BUFFALO, NY — August 12, 2026 — A new #research paper was #published in Volume 18 of Aging on July 27, 2026, titled “Transcriptomic aging clock analysis identifies key genes in opioid dependence.”

The study was led by first author Hai Duc Nguyen from the Division of Microbiology, Tulane National Biomedical Research Center, Tulane University. The corresponding author is Woong-Ki Kim, who is affiliated with the Division of Microbiology, Tulane National Biomedical Research Center, Tulane University, and the Department of Microbiology and Immunology at Tulane University School of Medicine.

Opioid dependence is a chronic and relapsing condition associated with substantial health and societal burdens. Chronic opioid exposure can affect neuronal signaling, immune function, metabolism, and other biological processes, yet the molecular mechanisms underlying dependence remain incompletely understood. Increasing evidence also suggests that substance use disorders may be associated with molecular changes related to aging, raising questions about how chronic opioid exposure interacts with age-dependent processes in the brain.

To investigate these relationships, the researchers conducted an in silico study integrating three complementary approaches: RNA sequencing-based transcriptomic profiling, transcriptomic aging-clock modeling, and analysis of previously published genome-wide association studies (GWAS). The transcriptomic analysis used a publicly available brain RNA-seq dataset containing 42 samples—21 healthy controls and 21 individuals with opioid dependence—while the genetic analysis incorporated findings from six independent GWAS.

Full press release - https://www.aging-us.com/news-room/transcriptomic-aging-clock-reveals-age-related-molecular-patterns-in-opioid-dependence

DOI - https://doi.org/10.18632/aging.206405

Corresponding author - Woong-Ki Kim - [email protected]

Abstract video - https://www.youtube.com/watch?v=7VwU0mFGkbg

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Keywords - aging, opioids, GWAS, transcriptomic clock

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BUFFALO, NY — August 10, 2026 — A new #essay was #published in Volume 18 of Aging on August 6, 2026, titled “Misha Blagosklonny: a life of ideas.”

The article was written by Aging Editorial Board member David Gems from the Institute of Healthy Ageing and Research Department of Genetics, Evolution and Environment, University College London, United Kingdom, along with Aging Editor-in-Chief Marco Demaria from the European Research Institute for the Biology of Ageing (ERIBA), University Medical Center Groningen (UMCG), University of Groningen, the Netherlands. Rather than presenting new experimental findings, the essay examines the life, scientific contributions, and lasting influence of Mikhail (“Misha”) Blagosklonny, whose ideas had a major influence on modern thinking about the biological mechanisms of aging.

Dr. Blagosklonny was trained as a physician and experimental scientist before building an influential career in oncology and aging research after moving to the United States. His work combined cancer biology with theoretical biogerontology, leading to the proposal that aging is driven not primarily by the passive accumulation of molecular damage, but by developmental and growth-related programs that continue beyond their beneficial period. Through what he described as conceptual research, Misha synthesized evidence from diverse experimental studies to generate new hypotheses about aging and reinterpret existing biological observations.

A central theme of the essay is Dr. Blagosklonny’s development of the hyperfunction theory of aging. Building on observations that persistent activation of the mechanistic target of rapamycin (mTOR) pathway can drive cellular senescence, he proposed that many features of aging arise from the continued activity of biological programs that promote growth and reproduction earlier in life. Rather than viewing aging as an adaptive genetic program, Misha argued that it represents a quasi-program—a genetically determined continuation of normal developmental processes that become harmful later in life. This framework provided a mechanistic explanation linking evolutionary concepts such as antagonistic pleiotropy with molecular pathways that regulate growth, metabolism, and cellular senescence.

Full press release - https://www.aging-us.com/news-room/misha-blagosklonnys-scientific-legacy-continues-to-shape-modern-aging-research

DOI - https://doi.org/10.18632/aging.206412

Corresponding author - David Gems - [email protected]

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Keywords - aging, hyperfunction, programmatic theory, disposable soma 2, quasi-program, biogerontology, evolutionary physiology, Mikhail Blagosklonny

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BUFFALO, NY — August 6, 2026 — A new #research perspective was #published in Volume 18 of Aging on July 24, 2026, titled “A brief history of the hyperfunction theory of aging and future directions.”

The article was written by João Pedro de Magalhães from the Genomics of Ageing and Rejuvenation Lab, Department of Inflammation and Ageing, College of Medicine and Health, University of Birmingham, United Kingdom.

Rather than presenting new experimental findings, the perspective examines the historical development of the hyperfunction theory of aging, reviews evidence supporting programmatic mechanisms of aging, and discusses future directions for understanding why organisms age and how aging might eventually be modified.

For decades, most aging research has been dominated by the idea that aging results primarily from the gradual accumulation of molecular damage, including DNA damage, oxidative stress, mitochondrial dysfunction, and protein deterioration. In contrast, the hyperfunction theory proposes that aging is driven largely by developmental and growth programs that continue operating beyond their beneficial period. Rather than being intentionally programmed, aging is viewed as a consequence of biological pathways that promote growth and reproduction early in life but become harmful when they continue later in adulthood.

The perspective traces the historical roots of these ideas from early theories proposed in the nineteenth century through Clive McCay’s pioneering caloric restriction experiments and George Williams’ concept of antagonistic pleiotropy. Particular attention is given to the contributions of the late Mikhail Blagosklonny, whose hyperfunction theory proposed that aging results from “quasi-programs”—developmental processes that fail to switch off after their normal biological role has ended. The author argues that this framework provides a mechanistic explanation linking evolutionary theory with many biological features of aging.

Full press release - https://www.aging-us.com/news-room/hyperfunction-theory-offers-a-new-perspective-on-why-we-age

Paper DOI - https://doi.org/10.18632/aging.206403

Corresponding author - João Pedro de Magalhães - [email protected]

Abstract video - https://www.youtube.com/watch?v=VwC6aJoUUQo

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Keywords - aging, antagonistic pleiotropy, longevity, programmatic aging, quasi-program

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In this episode of the Longevity & Aging Series (S4, E5), Dr. Kan Cao of the Department of Cell Biology and Molecular Genetics at the University of Maryland joins host Dr. Yuan Zhao to discuss the research paper she co-authored in Volume 18 of Aging, titled “Methylene blue protects hair follicle stem cells from oxidative and metabolic stress to enhance hair regeneration.”

Interview video - https://www.youtube.com/watch?v=2Por-Wh3AWo

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

Corresponding author - Kan Cao - [email protected]

Longevity & Aging Series - https://www.aging-us.com/longevity

About Dr. Yuan Zhao - https://www.qmul.ac.uk/sbbs/staff/yuan-zhao.html

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Keywords - aging, methylene blue, minoxidil, HFSCs, Wnt/β-catenin, GLP-1 RA

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BUFFALO, NY — August 5, 2026 — A new #research paper was #published in Volume 18 of Aging on July 23, 2026, titled “Adipo-neuroinflammation, cognitive impairment and surrogate markers of cardiovascular risk in patients with Metabolic Dysfunction Associated Steatotic Liver Disease (MASLD).”

The study was led by co-first authors Gaetano Pacinella from the University of Palermo, and the Internal Medicine and Stroke Care Ward, Policlinico “P. Giaccone”, Palermo, and Alessandro Del Cuore from the same institutions. Gaetano Pacinella also served as the corresponding author.

Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as nonalcoholic fatty liver disease, is increasingly recognized as a systemic condition that extends beyond the liver. People with MASLD have an elevated risk of cardiovascular disease, cognitive decline, and other metabolic complications, yet the biological mechanisms connecting these conditions remain incompletely understood. In this study, researchers investigated whether lipocalin-2 (LCN2), a protein involved in inflammatory and metabolic signaling, is associated with early vascular dysfunction, cognitive impairment, and cardiovascular risk in patients with MASLD.

Full press release - https://www.aging-us.com/news-room/fatty-liver-disease-linked-to-early-cardiovascular-and-cognitive-changes

DOI - https://doi.org/10.18632/aging.206397

Corresponding author - Gaetano Pacinella - [email protected]

Abstract video - https://www.youtube.com/watch?v=CrqTayKl8KI

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Keywords - aging, metabolic dysfunction, cardiovascular risk, lipocalin-2, cognitive impairment, endothelial dysfunction

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Heart failure remains one of the leading causes of hospitalization among older adults worldwide. During episodes of acute decompensated heart failure (ADHF), excess fluid builds up in the lungs and body, making breathing difficult and increasing the risk of serious complications. Although intravenous loop diuretics such as furosemide are the standard treatment for relieving congestion, many patients continue to experience persistent inflammation, ongoing cardiac remodeling, and worsening heart function despite therapy.

A research paper published in Volume 18 of Aging titled “Effects of intravenous furosemide plus small-volume hypertonic saline solutions on inflammatory, remodelling markers and epigenetics signatures of patients with congestive acute decompensated heart failure (ADHF),” investigated whether combining intravenous furosemide with small volumes of hypertonic saline solution (HSS) could improve biological markers associated with heart failure compared with furosemide alone.

Full blog post - https://aging-us.org/2026/08/hypertonic-saline-plus-furosemide-improves-heart-failure-biomarkers-in-randomized-trial/

DOI - https://doi.org/10.18632/aging.206364

Corresponding author - Antonino Tuttolomondo - [email protected]

Abstract video - https://www.youtube.com/watch?v=EG65XlcDJ3U

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Keywords - aging, heart failure, acute decompensated heart failure, furosemide, hypertonic saline solution

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BUFFALO, NY — August 3, 2026 — A new #research paper was #published in Volume 18 of Aging on July 17, 2026, titled “Selective targeting of cancer and senescence via shared metabolic shifts extends lifespan of old mice.”

The study was led by first author Zachery R. Robinson, and corresponding author and Aging editorial board member Irina M. Conboy, both from the Department of Bioengineering and QB3 Institute, University of California, Berkeley. The researchers developed a new combination therapy that selectively targets both cancer cells and senescent cells by exploiting metabolic vulnerabilities shared by these two cell types. In laboratory studies and aged mice, the treatment selectively eliminated senescent cells and reduced cancer cell viability while improving physical performance and extending lifespan without significant toxicity to healthy tissues.

Cancer and aging are closely linked. As people age, senescent cells accumulate throughout the body. Although these cells no longer divide, they remain metabolically active and release inflammatory molecules known as the senescence-associated secretory phenotype (SASP), which contributes to chronic inflammation, tissue dysfunction, and tumor progression. Existing therapies such as the BCL-2/BCL-xL inhibitor navitoclax (ABT-263) can eliminate both cancer cells and senescent cells but require doses that frequently cause thrombocytopenia, a potentially serious reduction in platelet counts that has limited their clinical use.

Full press release - https://www.aging-us.com/news-room/new-drug-combination-targets-cancer-and-senescent-cells-while-extending-lifespan-in-old-mice

DOI - https://doi.org/10.18632/aging.206399

Corresponding author - Irina M. Conboy - [email protected]

Abstract video - https://www.youtube.com/watch?v=7p5JMvy9Twg

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Keywords - aging, senescence, cancer, metabolic shift, ATP

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BUFFALO, NY — July 30, 2026 — A new #research perspective was #published in Volume 18 of Aging on July 16, 2026, titled “Towards integration of healthspan strategies into the Italian National Health Service.”

The article was led by co-first authors Nicola Marino, affiliated with the AEON Foundation and the Women’s Brain Foundation, and Matteo Fiore from the University of Bologna, with both serving as corresponding authors. Rather than presenting new clinical trial results, the authors propose a prevention-focused framework for the staged, evidence-based evaluation and integration of healthspan strategies into Italy’s National Health Service (Servizio Sanitario Nazionale, SSN) to help address the challenges of an aging population.

Italy has one of the oldest populations in the world. Although life expectancy has continued to increase, many older adults spend a substantial portion of those additional years living with chronic disease, disability, or reduced physical and cognitive function. The authors describe this mismatch as the lifespan–healthspan divide and argue that healthcare systems should increasingly focus not only on helping people live longer, but also on extending the years they remain healthy and functionally independent.

To address this challenge, the authors outline the concept of longevity medicine, describing it as a prevention-oriented, life-course framework rather than a new medical specialty. The approach integrates principles from geroscience, preventive medicine, and personalized healthcare with the goal of identifying age-related risks earlier and promoting healthy aging before chronic diseases and functional limitations accumulate. At the same time, the paper emphasizes that many emerging tools—including biological-age biomarkers, multi-omic profiling, wearable sensor data, and artificial intelligence-based risk stratification—remain exploratory and should not be adopted routinely until they demonstrate clear clinical utility, cost-effectiveness, and meaningful benefits for patients.

Full press release - https://www.aging-us.com/news-room/italy-proposes-a-healthspan-focused-framework-for-healthy-aging

DOI - https://doi.org/10.18632/aging.206402

Corresponding authors - Nicola Marino - [email protected], and Matteo Fiore - [email protected]

Abstract video - https://www.youtube.com/watch?v=uc1tGVfiHMw

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Keywords - aging, preventive, longevity, national health system, health span, biomarkers

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BUFFALO, NY — July 27, 2026 — A new #research paper was #published in Volume 18 of Aging on July 13, 2026, titled “Slowing intervertebral disc aging in mice through long-term systemic treatment with the senolytic BCL-2/BCL-xL proteolysis targeting chimera (PROTAC) 753b.”

The study was led by first author Peter G. Alexander from the Ferguson Laboratory for Spine Research, Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine, and corresponding author Nam Viet Vo from the same institution.

Intervertebral disc degeneration is a leading cause of chronic low back pain and disability. As discs age, they lose important structural components, become less able to absorb mechanical stress, and accumulate senescent cells—dysfunctional cells that stop dividing but continue releasing inflammatory molecules that contribute to tissue degeneration. Senolytic therapies, which selectively eliminate these cells, have emerged as a promising strategy to slow age-related diseases. In this study, researchers evaluated PROTAC 753b, a next-generation senolytic designed to target the anti-apoptotic proteins BCL-2 and BCL-xL while reducing the platelet toxicity associated with earlier drugs in this class.

The researchers treated 16-month-old male and female mice with PROTAC 753b for six months and evaluated their intervertebral discs at 22 months of age using histology, molecular analyses, and measurements of inflammatory markers. The treatment significantly improved several measures of intervertebral disc health in aged male mice, preserving the extracellular matrix protein aggrecan and reducing matrix metalloproteinase (MMP)-mediated aggrecan breakdown, a hallmark of disc degeneration. In contrast, female mice showed little overall improvement, revealing a sex-specific response to treatment.

Full press release - https://www.aging-us.com/news-room/senolytic-protac-slows-age-related-intervertebral-disc-degeneration-in-male-mice

DOI - https://doi.org/10.18632/aging.206394

Corresponding author - Nam Viet Vo - [email protected]

Abstract video - https://www.youtube.com/watch?v=t0z4MULDr1A

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Keywords - aging, intervertebral disc aging, cellular senescence, senolytic, anti-apoptosis, PROTAC-753b

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BUFFALO, NY — July 23, 2026 — A new #research paper was #published in Volume 18 of Aging on July 8, 2026, titled “TM4SF1 is a surface marker of senescent pancreatic β-cells.”

The study was led by first author Ana Beathriz Leite Lorente from Joslin Diabetes Center and Harvard Medical School, and São Paulo State University (UNESP), Brazil, and corresponding author Cristina Aguayo-Mazzucato from Joslin Diabetes Center and Harvard Medical School.

Type 2 diabetes is characterized by insulin resistance and the progressive loss of pancreatic β-cell function. With aging and metabolic stress, senescent β-cells accumulate within the pancreas, producing less insulin while releasing inflammatory signals that contribute to disease progression. Although eliminating these dysfunctional cells has emerged as a promising therapeutic strategy, a major challenge has been identifying markers that distinguish senescent β-cells from healthy cells with sufficient precision. This study identifies transmembrane 4 L six family member 1 (TM4SF1) as a highly selective surface marker of senescent β-cells, providing a promising candidate for the future development of more selective therapies for type 2 diabetes.

In this study, the researchers searched for cell-surface proteins that specifically identify senescent β-cells. Using RNA sequencing, flow cytometry, immunofluorescence, and analyses of both mouse and human pancreatic tissue, they compared TM4SF1 with the previously established senescence marker urokinase-type plasminogen activator receptor (uPAR/PLAUR). Their findings showed that TM4SF1 is expressed predominantly in senescent β-cells while exhibiting much lower expression in non-senescent β-cells and other tissues, making it a more β-cell-specific surface marker than uPAR.

Full press release - https://www.aging-us.com/news-room/new-surface-marker-could-advance-precision-therapies-for-type-2-diabetes

DOI - https://doi.org/10.18632/aging.206398

Corresponding author - Cristina Aguayo-Mazzucato - [email protected]

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

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Keywords - aging, senescent β-cell, type 2 diabetes, transmembrane 4 l six family member 1, urokinase-type plasminogen activator receptor

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