-based therapies to address age-related decline. Advances in automation, scalability, and precision are making neuroreplacement strategies more feasible, though cost and access remain significant challenges, and prevention remains key.

Equally important was the focus on patient advocacy. Speakers stressed the need to incorporate patient and caregiver perspectives into research and clinical trials, ensuring that scientific progress aligns with real-world needs and experiences.

Patient Advocacy

A powerful breakout session on patient advocacy emphasized the importance of integrating lived experiences into research and clinical development.

Kevin Rhodes of the Association for Frontotemporal Degeneration (AFTD), who is living with frontotemporal dementia, highlighted the session as he underscored the challenges of diagnosis and access. With advanced imaging often required for confirmation, many patients face barriers to timely diagnosis. He emphasized the need for stronger connections between patients and biotechnology companies, enabling researchers to better understand patient needs while helping individuals identify and access clinical trials.

The perspectives discussed overall highlighted a critical shift in the field: advancing brain aging research will require not only scientific innovation, but also meaningful engagement with the individuals most directly affected.

Looking Ahead

The conference concluded with a keynote by Dr. Dennis Selkoe from the Ann Romney Center for Neurologic Diseases, discussing the biology of Alzheimer’s disease and ongoing efforts to target amyloid-related mechanisms through immunotherapy. With millions affected worldwide, the urgency of advancing effective treatments remains clear.

Next year’s event will be the Cardiovascular Aging Research & Development (CARD) Symposium on May 6, 2027, with Opening Keynote Speaker Dr. John Maraganore of Alnylam.

Overall, the NOVA Conference highlighted a field that is rapidly evolving and is driven by technological innovation, interdisciplinary collaboration, and a shared commitment to improving outcomes for aging populations. As research continues to advance, the integration of science, investment, and patient engagement will be essential to translating discoveries into meaningful impact.

Photo Credit: Tony Zhang
Photo Credit: Tony Zhang
Photo Credit: Tony Zhang
Photo Credit: Tony Zhang
Photo Credit: Tony Zhang
Photo Credit: Tony Zhang
Photo Credit: Tony Zhang
Photo Credit: Tony Zhang
Photo Credit: Tony Zhang
Photo Credit: Tony Zhang
Photo Credit: Tony Zhang
Photo Credit: Tony Zhang
Photo Credit: Tony Zhang
Photo Credit: Tony Zhang
Photo Credit: Tony Zhang
Photo Credit: Tony Zhang
Photo Credit: Tony Zhang
Photo Credit: Tony Zhang
Photo Credit: Tony Zhang
Photo Credit: Tony Zhang
Photo Credit: Tony Zhang
Photo Credit: Tony Zhang
Photo Credit: Tony Zhang
Photo Credit: Tony Zhang
Photo Credit: Tony Zhang
Photo Credit: Tony Zhang
Photo Credit: Tony Zhang
Photo Credit: Tony Zhang
Photo Credit: Tony Zhang
Photo Credit: Tony Zhang

Our Continued 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 NOVA Conference 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-US 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-US publication updates.

For media inquiries, please contact [email protected].

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IL6 and IL6R: Opposing Forces of Inflammation That Shape Human Survival

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“The IL6 axis plays a pivotal role in both acute and chronic inflammatory responses, operating through two distinct pathways: classical signalling via a membrane-bound IL6 receptor and trans-signalling mediated by a soluble IL6 receptor (IL6R), which enables IL6 activity in cells lacking the membrane receptor.”

Inflammation is a double-edged sword. It defends the body against infection and injury, yet when it becomes chronic, it can accelerate aging and fuel the very diseases that shorten human life. For decades, scientists have observed that people with higher levels of inflammatory markers like interleukin-6 (IL6) and C-reactive protein (CRP) tend to have shorter lifespans. But the critical question has always been: does inflammation cause mortality, or does it merely reflect underlying disease?

A research paper, titled “Causal effects of inflammation on long-term mortality: A mendelian randomization study” was published in  Volume 18 of Aging-US by an international team of researchers, provides a definitive answer by using a powerful genetic technique to untangle cause from effect.

The team’s investigation demonstrates that the IL6 inflammatory pathway has a direct causal impact on human survival—but with a surprising twist: two components of the same pathway pull in opposite directions.

The Method: Mendelian Randomization

To establish causation, the researchers employed Mendelian randomization (MR), a technique that uses genetic variants as natural experiments. Because genes are randomly assigned at conception and fixed throughout life, they are not subject to the confounding factors—such as lifestyle, diet, or socioeconomic status—that plague traditional observational studies.

The team analyzed genetic data from approximately 750,000 individuals of European ancestry, focusing on four inflammatory biomarkers: interleukin-6 (IL6), its soluble receptor (IL6R), C-reactive protein (CRP), and growth differentiation factor-15 (GDF15). The primary outcome was all-cause mortality over a median follow-up of 11.7 years, with secondary outcomes including cardiovascular events and cancer.

Key Findings: Opposing Forces in the IL6 Pathway

The results revealed a remarkable biological duality. Genetically higher levels of the soluble IL6 receptor (IL6R) were associated with a reduced risk of all-cause mortality (odds ratio 0.95 per 1-standard deviation increase; p = 0.007). Higher IL6R levels also lowered the risk of atrial fibrillation, coronary artery disease, stroke, and lung cancer.

In stark contrast, genetically higher levels of IL6 itself were linked to an increased risk of mortality (odds ratio 1.05; p = 0.002). These findings suggest that IL6 and IL6R are biological opposites: IL6 drives harm, while IL6R protects.

The protective effects of IL6R were consistent across multiple sensitivity analyses, with no evidence of pleiotropy (where genetic variants influence outcomes through unintended pathways). A cis-Mendelian randomization analysis restricted to variants within the IL6R gene locus confirmed the protective association, reinforcing the causal relevance of this pathway.

CRP and GDF15: Biomarkers, Not Drivers

Notably, neither CRP nor GDF15 showed any significant causal effect on mortality or cardiovascular outcomes. Despite their well-established epidemiological associations with disease, these markers appear to be downstream indicators of inflammation rather than active drivers. As the authors note, this distinction is critical: CRP and GDF15 may be useful for predicting risk, but they are not themselves targets for intervention.

The Biological Mechanism: Classical vs. Trans-Signaling

The opposing effects of IL6 and IL6R are explained by the unique biology of the IL6 pathway. IL6 signals through two distinct routes. Classical signaling occurs when IL6 binds to membrane-bound IL6 receptors on certain cell types. Trans-signaling, however, occurs when IL6 binds to soluble IL6 receptors (sIL6R), allowing it to act on cells that lack membrane-bound receptors—including vascular and myocardial cells.

The genetic variants associated with higher sIL6R levels shift the balance away from trans-signaling, effectively dampening the inflammatory effects of IL6 in cardiovascular tissues. This reduces vascular inflammation, endothelial dysfunction, and thrombotic risk—mechanisms that directly contribute to atrial fibrillation, coronary artery disease, and stroke.

Clinical Implications: A Precision Target for Prevention

These findings have direct implications for drug development. IL6 receptor antagonists such as tocilizumab are already approved for inflammatory conditions like rheumatoid arthritis and giant cell arteritis, and have shown survival benefits in severe COVID-19. The genetic evidence presented here suggests that targeting IL6R could be an effective strategy for preventing cardiovascular disease and reducing mortality in high-risk populations.

Importantly, the neutral findings for CRP and GDF15 argue against broad anti-inflammatory approaches that target downstream markers. Instead, precision targeting of the IL6 signaling pathway—specifically through modulation of trans-signaling—appears to offer a more focused and potentially safer therapeutic avenue.

Limitations and Future Directions

The authors acknowledge several limitations. The analysis was restricted to individuals of European ancestry, which may limit generalizability to other populations. Additionally, while the study identified cardiovascular mechanisms as key mediators of IL6R’s mortality benefits, other potential pathways—such as metabolic or inflammatory diseases—remain to be explored.

Future research should focus on validating these findings in more diverse populations and conducting dedicated cardiovascular prevention trials with IL6R antagonists. The long-term safety of such interventions also warrants careful evaluation.

Future Perspectives and Conclusion

This study does not merely confirm that inflammation matters for longevity. It goes further, identifying a specific molecular axis—IL6 and its receptor—as a causal driver of human survival, with one component harming and the other protecting.

The perspective that emerges is one where the immune system’s inflammatory machinery can be precisely tuned. Rather than broadly suppressing inflammation—which could impair host defense—targeting IL6 trans-signaling offers a way to reduce cardiovascular risk while preserving essential immune functions.

As the authors conclude, “These results support IL6R antagonism as a potential strategy for cardiovascular disease prevention.” In an era where cardiovascular disease remains the leading cause of death globally, this genetic evidence provides a clear roadmap for translating inflammation biology into clinical practice.

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

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Aging-US 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-US publication updates.

For media inquiries, please contact [email protected].

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Acknowledgment of 2025 Reviewers

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Aging-US sincerely thanks all reviewers who contributed their expertise and time during 2025.

Rigorous and constructive peer review is essential to scientific progress. Through their careful evaluations, our reviewers played a central role in maintaining the scientific quality, integrity, and credibility of the journal.

Their efforts also directly support one of the core missions of Aging-US, which is to increase the visibility and impact of high-quality research in the biology of aging and age-related disease.

We are deeply grateful for this commitment to excellence and to the aging research community, and we look forward to continued collaboration in the coming year.

–Marco Demaria
Editor-in-Chief, Aging-US

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Aging-US 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-US publication updates.

For media inquiries, please contact [email protected].

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How Aging Leads to Disease: New Two-Stage Model Explains Age-Related Illness

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“Here we propose a general account of how different determinants of aging can interact to generate late-life disease.”

BUFFALO, NY — January 20, 2026 — A new review was published in Volume 17, Issue 12 of Aging-US on December 30, 2025, titled “Aging as a multifactorial disorder with two stages.”

“This article is a contribution to the special issue of Aging celebrating the life and work of Misha Blagosklonny (more formally, Mikhail Vladimirovich Blagosklonny), who died in October 2024.”

In this review, David Gems and Alexander Carver from University College London, together with Yuan Zhao from Queen Mary University of London, present a new theoretical model to explain how aging leads to the development of chronic diseases. Drawing on evolutionary theory and biological research, the authors propose that aging is driven by a combination of early-life damage and harmful genetic activity in later life. This framework helps explain why diseases such as cancer, arthritis, and infections often appear in old age and offers insight into how they might be prevented.

Aging is the biggest risk factor for most chronic diseases, but the biological reasons for this association are still debated. The authors address this by introducing a two-stage model. In the first stage, individuals experience disruptions early in life, such as infections, injuries, or genetic mutations. Although the body can often contain or repair this damage, it does not fully eliminate it. In the second stage, which begins in later life, normal genetic processes begin to act in ways that are no longer beneficial. These late-life changes weaken the body’s ability to contain earlier damage, allowing it to develop into disease.

The review emphasizes that aging is a multifactorial process, shaped by many interacting causes rather than a single underlying mechanism. The model suggests that early-life disruptions and later-life genetic activity work together to drive age-related diseases. For example, dormant viruses can re-emerge as infections like shingles due to weakened immunity in older adults. Similarly, injuries to joints in youth can lead to osteoarthritis as tissues change with age. Inherited mutations may also remain silent for decades before contributing to conditions such as cancer or fibrosis later in life.

This two-stage model builds on long-standing ideas from evolutionary biology, particularly the theory that aging occurs because natural selection has less influence in later life. The authors also draw on studies in the roundworm Caenorhabditis elegans, where early mechanical damage can lead to fatal infections in old age, suggesting similar patterns may occur in humans.

Overall, this review presents a new framework for understanding how different causes of aging interact over time. By identifying two key stages, early-life damage and late-life genetic activity, it highlights potential strategies for promoting healthier aging through prevention and targeted intervention.

Paper DOI: https://doi.org/10.18632/aging.206339

Corresponding author: David Gems – [email protected]

Keywords: aging, C. elegans, disease, hyperfunction, multifactorial model

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How Two Russian Scientists Changed the Way We Understand Aging and Cancer

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“Here, conceptual similarities between Mikhail Blagosklonny’s hyperfunction theory of aging and Vladimir Dilman’s elevation theory of aging are considered.”

BUFFALO, NY — December 3, 2025 — A new essay was published in Volume 17, Issue 11 of Aging-US on November 19, 2025, titled “On the intergenerational transfer of ideas in aging and cancer research: from the hypothalamus according to V.M. Dilman to the mTOR protein complex according to M.V. Blagosklonny.”

In this work, Aleksei G. Golubev from the N.N. Petrov National Medical Research Center of Oncology reflects on the legacy of two influential Russian scientists, Vladimir M. Dilman and his son Mikhail V. Blagosklonny, who each introduced groundbreaking ideas about aging and cancer. Drawing from his own experience working in Dilman’s lab, Golubev explores how their ideas remain deeply relevant to today’s scientific understanding.

The essay connects Dilman’s “elevation theory” with Blagosklonny’s “hyperfunction theory,” two frameworks that challenge the conventional view of aging as a process of decline. Instead, both propose that aging results from continued biological processes that once supported growth but eventually become harmful when left unchecked.

Dilman believed that aging begins with reduced sensitivity in the hypothalamus, a brain region that regulates the body’s balance. This desensitization disrupts metabolism and hormone levels, setting the stage for many chronic illnesses. Decades later, Blagosklonny expanded on this idea at the molecular level. Central to his theory is the mTOR protein complex, which regulates growth and metabolism and is now a major focus in aging research.

Golubev also explores the historical and personal connections between the two scientists. Dilman, an endocrinologist trained in the Soviet Union, and Blagosklonny, a molecular biologist educated during the post-Soviet period, represent two generations shaped by a shared scientific tradition. 

“Dilman’s scientific legacy is not as well recognized as it should be, partly due to bias in citation practices.”

The essay also draws attention to a troubling trend in science: the tendency to overlook early contributions, especially from non-Western scholars. Many of Dilman’s insights, such as the connection between high blood sugar, insulin resistance, and cancer, have since been validated by modern tools, yet his work is rarely cited. Golubev points out how citation practices, language barriers, and historical isolation have contributed to this lack of recognition.

Finally, Golubev encourages the scientific community to look back and acknowledge the foundational work that shaped modern aging science. It also highlights the importance of cross-generational knowledge in moving science forward. By tracing the intellectual journey from hormonal regulation in the brain to molecular pathways in cells, this essay demonstrated the relevance of old ideas in a new biological era.

Paper DOI: https://doi.org/10.18632/aging.206338

Corresponding author: Aleksei G. Golubev – [email protected]

Keywords: aging, gerontology, history of science, hyperfunction, mTOR, hypothalamus, cancer, metabolism, immunity.

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

Click here to subscribe to Aging-US publication updates.

For media inquiries, please contact [email protected].

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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).

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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Aging Sponsors Open Access Team in 2025 Ride for Roswell

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Impact Journals, the publisher of Aging, is once again proudly sponsoring the Open Access Team in the annual Ride for Roswell.


BUFFALO, NY — June 10, 2025 — The Ride for Roswell, one of the USA’s largest cycling events supporting cancer research, returns to Buffalo on Saturday, June 28, 2025. Hosted annually by Roswell Park Comprehensive Cancer Center, this community-wide event brings together riders, volunteers, and supporters to raise funds for cancer research, celebrate survivors, and honor those lost to the disease. 

Among the returning participants is the Open Access Team, led by team captain Sergei Kurenov. This year, the team is once again proudly sponsored by Impact Journals, the publisher of open access journals Aging, Oncotarget, Genes & Cancer, and Oncoscience.

“For the last 10 years, I have continuously participated in the Ride for Roswell in honor of those who have bravely fought cancer,” said Kurenov. “This journey is deeply personal for me. My father battled cancer, and some of my closest friends have fought through prostate and lung cancer with incredible strength.”

This year, the Open Access Team rides in honor of Dr. Mikhail (Misha) Blagosklonny, a visionary scientist who dedicated his career to advancing cancer and aging research. As the founding Editor-in-Chief of Aging, Oncotarget and Oncoscience, Dr. Blagosklonny was a pioneer of open-access publishing. His groundbreaking work on mTOR signaling and rapamycin transformed our understanding of cancer biology and healthy lifespan extension.

The 2025 Ride for Roswell features nine route options, ranging from 4 to 100 miles, all beginning at the University at Buffalo North Campus. Riders from across the USA and beyond are invited to participate and make a meaningful impact in the fight against cancer.

This ride is more than just a journey on two wheels—it’s a commitment to building a future where no one has to fear a cancer diagnosis. There is still time to support the Open Access Team in the 2025 Ride for Roswell. Whether by donating, joining the team, or sharing their story, every action brings us closer to better treatments, deeper understanding, and, ultimately, a cure.

Visit the Open Access Team page to join or donate today.

Click here to learn more about the 2025 Ride for Roswell.

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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:

Click here to subscribe to Aging publication updates.

For media inquiries, please contact [email protected].

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Longevity & Aging Series Wins Silver Award for Excellence in Video/Film at SSP EPIC Awards

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The EPIC Awards recognize the achievements of those who are advancing scholarly publishing through creativity, collaboration, and cutting-edge innovation.

Buffalo, NY — June 4, 2025 — The Longevity & Aging Series has been honored with the Silver Award for “Excellence in Video/Film” at the inaugural EPIC Awards celebration on May 29, 2025, during the Society for Scholarly Publishing (SSP) 47th Annual Meeting in Baltimore, Maryland.

The EPIC Awards recognize the achievements of those who are advancing scholarly publishing through creativity, collaboration, and cutting-edge innovation. The Longevity & Aging Series, hosted by Aging (Aging-US) Editorial Board member Dr. Evgeniy Galimov, stood out for its impactful storytelling, production quality, and commitment to advancing understanding in the field of aging research.

The Longevity & Aging Series brings together leading experts to discuss the latest developments in the biology of aging, healthy longevity, and interventions to improve healthspan. Now in its third season, the series is a trusted resource for scientists, clinicians, and the broader public interested in the future of aging research.

For more information about the Aging (Aging-US) Longevity & Aging Series and to view the award-winning videos, please visit our show page or YouTube channel. If you are interested in becoming a guest or would like to know more about the series, please email us at [email protected].

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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:

Click here to subscribe to Aging publication updates.

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Call for Papers: Commemorative Collection Honoring Dr. Judith Campisi

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Dr. Judith Campisi

“This collection is published in memory of Professor Judith Campisi, a pioneering force in the field of cellular senescence whose groundbreaking work shaped the understanding of senescence in aging, cancer, and tissue homeostasis.”

BUFFALO, NY — May 1, 2025 — Aging (Aging-US) invites submissions for a Special Collection dedicated to the theme of cellular senescence, spanning its basic mechanisms, physiological and pathological functions, and clinical applications.

This collection is published in memory of Professor Judith Campisi, a pioneering force in the field of cellular senescence whose groundbreaking work shaped the understanding of senescence in aging, cancer, and tissue homeostasis. Her legacy continues to inspire generations of scientists working to decode the complex biology of senescent cells and their impact on health and disease.

We welcome original research articles, reviews, and perspectives on topics including:

  • Fundamental mechanisms of senescence induction and maintenance
  • Regulation and context-specific roles of the senescence-associated secretory phenotype (SASP)
  • Beneficial and detrimental effects of senescent cells in vivo
  • Senescence in development, aging, regeneration, and age-related diseases
  • Biomarkers, imaging, and tools for senescence detection and quantification
  • Therapeutic targeting of senescent cells: senolytics, senomorphics, and clinical translation

This Special Collection is guest edited by Han Li and Irina Conboy, both internationally recognized leaders in the study of senescence and aging.

Submission Details:

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