Aging-US

BUFFALO, NY — October 5, 2026 — Aging is pleased to support the 11th International Cell Senescence Association (ICSA) Conference, taking place November 3–5, 2026, at Seoul National University’s Siheung Convention Center in South Korea.

The conference will bring together researchers from around the world to advance understanding of cellular senescence and its roles in aging, cancer, health, and disease. ICSA is an open, global community dedicated to fostering collaboration and scientific progress across the field of cellular senescence.

A key speaker at the conference will be Aging Editor-in-Chief Marco Demaria, Professor of Cellular Ageing and Senescence at the University Medical Center Groningen and also the President of ICSA.

As part of its support for the conference, Aging will also sponsor a $200 cash poster prize recognizing outstanding scientific research presented at the conference.

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BUFFALO, NY — October 1, 2026 — A new #research paper was #published in Volume 18 of Aging on September 10, 2026, titled “Social determinants of health and risk of dementia in people with and without type 2 diabetes – findings from two large national-scale cohorts.”

The study found that unfavorable social determinants of health (SDOH) were associated with a higher risk of dementia in adults with and without type 2 diabetes (T2D), with particularly strong associations observed among women with T2D.

The research was authored by You Lu and Yilin Yoshida. Both researchers are affiliated with the Section of Endocrinology, Deming Department of Medicine, Tulane University, New Orleans, Louisiana.

People with T2D already face an elevated risk of dementia and cognitive impairment. The researchers examined whether social and environmental circumstances could further shape this risk. Rather than evaluating individual social factors separately, they developed a weighted multidomain SDOH score designed to capture the cumulative and unequal contributions of multiple forms of social disadvantage.

The primary analysis included 10,071 UK Biobank participants with T2D and 11,780 euglycemic participants. SDOH indicators were weighted using an elastic-net approach and grouped into favorable, medium and unfavorable categories. Associations with incident dementia were examined using multivariable models and further evaluated using data from the U.S. All of Us Research Program.

Full press release - https://www.aging-us.com/news-room/adverse-social-determinants-linked-to-higher-dementia-risk-in-people-with-type-2-diabetes

DOI - https://doi.org/10.18632/aging.206417

Corresponding author - Yilin Yoshida - [email protected]

Abstract video - https://www.youtube.com/watch?v=Aql6kZZDrEI

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Keywords - aging, dementia, SDOH, type 2 diabetes, sex difference

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Aging is commonly associated with the gradual loss of skeletal muscle mass and function. While preserving muscle mass is important, muscle health also depends on the mitochondria that provide energy for contraction and help muscles respond to physical stress. A new study suggests that a protein called Activating Transcription Factor 5 (ATF5) plays a complex role in balancing these processes during aging.

A research paper published in Volume 18 of Aging titled “ATF5 is required for the maintenance of mitochondrial homeostasis and skeletal muscle health during aging,” investigated how ATF5 influences mitochondrial quality control, muscle mass, and endurance as mice age.

Full blog - https://aging-us.org/2026/09/atf5-helps-preserve-mitochondrial-quality-and-muscle-endurance-during-aging/

DOI - https://doi.org/10.18632/aging.206365

Corresponding author - David A. Hood - [email protected]

Abstract video - https://www.youtube.com/watch?v=u2OeppqIPN4

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Keywords - aging, skeletal muscle, ATF5, mitochondria, stress response

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BUFFALO, NY — September 29, 2026 — A new #review was #published in Volume 18 of Aging on September 8, 2026, titled “Developmental senescence misregulation in congenital disorders: CHARGE syndrome as a candidate model.”

The article proposes that disruption of developmental senescence—a tightly controlled cellular program involved in embryonic tissue remodeling—may contribute to congenital abnormalities associated with CHARGE syndrome.

The review was led by co-first authors Álvaro J. Arana and Pablo Palau-Irisarri, who contributed equally. Arana is affiliated with the Departamento de Zoología, Genética y Antropología Física, Facultad de Veterinaria, Universidad de Santiago de Compostela, Spain, while Palau-Irisarri is affiliated with the Departamento de Biología, Facultad de Ciencias, Universidad Autónoma de Madrid, Spain. Arana is also the corresponding author.

Cellular senescence is commonly associated with aging, cellular stress and tumor suppression, but it also occurs naturally during embryonic development. Unlike classical stress-induced senescence, developmental senescence is transient and restricted to particular tissues and developmental stages. These cells can contribute to tissue remodeling and patterning before being cleared, helping shape developing organs.

Because this process must occur at the right place and time, the authors propose that excessive, insufficient, prolonged or misplaced senescence could interfere with normal morphogenesis. CHARGE syndrome provides a particularly relevant model for investigating this possibility. The rare developmental disorder can involve coloboma, heart defects, choanal atresia, growth and developmental delay, genitourinary abnormalities and characteristic ear defects. Most patients with CHARGE syndrome carry pathogenic variants in CHD7, which encodes an ATP-dependent chromatin remodeler.

Full press release - https://www.aging-us.com/news-room/developmental-senescence-emerges-as-a-candidate-mechanism-in-charge-syndrome

DOI - https://doi.org/10.18632/aging.206396

Corresponding author - Álvaro J. Arana - [email protected]

Abstract video - https://www.youtube.com/watch?v=QtB5390b1To

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Keywords - aging, CHD7, morphogenesis, p53/p21 pathway, TGFβ signaling, congenital disorders

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In this episode of the Longevity & Aging Series (S4, E6), Dr. Adam Bohnert from the Department of Biological Sciences at Louisiana State University (Baton Rouge, LA) joins host Dr. Yuan Zhao to discuss the research paper he co-authored in Volume 18 of Aging, titled “Inhibition of peroxisomal protein PRX-11 promotes longevity in Caenorhabditis elegans via enhancements to mitochondria.”

DOI - https://doi.org/10.18632/aging.206395

Corresponding author - K. Adam Bohnert - [email protected]

Video interview - https://www.youtube.com/watch?v=ztK336BflJ4

Abstract video - https://www.youtube.com/watch?v=fbcqBsP90CY

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

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Keywords - aging, cellular aging, lifespan, pexophagy, mitochondrial tubulation, inter-organelle crosstalk

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BUFFALO, NY — September 24, 2026 — A new #review was #published in Volume 18 of Aging on September 8, 2026, titled “How to live for centuries: common denominators of organisms with exceptional longevity.”

The review examines what some of the world’s longest-lived organisms may reveal about the biology of exceptional longevity.

The review was led by first author Stefania E. Kapsetaki from the Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology-Hellas (FORTH), in Heraklion, Crete, Greece. Corresponding author Nektarios Tavernarakis is affiliated with the same institute and with the Division of Basic Sciences, School of Medicine, University of Crete.

Kapsetaki and Tavernarakis surveyed molecular and cellular evidence from 101 multicellular species with maximum lifespans of at least 250 years, including 90 plants and 11 animals. Some reach only slightly beyond 250 years, while others may persist for thousands or even tens of thousands of years. The freshwater planarian Schmidtea mediterranea and the jellyfish Turritopsis dohrnii are even considered potentially immortal.

Rather than looking only at why certain species live longer than others, the authors compared two dimensions of longevity: variation within exceptionally long-lived species and variation between long- and shorter-lived species. Their analysis covered genetic, genomic, transcriptomic, proteomic and metabolomic findings, as well as telomere maintenance, stress resistance, regeneration and tumorigenesis.

Full press release - https://www.aging-us.com/news-room/exceptional-longevity-across-species-linked-to-dna-maintenance-stemness-and-stress-resistance

DOI - https://doi.org/10.18632/aging.206419

Corresponding author - Nektarios Tavernarakis - [email protected]

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

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Keywords - aging, healthspan, interspecific variation, intraspecific variation, stemness

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BUFFALO, NY — September 21, 2026 — A new #review was #published in Volume 18 of Aging on August 31, 2026, titled “The guardian paradox: DNA damage response overactivation as an integrative driver of aging – a tumor suppressor–negative regulator framework.”

The review presents a new framework proposing that chronic overactivation of the DNA damage response (DDR) may serve as a major integrating driver of biological aging. Rather than framing aging in the same mutation-centered terms often applied to cancer, the framework suggests that many tumor-suppressor pathways remain structurally intact but become persistently overactivated or otherwise dysregulated as tissues age.

The review was authored by Patrick E. Sewell from Triple Helix Science in Santa Ana, California. The paper organizes 16 candidate tumor suppressor–negative regulator axes into three evidence tiers and proposes experiments designed to determine whether chronic DDR signaling plays a causal role in aging.

The DNA damage response is the cellular surveillance system that detects genomic damage and coordinates repair. In young, healthy tissues, DDR signaling normally activates temporarily following stresses such as DNA double-strand breaks, replication stress or oxidative lesions and subsides after repair. With aging, however, persistent signals associated with telomere attrition, epigenetic erosion, mitochondrial dysfunction and transposable-element activity may maintain DDR activation even without new driver mutations.

According to the proposed model, chronic DDR signaling can stabilize p53 and increase p21 and p16INK4a, promoting cell-cycle arrest and cellular senescence. Senescent cells can then produce the senescence-associated secretory phenotype (SASP), releasing inflammatory mediators that may spread senescence to neighboring cells, reduce stem-cell function, disrupt tissue homeostasis and contribute to systemic inflammaging. Importantly, these effects can occur while the underlying tumor-suppressor genes remain intact.

Full press release - https://www.aging-us.com/news-room/the-guardian-paradox-links-chronic-dna-damage-response-to-aging

DOI - https://doi.org/10.18632/aging.206416

Corresponding author - Patrick E. Sewell - [email protected]

Abstract video - https://www.youtube.com/watch?v=rBMe9uWMpBU

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Keywords - aging, biological aging, DNA damage response, tumor suppressor pathways, gene therapy, adeno-associated virus

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A research paper recently published in Aging, titled “Human-relevant Ptpn6 mutation alters immune and hepatic functions during aging,” investigated how a human-relevant mutation in the PTPN6 gene, which encodes the immune and metabolic regulator SHP-1, affects immune and liver function during aging. Using mice carrying the mutation, the researchers found that older mutant mice had improved glucose tolerance and hepatic insulin sensitivity, but also developed liver abnormalities characterized by increased fibrosis and the accumulation of immune cells, particularly B lymphocytes and macrophages. Further analyses indicated that these age-related changes were driven primarily by altered immune activity rather than direct effects within liver cells.

The findings identify SHP-1 as an important regulator of liver immune homeostasis and provide new insight into how immune-cell infiltration may contribute to age-related changes in the liver.

DOI - https://doi.org/10.18632/aging.206413

Corresponding author - André Marette - [email protected]

Abstract video - https://www.youtube.com/watch?v=lyn__UY9Buk

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Keywords - aging, SHP-1/Ptpn6, B cell, macrophage, aging, Ptpn6Ala457Thr

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BUFFALO, NY — September 16, 2026 — A new #research paper was #published in Volume 18 of Aging on August 28, 2026, titled “Human-relevant Ptpn6 mutation alters immune and hepatic functions during aging.”

The study examines how a mutation affecting the immune and metabolic regulator SHP-1 reshapes liver function during aging, revealing that improved glucose metabolism can coexist with immune-cell accumulation and liver fibrosis.

The research was led by first author Beisy Laborit Labrada from the Institut Universitaire de Cardiologie et de Pneumologie de Québec (CRIUCPQ), Université Laval, Québec, Canada. André Marette, from CRIUCPQ and the Department of Medicine at Université Laval, is the corresponding author.

SHP-1, encoded by the PTPN6 gene, is a protein tyrosine phosphatase that helps regulate both immune responses and metabolic signaling. In immune cells, it generally restrains signaling pathways that control cellular activation, while in metabolic tissues it acts as a negative regulator of insulin signaling. This dual function places SHP-1 at an important intersection between immunity and metabolism, two systems that undergo substantial changes during aging.

The study centered on a rare PTPN6Ala455Thr variant originally identified in a French-Canadian family with early-onset severe emphysema. The human mutation moderately reduces SHP-1 phosphatase activity. To investigate its longer-term effects, the researchers used mice carrying the corresponding Ptpn6Ala457Thr mutation and compared young adult mice at 5.6 months with older animals at 16–19 months. Unlike more severe SHP-1-deficient mouse models, these animals have lifespans comparable to wild-type mice, allowing the consequences of partial SHP-1 dysfunction to be examined across aging.

Full press release - https://www.aging-us.com/news-room/human-relevant-ptpn6-mutation-reveals-complex-links-between-immunity-metabolism-and-liver-aging

DOI - https://doi.org/10.18632/aging.206413

Corresponding author - André Marette - [email protected]

Abstract video - https://www.youtube.com/watch?v=lyn__UY9Buk

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Keywords - aging, SHP-1/Ptpn6, B cell, macrophage, aging, Ptpn6Ala457Thr

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BUFFALO, NY — September 14, 2026 — A new #review was #published in Volume 18 of Aging on August 26, 2026, titled “Assessing mechanisms and evidence of a causal role for cellular senescence and somatic mutations in aging.”

The review examines two biological processes strongly associated with aging—cellular senescence and somatic DNA mutations—and evaluates whether the evidence supports their causal contribution to age-related functional decline.

The review was authored by Lucrezia A. Trastus and Fabrizio d’Adda di Fagagna from IFOM ETS – The AIRC Institute of Molecular Oncology in Milan, Italy. d’Adda di Fagagna is also affiliated with the Istituto di Genetica Molecolare, Consiglio Nazionale delle Ricerche (IGM-CNR) in Pavia, Italy. Both authors are corresponding authors.

Aging involves many interconnected molecular and cellular changes, making it difficult to distinguish processes that actively drive deterioration from those that simply accompany it. Trastus and d’Adda di Fagagna assess cellular senescence and somatic mutations using necessity and sufficiency as key criteria for causal inference.

For cellular senescence, the evidence for causality is comparatively strong. Senescent cells undergo stable proliferative arrest, which can impair tissue regeneration, particularly when stem cells are affected. Their influence can extend far beyond individual cells through the senescence-associated secretory phenotype (SASP), a complex secretory program that allows senescent cells to alter surrounding tissues and promote senescence in neighboring cells.

Full press release - https://www.aging-us.com/news-room/evidence-for-cellular-senescence-as-a-driver-of-aging-stronger-than-for-somatic-mutations

DOI - https://doi.org/10.18632/aging.206414

Corresponding authors - Lucrezia A. Trastus - [email protected], Fabrizio d’Adda di Fagagna - [email protected]

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

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Keywords - aging, cellular senescence, somatic mutations, DNA damage, SASP

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