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BUFFALO, NY — September 3, 2026 — A new #research paper was published in Volume 18 of Aging on August 12, 2026, titled “Indy reduction decreases aging-related dysbiosis in Drosophila.”

The study was led by first author Danielle N. A. Lesperance from the University of Connecticut. Corresponding authors Blanka Rogina and Nichole A. Broderick are affiliated with the University of Connecticut Health and Johns Hopkins University, respectively. Broderick is also affiliated with the University of Connecticut.

The Indy gene—short for “I’m not dead yet”—encodes a plasma membrane citrate transporter in Drosophila melanogaster. Previous research has shown that reducing Indy activity can extend lifespan and preserve metabolic and intestinal health in flies. Because aging is also associated with disruption of the gut microbiota, the researchers investigated whether changes in intestinal microbes contribute to the longevity effects associated with reduced Indy activity.

The researchers compared control flies with Indy heterozygous flies under conventional conditions and axenic conditions, in which microbes were absent. They also examined bacterial load and microbiota composition and performed RNA sequencing of the midgut to investigate molecular pathways connecting Indy, the microbiota, intestinal homeostasis, and aging.

Full press release - https://www.aging-us.com/news-room/indy-gene-reduction-linked-to-healthier-gut-microbiota-and-longer-lifespan-in-fruit-flies

DOI - https://doi.org/10.18632/aging.206408

Corresponding authors - Blanka Rogina - [email protected], and Nichole A. Broderick - [email protected]

Abstract video - https://www.youtube.com/watch?v=d0PfTj_Pg7U

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Keywords - aging, Indy, host-microbe interactions, lifespan, Drosophila melanogaster

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Why do we age? For decades, one of the dominant explanations has been that cells and tissues gradually accumulate molecular damage until they can no longer function normally. DNA mutations, damaged proteins, mitochondrial dysfunction, epigenetic alterations, and other forms of cellular wear have all been proposed as major drivers of aging. But another theory offers a very different possibility: some aspects of aging may result not from biological systems breaking down, but from developmental programs continuing to operate after they are no longer beneficial.

A research perspective published in Volume 18 of Aging titled “A brief history of the hyperfunction theory of aging and future directions,” traces the development of this idea and examines where the field may go next.

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 a new experiment, the paper combines historical analysis, evolutionary theory, experimental evidence, and the author’s own perspective on how programmatic models could reshape aging research.

Full blog post - https://aging-us.org/2026/09/developmental-programs-could-help-drive-the-aging-process/

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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BUFFALO, NY — August 31, 2026 — A new research paper was published in Volume 18 of Aging on August 11, 2026, titled “TMAO is associated with higher age, cardiometabolic risk factors and degenerative alterations of the brain in healthy elderly adults.”

The study was led by first author Gunter Almer from the Clinical Institute of Medical and Chemical Laboratory Diagnostics at the Medical University of Graz in Austria. The corresponding author is Markus Herrmann from the same institution.

Trimethylamine N-oxide (TMAO) is a metabolite linked to the gut microbiome. Its precursor, trimethylamine (TMA), is produced by gut bacteria from dietary compounds such as L-carnitine and choline and is subsequently converted to TMAO in the liver. Higher circulating TMAO concentrations have previously been associated with cardiovascular and metabolic diseases, but evidence concerning its role in aging and neurodegeneration remains inconsistent.

To investigate these relationships, the researchers measured serum TMAO in 487 neurologically normal, community-dwelling adults from the Austrian Stroke Prevention Study and Austrian Stroke Prevention Family Study. Participants had a mean age of 67.8 years and underwent cognitive testing assessing memory, executive function, and motor abilities. Brain MRI data were also available for 180 participants, allowing the researchers to examine structural and vascular brain changes.

Full press release - https://www.aging-us.com/news-room/higher-tmao-levels-linked-to-cardiometabolic-risk-and-brain-atrophy-in-older-adults

Paper DOI: https://doi.org/10.18632/aging.206401

Corresponding author: Markus Herrmann - [email protected]

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Keywords: TMAO, aging, risk factors, cognitive function, brain atrophy

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BUFFALO, NY — August 26, 2026 — A new #review was #published in Volume 18 of Aging on August 10, 2026, titled “Metformin at the convergence of aging and longevity.”

The review was authored by Jarra Manneh, May Alasmar and Nady El Hajj from the College of Health and Life Sciences at Hamad Bin Khalifa University, Qatar Foundation, Doha, Qatar. Corresponding author Nady El Hajj is also affiliated with the College of Science and Engineering at Hamad Bin Khalifa University, Doha, Qatar.

Metformin has been used for decades as a first-line treatment for type 2 diabetes, but increasing interest in geroscience has raised a broader question: could this widely used metabolic drug also influence the biological processes that drive aging? The review brings together evidence from cellular studies, animal models, human observational research, and clinical trials examining how metformin interacts with multiple hallmarks of aging.

A central mechanism involves AMP-activated protein kinase (AMPK), a major cellular energy sensor. By inhibiting mitochondrial complex I and altering cellular energy balance, metformin can activate AMPK, triggering downstream effects that include suppression of mechanistic target of rapamycin (mTOR) signaling, increased autophagy and mitochondrial biogenesis, and reduced oxidative stress. Metformin also improves insulin sensitivity and reduces hepatic gluconeogenesis, connecting its established metabolic effects with nutrient-sensing pathways involved in aging biology.

Full press release - https://www.aging-us.com/news-room/metformin-emerges-as-a-promising-candidate-at-the-intersection-of-aging-and-longevity

DOI - https://doi.org/10.18632/aging.206407

Corresponding author - Nady El Hajj - [email protected]

Abstract video - https://www.youtube.com/watch?v=5Ws-x8e1klI

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Keywords - aging, metformin, AMPK, mTOR, epigenetic modifications

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BUFFALO, NY — August 24, 2026 — A new research paper was published in Volume 18 of Aging on August 8, 2026, titled “Investigating POLG-driven modulation of cancer stemness: a pilot study in breast cancer cells.”

The study was led by first author Chiara Chinigò from the Italian National Research Center on Aging (IRCCS INRCA), Cosenza, Italy. Corresponding authors Federica Sotgia and Michael P. Lisanti are affiliated with the University of Salford, United Kingdom, and Lunella Biotech in Ottawa, Canada, with Lisanti additionally affiliated with the Institute of Mental Health Research at the University of Ottawa and The Royal Ottawa Hospital, and Université Laval in Québec.

Breast cancer stem cells (CSCs) are a small population of tumor cells with self-renewal and differentiation capabilities that are associated with tumor progression, metastasis, and therapy resistance. These cells rely heavily on mitochondrial biogenesis and oxidative metabolism, making mitochondrial function a potential metabolic vulnerability. The researchers focused on mitochondrial DNA polymerase gamma (POLG), the enzyme responsible for mitochondrial DNA (mtDNA) replication and repair. POLG contains a catalytic subunit encoded by POLG1 and an accessory subunit encoded by POLG2.

Using estrogen receptor-positive MCF-7 breast cancer cells, the researchers genetically silenced POLG1 and POLG2 to determine whether disrupting mtDNA maintenance would affect cancer stemness. POLG1 knockdown reduced mtDNA content by approximately 80%, while POLG2 knockdown produced an approximately 70% reduction. Both interventions impaired mitochondrial function, lowering the mtDNA-encoded respiratory-chain protein MTCO2, mitochondrial membrane potential, respiration, and ATP production.

Full press release - https://www.aging-us.com/news-room/targeting-polg-reduces-breast-cancer-stemness-through-mitochondrial-dysfunction

DOI - https://doi.org/10.18632/aging.206406

Corresponding authors - Federica Sotgia - [email protected] (ORCiD: 0000-0003-2826-4529), Michael P. Lisanti - [email protected] (ORCiD: 0000-0003-2034-1382)

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Keywords - aging, breast cancer, cancer stem cells, cancer metabolism, POLG, mitochondrial DNA

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BUFFALO, NY — August 24, 2026 — Aging is pleased to announce its partnership as a media partner of the 13th Aging Research and Drug Discovery Meeting (ARDD), taking place October 1–3, 2026, at the David Rubenstein Treehouse at Harvard University in Boston, Massachusetts.

ARDD brings together leading researchers, clinicians, biotech innovators and industry experts to advance the understanding of aging and accelerate the development of interventions targeting age-related diseases. The partnership reflects Aging’s continued commitment to supporting the growth and visibility of research in the fields of aging and longevity.

As a media partner, Aging will help promote ARDD and raise awareness of the meeting through its digital and social media channels, connecting the event with the journal’s global audience. Together, Aging and ARDD will help bring greater visibility to the growing scientific community working to advance healthy longevity and address age-related diseases.

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A #Research paper recently #Published in Volume 18 of Aging, titled “Slowing intervertebral disc aging in mice through long-term systemic treatment with the senolytic BCL-2/BCL-xL proteolysis targeting chimera (PROTAC) 753b,” examines whether the senolytic PROTAC 753b can slow age-related intervertebral disc degeneration (IDD) in mice. Long-term systemic treatment with 753b reduced key features of disc degeneration in 22-month-old male mice, including matrix breakdown, loss of disc aggrecan, age-related structural changes, and inflammatory markers such as IL-6 and TNFα. These benefits, however, were not observed in female mice, highlighting potential sex-based differences in the role of cellular senescence in IDD and the response to senolytic therapies.

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 — 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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