Aging-US

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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Scientific progress often begins with questioning assumptions that have shaped a field for decades. Few researchers embodied this approach as strongly as Dr. Mikhail “Misha” Blagosklonny, an oncologist and biogerontologist whose unconventional theories challenged traditional explanations of why organisms age.

An essay published in Volume 18 of Aging titled “Misha Blagosklonny: a life of ideas,” reflects on Dr. Blagosklonny’s life, scientific career, and contributions to the biology of aging.

Full blog post - https://aging-us.org/2026/09/misha-blagosklonnys-ideas-reshaped-thinking-about-aging/

Paper 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 — September 10, 2026 — A new #research paper was #published in Volume 18 of Aging on August 24, 2026, titled “Disruption of the insulin/IGF-1 signaling pathway in Caenorhabditis elegans dramatically increases male longevity and enhances reproductive health late in life.”

The research was conducted by Rose S. Al-Saadi, Hannah B. Lewack and Patrick C. Phillips. Al-Saadi and Lewack contributed equally to the study. Al-Saadi and Phillips are from the Institute of Ecology and Evolution at the University of Oregon, while Lewack is affiliated with both the Institute of Ecology and Evolution at the University of Oregon and the Department of Molecular Biology at the University of California, San Diego. Phillips is the corresponding author.

Insulin/IGF-1 signaling (IIS) is one of the best-established molecular pathways regulating longevity across animal species. In C. elegans, the gene DAF-2 encodes an insulin/IGF-1 receptor, and reducing its activity can substantially extend lifespan. However, most previous aging studies in this model have focused on hermaphrodites, leaving considerably less known about how males respond to interventions targeting the same pathway.

To investigate these sex-specific effects, the researchers used an auxin-inducible degron system to selectively degrade the DAF-2 receptor throughout the body or within particular tissues. When DAF-2 was degraded throughout the body, the effect on male longevity was striking: median lifespan increased by 446%, compared with a 109% increase in hermaphrodites exposed to the same intervention. The age at which 10% of the population remained alive reached 106 days in treated males, compared with 15 days in controls. The authors describe this as one of the largest lifespan extensions reported in C. elegans—or any animal—from a single intervention.

Full press release - https://www.aging-us.com/news-room/reduced-insulin-igf-1-signaling-dramatically-extends-male-lifespan-in-c-elegans

DOI - https://doi.org/10.18632/aging.206411

Corresponding author - Patrick C. Phillips - [email protected]

Abstract video - https://www.youtube.com/watch?v=zQ32BnBwEBI

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Keywords - aging, Insulin/IGF-1 signaling, sex differences, Caenorhabditis elegans, reproductive health

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BUFFALO, NY — September 9, 2026 — A new #research paper was #published in Volume 18 of Aging on August 13, 2026, titled “Protective effects of three herbal extracts on mitochondrial dysfunction in VPS13C-knockdown SH-SY5Y cells: implications for Parkinson’s disease.”

The study was led by co-first authors Yih-Ru Wu and Chih-Hsin Lin from the Chang Gung Memorial Hospital, Chang Gung University College of Medicine in Taoyuan, Taiwan, and Pei-Syuan Huang from the School of Life Science at National Taiwan Normal University in Taipei, Taiwan. Corresponding authors I-Cheng Chen and Guey-Jen Lee-Chen are from the School of Life Science at National Taiwan Normal University. The paper identifies Wu, Lin, and Huang as equal contributors.

Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized primarily by dysfunction and loss of dopaminergic neurons in the substantia nigra. Although its causes are complex, mitochondrial dysfunction and oxidative stress are important biological processes implicated in both sporadic and inherited forms of the disease. The researchers focused on VPS13C, also known as PARK23, a gene associated with a rare autosomal recessive form of early-onset parkinsonism. Loss of VPS13C function has previously been linked to impaired mitochondrial function.

The study investigated three extracts used in traditional Chinese medicine: Uncaria rhynchophylla (UR), Gardenia jasminoides (GJ), and Scutellaria baicalensis (SB). Previous experimental studies have reported neuroprotective effects from these plants or their bioactive constituents in models relevant to PD. The researchers examined whether the extracts could protect cells against mitochondrial dysfunction associated with reduced VPS13C expression.

Chemical analyses identified several potentially bioactive constituents in the extracts. UR contained rhynchophylline and isorhynchophylline; GJ contained geniposide and crocin; and SB contained several flavonoids, including baicalin, wogonoside, baicalein, wogonin, and oroxylin A. Across the concentrations initially tested, the three extracts maintained greater than 90% viability in SH-SY5Y cells after 24 hours, indicating low cytotoxicity under these experimental conditions.

Full press release - https://www.aging-us.com/news-room/three-herbal-extracts-protect-mitochondrial-function-in-a-cellular-model-of-parkinsons-disease

DOI - https://doi.org/10.18632/aging.206409

Corresponding authors - I-Cheng Chen - [email protected], Guey-Jen Lee-Chen - [email protected]

Abstract video - https://www.youtube.com/watch?v=kM8hO89d_9k

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Keywords - aging, Parkinson’s disease, traditional Chinese medicine, VPS13C knockdown, mitochondrial dysfunction, oxidative stress

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Dr. Falak Pahwa, Dr. Ranjan Kumar Nanda, and Mr. Ashish Gupta from the International Centre for Genetic Engineering and Biotechnology (ICGEB) in New Delhi, India, discuss their research paper, recently published in Volume 18 of Aging, titled “Host immunosenescence compromises Mycobacterium tuberculosis clearance.”

Video interview - https://www.youtube.com/watch?v=bSaJaB751kM

DOI - https://doi.org/10.18632/aging.206374

Corresponding author - Ranjan Kumar Nanda - [email protected]

Abstract video - https://www.youtube.com/watch?v=isPD8ZmUjv8

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Keywords - aging, tuberculosis, immunosenescence, TFH cells, proteomics

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