BUFFALO, NY — June 16, 2026 — A new #research paper was #published in Volume 18 of Aging on May 22, 2026, titled “Systemic cancer risk profile in neovascular age-related macular degeneration: insights into shared aging-related mechanisms from a nationwide population-based study.”

The study was led by first author Hyeong Min Kim and corresponding author Hyewon Chung from Konkuk University College of Medicine and Konkuk University Medical Center in Seoul, Republic of Korea.

Neovascular age-related macular degeneration (nAMD) is one of the leading causes of severe vision loss in older adults. Although the disease primarily affects the retina, researchers increasingly recognize that it may reflect broader biological processes associated with aging, including chronic inflammation, vascular dysfunction, and immune dysregulation. These same mechanisms have also been implicated in the development of several cancers, raising questions about whether the two conditions may be biologically connected.

To explore this possibility, investigators analyzed data from the Korean National Health Insurance Service, one of the world’s largest population-based healthcare databases. The study included 334,091 individuals aged 50 years and older, including 83,742 patients with nAMD and 250,349 matched controls without the disease. Participants were followed for up to 10 years, allowing researchers to evaluate both overall cancer incidence and risks for specific cancer types.

The analysis revealed that individuals with nAMD had a modest but statistically significant increase in overall cancer risk compared with matched controls. However, the increased risk was not observed across all cancers. Instead, patients with nAMD showed elevated risks for several specific malignancies, including thyroid, kidney, pancreatic, lung, bladder, and prostate cancers, while no significant associations were found for many other cancer types.

Full press release - https://aging-us.net/2026/06/16/common-aging-mechanisms-may-link-vision-loss-disorder-to-increased-risk-of-certain-cancers/

DOI - https://doi.org/10.18632/aging.206383

Corresponding author - Hyewon Chung - [email protected]

Abstract video - https://www.youtube.com/watch?v=hViOqGLYr1Y

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Keywords - aging, neovascular age-related macular degeneration, cancer, population cohort, polygenic risk, shared susceptibility

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BUFFALO, NY — June 11, 2026 — A new #meetingreport was #published in Volume 18 of Aging on May 14, 2026, titled “Foundations of Gerophysics.”

The report was led by corresponding authors Maximilian Unfried and Brian K. Kennedy from the National University of Singapore.

Aging is often studied through biology, genetics, and medicine. Yet despite tremendous advances, many fundamental questions remain unanswered: Why do organisms age at different rates? Why does resilience decline over time? And can the trajectory of aging be predicted before disease develops? Researchers participating in the inaugural Global Conference on Gerophysics explored whether answering these questions may require integrating biology with the quantitative principles of physics.

Held in Singapore on March 5–6, 2025, the conference brought together 160 researchers from physics, biology, computation, and medicine and featured 31 speakers from institutions around the world. The meeting focused on developing a predictive and testable science of aging by applying concepts from dynamical systems, thermodynamics, network theory, stochastic processes, and artificial intelligence to biological aging.

Full press release - https://aging-us.net/2026/06/11/physics-meets-aging-researchers-lay-the-foundations-of-gerophysics/

DOI - https://doi.org/10.18632/aging.206378

Corresponding authors - Maximilian Unfried - [email protected], and Brian K. Kennedy - [email protected]

Abstract video - https://www.youtube.com/watch?v=hgsA8EhjF0U

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Keywords - gerophysics, geroscience, aging biology, longevity, complex systems, theoretical physics

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BUFFALO, NY — June 10, 2026 — A new #research paper was #published in Volume 18 of Aging on May 18, 2026, titled “Transcriptional programs diverge in aging mouse and human skeletal muscle.”

The study was led by co-first authors Charles D. Hwang and Siti Rahmayanti and corresponding author Indranil Sinha from Brigham and Women’s Hospital, Harvard University.

Aging is widely associated with the gradual loss of muscle mass, strength, and physical function. Much of what scientists know about these changes comes from studies in laboratory mice, which are frequently used to investigate the biological mechanisms of aging and to identify potential therapeutic targets. However, an important question remains: how closely do aging-related changes in mouse muscle reflect what actually occurs in humans?

To address this question, researchers performed a detailed comparison of gene expression patterns in skeletal muscle from young and old mice and humans. The team analyzed RNA sequencing data from mouse gastrocnemius muscle and compared it with transcriptomic data from healthy young and older adults obtained through the National Institute on Aging’s GESTALT study.

The results revealed substantial differences between the two species. Despite both mice and humans experiencing age-related muscle decline, fewer than 5% of significantly altered biological pathways were shared between them. Many of the genetic programs that changed with aging in mice showed little resemblance to those observed in human skeletal muscle.

Full press release - https://aging-us.net/2026/06/10/aging-muscle-follows-different-genetic-programs-in-mice-and-humans/

DOI - https://doi.org/10.18632/aging.206382

Corresponding author - Indranil Sinha - [email protected]

Abstract video - https://www.youtube.com/watch?v=CYKh4X1w8H0

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Keywords - hypoxia, angiogenesis, aging, skeletal muscle, regeneration

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Why do some people appear to age faster than others, even when they are the same age? Researchers increasingly believe that chronological age tells only part of the story. Biological age attempts to capture how well the body’s systems are functioning and may provide a more meaningful picture of overall health.

A research paper on this topic was published in Volume 18 of Aging titled “Blood biochemical and gut microbiotic neural network models forecasting human biological age.” In the study, Russian researchers explored whether information from routine blood tests and the gut microbiome could be used to estimate biological age.

Full blog - https://aging-us.org/2026/06/blood-tests-and-gut-bacteria-may-help-reveal-your-biological-age/

DOI - https://doi.org/10.18632/aging.206360

Corresponding author - Alexey Moskalev - [email protected]

Abstract video - https://www.youtube.com/watch?v=wg3YEwXMKWY

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Keywords - aging, biological age, blood biochemistry, gut microbiome, neural network

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BUFFALO, NY — June 5, 2026 — A new #review was #published in Volume 18 of Aging on May 15, 2026, titled “Blue period – features of senescence 30 years after beta-galactosidase.”

The review was led by first author Chisaka Kuehnemann and corresponding author Christopher D. Wiley from Tufts University.

Cellular senescence has emerged as one of the most important biological processes linked to aging and age-related disease. Senescent cells stop dividing in response to stress or damage, yet they remain metabolically active and release a variety of signaling molecules that can influence surrounding tissues. Over the past three decades, evidence has increasingly shown that the accumulation of these cells contributes to chronic inflammation, tissue dysfunction, and many degenerative conditions associated with aging.

In this review, the authors examine how the field has evolved since the landmark discovery of senescence-associated beta-galactosidase (SA-β-gal) in 1995. That finding provided one of the first practical methods for identifying senescent cells and helped establish that these cells accumulate in aging tissues. Since then, researchers have identified numerous additional characteristics of senescence and developed new approaches to study their role in health and disease.

The review highlights several major features now recognized as hallmarks of senescent cells. These include stable proliferative arrest, increased lysosomal activity, secretion of inflammatory and signaling molecules collectively known as the senescence-associated secretory phenotype (SASP), mitochondrial dysfunction, alterations in nuclear architecture, accumulation of metals and lipofuscin, and enhanced survival despite exposure to cellular stress.

Full press release - https://aging-us.net/2026/06/05/thirty-years-after-the-discovery-of-sa-%ce%b2-gal-researchers-revisit-the-hallmarks-of-cellular-senescence/

DOI - https://doi.org/10.18632/aging.206380

Corresponding author - Christopher D. Wiley - [email protected]

Abstract video - https://www.youtube.com/watch?v=lfMPJF6No7M

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Keywords - aging, senescence, biomarkers, SASP, cell death

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BUFFALO, NY — June 3, 2026 — A new #research paper was #published in Volume 18 of Aging-US on May 15, 2026, titled “Extracellular vesicles released by senescent myoblasts affect recipient cells via miRNA-target interactions.”

The study was led by first author Michael Kamal from the Department of Kinesiology at McMaster University and corresponding author Gianni Parise from the same university.

As people age, skeletal muscle gradually loses strength, size, and regenerative capacity. Scientists have increasingly linked these changes to cellular senescence—a state in which damaged cells permanently stop dividing but remain metabolically active. These senescent cells release a complex mixture of signaling molecules known as the senescence-associated secretory phenotype (SASP), which can influence neighboring cells and contribute to tissue dysfunction.

In this study, the researchers investigated whether extracellular vesicles (EVs)—tiny membrane-bound particles released by cells—play a role in this process. Specifically, they examined EVs released by senescent muscle precursor cells, known as myoblasts, and analyzed the microRNAs (miRNAs) carried within these vesicles.

The team found that senescent myoblasts released factors that impaired normal muscle cell development. When healthy muscle cells were exposed to signals from senescent cells, the resulting muscle fibers became significantly smaller and displayed increased expression of genes associated with cellular stress and senescence.

Further analysis revealed that EVs released by senescent myoblasts carried a distinct set of miRNAs. The researchers identified 22 significantly altered miRNAs, including several previously linked to cellular senescence, such as miR-34a, miR-34b, miR-34c, and miR-22. The study also identified miR-301a-3p as a potentially novel senescence-associated miRNA.

Full press release - https://aging-us.net/2026/06/03/senescent-muscle-cells-send-molecular-messages-that-may-contribute-to-age-related-muscle-decline/

DOI - https://doi.org/10.18632/aging.206379

Corresponding author - Gianni Parise - [email protected]

Abstract video - https://www.youtube.com/watch?v=HKBbraYg8ew

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Keywords - aging, cellular senescence, extracellular vesicles, myoblasts, miRNA, multi-omics

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BUFFALO, NY — May 27, 2026 — A new #research paper was #published in Volume 18 of Aging-US on May 8, 2026, titled “The mediating role of DNA methylation clocks in associations of race, ethnicity, education, income, and occupation with mortality: findings from NHANES 1999-2002.”

The study was led by first and corresponding author Hanyang Shen from the Department of Epidemiology and Population Health at Stanford University. In this study, the authors investigated whether DNA methylation aging biomarkers—often called epigenetic aging clocks—may help explain how social inequalities become biologically embedded and contribute to differences in mortality risk. Social factors such as race, ethnicity, educational attainment, household income, and occupation have long been associated with disparities in health outcomes and life expectancy. However, the biological mechanisms linking these social exposures to long-term disease risk and mortality remain incompletely understood.

Using nationally representative data from 2,402 adults in the U.S. National Health and Nutrition Examination Survey (NHANES) 1999–2002 linked to mortality follow-up data through 2019, the researchers examined thirteen different DNA methylation biomarkers alongside traditional clinical and behavioral risk factors. The study evaluated whether these epigenetic aging measures mediated associations between social stratification factors and all-cause mortality.

The findings showed that several DNA methylation clocks significantly mediated the relationship between social disadvantage and mortality risk. Among all biomarkers examined, GrimAge2 consistently demonstrated the strongest mediation effects, accounting for up to 52% of mortality disparities in some occupational comparisons. DunedinPoAm, a pace-of-aging biomarker, also demonstrated substantial mediation effects across multiple socioeconomic categories.

Importantly, the mediation effects observed for several DNA methylation biomarkers frequently exceeded those of traditional clinical risk factors measured in the study, including C-reactive protein and cholesterol-related markers. The results suggest that epigenetic aging measures may capture the cumulative biological effects of multiple social, environmental, behavioral, and physiological stressors simultaneously.

“Among all the 13 DNA methylation biomarkers available in NHANES, GrimAge2 consistently exhibited the strongest positive mediation capturing the social disparities on mortality up to 52% (95%CI: 26%-128%), followed by the DunedinPoAm.”

Full press release - https://aging-us.net/2026/05/27/dna-methylation-clocks-may-help-explain-how-social-inequality-influences-mortality/

DOI - https://doi.org/10.18632/aging.206377

Corresponding author - Hanyang Shen - [email protected]

Abstract video - https://www.youtube.com/watch?v=XObIyirTJok

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Keywords - aging, race and ethnicity, social position, epigenetic aging, mediation analysis, mortality disparities

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BUFFALO, NY — May 20, 2026 — A new #editorial was #published in Volume 18 of Aging-US on May 18, 2026, titled “Public health in the age of longevity interventions: from prevention to system-wide resilience.”

The editorial was authored by Jochen Mierau from the University of Groningen and Aging-US Editor-in-Chief Marco Demaria from the University of Groningen and European Research Institute for the Biology of Ageing (ERIBA). In this editorial, the authors examine how modern public health systems may need to evolve as aging populations increasingly face chronic disease, frailty, multimorbidity, and progressive loss of function rather than the acute infectious diseases that shaped 20th-century medicine.

The authors argue that many of the greatest gains in human lifespan historically came not from advanced medical technologies, but from broad public health interventions such as sanitation, vaccination, improved nutrition, occupational safety, safer housing, and access to education. While these measures remain essential, they suggest that modern aging societies now face a different challenge: extending healthspan alongside lifespan.

The editorial highlights how today’s health risks accumulate gradually across the life course through environmental, metabolic, social, and behavioral exposures. Ultra-processed foods, pollution, tobacco, alcohol, sedentary lifestyles, climate-related stressors, and social isolation are described as contributors to accelerated biological aging and increased vulnerability to chronic disease. The authors emphasize that these interconnected exposures cannot be fully addressed through disease-specific treatment alone.

“Rather than representing separate or competing domains, these approaches should be viewed as complementary components of a unified strategy to improve population health across aging societies.”

A major focus of the article is the growing scientific interest in longevity-directed interventions that target core biological mechanisms of aging. The authors discuss pathways including cellular senescence, chronic inflammation, metabolic dysfunction, and impaired proteostasis, noting that interventions directed at these processes may help delay or modify multiple age-related diseases simultaneously rather than treating each condition individually after it emerges.

Importantly, the editorial emphasizes that longevity interventions should not replace either public health or conventional clinical medicine. Instead, the authors propose a coordinated framework operating across the life course. In this model, public health strategies reduce baseline risk and environmental damage, clinical medicine treats established disease, and longevity-focused therapies may help slow biological decline before major pathology becomes clinically apparent. Figure 1 of the paper (page 2) illustrates this proposed multi-layered framework integrating public health, longevity interventions, and disease-specific care across different stages of life.

Full press release - https://www.aging-us.com/news-room/extending-healthspan-through-public-health-and-longevity-medicine

DOI - https://doi.org/10.18632/aging.206381

Corresponding author - Marco Demaria - [email protected]

Paper Preview Video - https://www.youtube.com/watch?v=KSjfmxpHer8

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BUFFALO, NY — May 19, 2026 — A new #research paper was #published in Volume 18 of Aging-US on May 5, 2026, titled “Methylene blue protects hair follicle stem cells from oxidative and metabolic stress to enhance hair regeneration.”

The study was led by first author Kavitha Sadashivaiah and corresponding author Kan Cao from the Department of Cell Biology and Molecular Genetics at the University of Maryland, College Park. In this study, the authors investigated how methylene blue (MB), a long-established mitochondrial-targeted antioxidant, affects human hair follicle stem cells (HFSCs) under conditions of oxidative and metabolic stress. Hair follicle stem cells are essential for maintaining hair growth and regeneration, but aging, ultraviolet radiation, oxidative stress, and metabolic dysfunction can impair their regenerative capacity and contribute to hair thinning and scalp aging.

Using cultured human HFSCs, the researchers found that methylene blue significantly enhanced stem cell proliferation and viability while reducing intracellular reactive oxygen species (ROS). Importantly, MB also increased activation of β-catenin signaling, a central pathway involved in hair follicle regeneration, stem cell maintenance, and wound repair. Functional scratch-assay experiments further demonstrated that MB accelerated wound closure and regenerative activity in HFSC cultures.

The study also explored how methylene blue interacts with other compounds commonly associated with scalp or hair health. While antioxidant vitamins A and C improved oxidative stress scavenging, they unexpectedly reduced MB-induced β-catenin activation when used in combination. In contrast, minoxidil—the widely used hair growth stimulant—worked synergistically with MB to further enhance β-catenin signaling and improve HFSC viability.

“Overall, these findings identify methylene blue as a multifunctional therapeutic candidate that reduces oxidative and metabolic stress while supporting HFSC–mediated hair regeneration.”

Another major focus of the paper involved glucagon-like peptide-1 receptor agonists (GLP-1 RAs), medications increasingly used for diabetes and weight management. Recent clinical observations have suggested that some patients receiving GLP-1 RA therapy may experience hair thinning or hair loss. The authors demonstrated that increasing GLP-1 RA concentrations caused dose-dependent reductions in HFSC viability in vitro. However, pretreatment with methylene blue substantially protected the stem cells from GLP-1 RA–associated metabolic stress and premature cell death.

Beyond stem cell protection, the paper discusses methylene blue’s broader potential role in scalp health. Because MB absorbs ultraviolet radiation and has previously demonstrated protective effects against UV-induced DNA damage in skin cells, the authors propose that it may help shield the scalp microenvironment from oxidative injury while supporting regenerative signaling pathways important for hair maintenance. The study also highlights MB’s possible antimicrobial properties and its potential influence on scalp microbiome balance.

Importantly, the authors emphasize that the findings are based on in vitro cellular models and that further in vivo studies will be necessary before clinical applications can be established. Additional research will be required to define appropriate dosing, pharmacokinetics, long-term safety, and therapeutic efficacy in living systems.

Overall, this study identifies methylene blue as a potentially multifunctional therapeutic candidate for supporting hair follicle stem cell health under conditions of oxidative, metabolic, and pharmacologic stress. By combining antioxidant activity with activation of regenerative β-catenin signaling, MB may represent a promising future strategy for protecting scalp health, enhancing hair regeneration, and improving the resilience of aging hair follicle stem cells.

DOI - https://doi.org/10.18632/aging.206376

Each month, we will highlight a paper published in Aging-US chosen as the “Editors’ Choice.” These selections are handpicked by our editors and accompanied by a brief summary, showcasing research with significant impact and novel insights in aging and age-related diseases.

__________

In the research paper, titled “Association of epigenetic age acceleration with MRI biomarkers of aging and Alzheimer’s disease neurodegeneration,” researchers investigated whether epigenetic clocks of biological aging are associated with MRI markers of brain aging and Alzheimer’s disease-related neurodegeneration in 1,196 older women. While none of the five epigenetic clocks examined were linked to accelerated overall brain aging, one measure (AgeAccelGrim2) was associated with MRI patterns related to neurodegeneration.

The findings suggest this relationship was largely driven by DNA methylation markers linked to smoking history and changes in frontal and temporal brain regions rather than areas typically affected early in Alzheimer’s disease.

Overall, the study indicates that epigenetic aging and brain aging may reflect different aspects of the aging process, while highlighting the potential role of smoking-related biological aging in increasing dementia risk.

DOI - https://doi.org/10.18632/aging.206369

Corresponding author - Linda K. McEvoy - [email protected]

Abstract video - https://www.youtube.com/watch?v=kZiRjlKnnsI

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Keywords - aging, epigenetic clocks, brain age, biological aging, smoking, frontal lobe

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