Aging-US

This month’s Editor’s Choice features the #research paper recently #published in Aging, titled “Social determinants of health and risk of dementia in people with and without type 2 diabetes – findings from two large national-scale cohorts.” Analyzing data from two large national-scale cohorts, researchers found that unfavorable social determinants of health (SDOH) were associated with a higher risk of developing dementia, with particularly strong associations among women with type 2 diabetes.

The findings highlight the importance of social and socioeconomic factors in dementia risk and the need to consider these factors when developing strategies for prevention and care.

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

Corresponding author - Yilin Yoshida - [email protected]

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

Sign up for free Altmetric alerts about this article -

https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206417

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

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

To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at:

Bluesky - https://bsky.app/profile/aging-us.bsky.social

ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589

X - https://twitter.com/AgingJrnl

Facebook - https://www.facebook.com/AgingUS/

Instagram - https://www.instagram.com/agingjrnl/

LinkedIn - https://www.linkedin.com/company/aging/

Reddit - https://www.reddit.com/user/AgingUS/

Pinterest - https://www.pinterest.com/AgingUS/

YouTube - https://www.youtube.com/@Aging-US

Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc

BUFFALO, NY — October 15, 2026 — A new #research paper was #published in Volume 18 of Aging on September 16, 2026, titled “Control theory of aging and longevity for gerotherapeutic drug discovery: state space, vector fields, modalities, safety, and the minimum safe cost of functional restoration.”

The paper introduces a mathematical framework for understanding aging and guiding the development of therapies aimed at preserving or restoring biological function. By applying principles from control theory, the researchers propose evaluating treatments according to their ability to move aging biological systems toward healthier functional states while accounting for treatment risks, intervention timing and irreversible damage.

The research was led by Aging Editorial Board member Alex Zhavoronkov, affiliated with Insilico Medicine and the Buck Institute for Research on Aging.

Aging research has identified numerous biological processes that contribute to functional decline, including cellular senescence, mitochondrial dysfunction, chronic inflammation, epigenetic alterations and loss of proteostasis. Established frameworks, such as the Hallmarks of Aging and the hyperfunction theory developed by Mikhail Blagosklonny, have helped explain these changes. However, identifying aging-related mechanisms does not automatically determine how, when or whether they should be targeted therapeutically.

The authors propose addressing this challenge using control theory, a mathematical discipline concerned with directing dynamic systems toward desired states. Their framework introduces the concept of biological state space, representing an organism’s condition across multiple dimensions, including inflammation, mitochondrial function, epigenetic stability, immune competence and regenerative capacity. Rather than aiming to restore every molecular feature to a youthful state, the framework prioritizes maintaining or recovering acceptable physiological function.

Full press release - https://www.aging-us.com/news-room/new-control-theory-framework-proposes-a-safer-approach-to-aging-drug-discovery

DOI - https://doi.org/10.18632/aging.206422

Corresponding author - Alex Zhavoronkov - [email protected]

Abstract video - https://www.youtube.com/watch?v=qXL5LMhQTVs

Sign up for free Altmetric alerts about this article -

https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206422

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

Keywords - aging, control theory, biological age, drug discovery, gerotherapeutics

To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at:

Bluesky - https://bsky.app/profile/aging-us.bsky.social

ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589

X - https://twitter.com/AgingJrnl

Facebook - https://www.facebook.com/AgingUS/

Instagram - https://www.instagram.com/agingjrnl/

LinkedIn - https://www.linkedin.com/company/aging/

Reddit - https://www.reddit.com/user/AgingUS/

Pinterest - https://www.pinterest.com/AgingUS/

YouTube - https://www.youtube.com/@Aging-US

Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc

Rare genetic disorders that cause features of aging to appear much earlier than expected can offer an unusual window into the biology of human aging. Yet information about these conditions is scattered across publications and databases, and the same genes or syndromes are sometimes described using different terminology. A new study brings much of this information together in a manually curated genetic and clinical resource.

A research paper published in Volume 18 of Aging titled “A manually curated gene–phenotype catalogue for progeroid syndromes and premature aging,” developed an integrated catalogue linking genes, premature aging syndromes, syndrome subtypes, and major clinical features.

Full blog post - https://aging-us.org/2026/10/new-gene-phenotype-catalogue-maps-the-genetic-landscape-of-premature-aging/

DOI - https://doi.org/10.18632/aging.206366

Corresponding author - Tanja Kunej - [email protected]

Abstract video - https://www.youtube.com/watch?v=Ov6Saz34ZpE

Sign up for free Altmetric alerts about this article -

https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206366

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

Keywords - aging, premature aging, progeroid syndromes, DNA repair, LMNA gene

To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at:

Bluesky - https://bsky.app/profile/aging-us.bsky.social

ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589

X - https://twitter.com/AgingJrnl

Facebook - https://www.facebook.com/AgingUS/

Instagram - https://www.instagram.com/agingjrnl/

LinkedIn - https://www.linkedin.com/company/aging/

Reddit - https://www.reddit.com/user/AgingUS/

Pinterest - https://www.pinterest.com/AgingUS/

YouTube - https://www.youtube.com/@Aging-US

Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc

BUFFALO, NY — October 13, 2026 — A new #research paper was #published in Volume 18 of Aging on September 16, 2026, titled “Targeting phospholipase Pla2g15 reduces long-chain BMP phospholipids abundance and senescence in kidney cells.”

The study found that disrupting the gene Pla2g15 reduced stress-induced cellular senescence in mouse kidney cells while altering the composition of phospholipids involved in lysosomal function. The findings identify a possible connection between lipid metabolism, mitochondrial pathways and kidney aging, suggesting that PLA2G15 could become a potential therapeutic target for age-related kidney disease.

The research was led by first author Sanne van der Rijt, affiliated with Amsterdam UMC. Corresponding authors Georges E. Janssens and Riekelt H. Houtkooper are also affiliated with Amsterdam UMC, while corresponding author Alessandra Tammaro is affiliated with Amsterdam UMC and Leiden University Medical Center.

Chronic kidney disease (CKD) becomes increasingly common with age and is associated with progressive loss of kidney function. One contributing factor is the accumulation of senescent cells, particularly proximal tubular epithelial cells (TECs), which play an important role in reabsorbing filtered substances and maintaining kidney function. Although cellular senescence can initially protect against damage, persistent senescent cells can release inflammatory and profibrotic factors that contribute to tissue injury, scarring and functional decline.

The researchers focused on the role of lysosomes, cellular compartments responsible for breaking down and recycling biological materials. Lysosomal function depends partly on specialized phospholipids, including bis(monoacylglycerol)phosphate (BMP), which helps maintain the organization and activity of the lysosomal system. Previous research has linked increased BMP abundance to aging and kidney disease, but its contribution to cellular senescence remains incompletely understood.

DOI - https://doi.org/10.18632/aging.206415

Corresponding authors - Georges E. Janssens - [email protected], Riekelt H. Houtkooper - [email protected], and Alessandra Tammaro - [email protected]

Abstract video - https://www.youtube.com/watch?v=cR_t76ZWZH0

Sign up for free Altmetric alerts about this article -

https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206415

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

Keywords - aging, phospholipids, bis(monoacylglycerol)phosphate (BMP), PLA2G15, tubular epithelial cell senescence

To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at:

Bluesky - https://bsky.app/profile/aging-us.bsky.social

ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589

X - https://twitter.com/AgingJrnl

Facebook - https://www.facebook.com/AgingUS/

Instagram - https://www.instagram.com/agingjrnl/

LinkedIn - https://www.linkedin.com/company/aging/

Reddit - https://www.reddit.com/user/AgingUS/

Pinterest - https://www.pinterest.com/AgingUS/

YouTube - https://www.youtube.com/@Aging-US

Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc

BUFFALO, NY — October 8, 2026 — A new #commentary was #published in Volume 18 of Aging on September 12, 2026, titled “Complexity, variability, and the behavioral layer of gerophysics: a commentary on Unfried et al. (2026).”

The commentary proposes expanding the emerging field of gerophysics to include behavioral complexity, offering a way to understand how aging affects the ability to adapt to everyday challenges. The authors argue that measuring changes in movement, physiological rhythms and other behavioral patterns could complement molecular and biological markers of aging, potentially helping researchers identify declining resilience and the transition toward frailty.

The commentary was authored by Jean-Jacques Temprado and Rita Sleimen-Malkoun, both affiliated with Aix Marseille Université, CNRS, and the Institute of Movement Sciences (ISM), Marseille, France. Temprado is also the corresponding author.

Gerophysics is an emerging interdisciplinary field that applies concepts from physics, mathematics and complex systems science to the study of aging. It draws on dynamical systems, entropy, network theory and stochastic processes to understand how biological systems change over time. A recent report from the Global Conference on Gerophysics, discussed by Unfried and colleagues, outlined a framework connecting aging processes across biological scales, from individual cells to the whole organism.

Temprado and Sleimen-Malkoun suggest that this framework could be strengthened by explicitly incorporating behavioral dynamics, particularly how people interact with and adapt to their environments. While molecular and physiological measurements reveal important aspects of aging, behavioral patterns may provide additional information about how effectively the body responds to changing demands in everyday life.

The authors build on earlier research suggesting that healthy physiological and behavioral systems exhibit complex fluctuations across multiple time scales. These patterns are neither entirely random nor perfectly regular. Instead, their variability reflects the flexibility needed to respond to different situations. With aging, this complexity may decline, producing patterns that become either more predictable or more random, potentially indicating a reduced capacity for adaptation.

Full press release - https://www.aging-us.com/news-room/behavioral-complexity-could-offer-new-insights-into-aging-and-frailty

DOI - https://doi.org/10.18632/aging.206421

Corresponding author - Jean-Jacques Temprado - [email protected]

Video preview - https://www.youtube.com/watch?v=7v2X8axjdgI

Sign up for free Altmetric alerts about this article -

https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206421

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

Keywords - aging, dynamical systems, complexity, behavior

To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at:

Bluesky - https://bsky.app/profile/aging-us.bsky.social

ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589

X - https://twitter.com/AgingJrnl

Facebook - https://www.facebook.com/AgingUS/

Instagram - https://www.instagram.com/agingjrnl/

LinkedIn - https://www.linkedin.com/company/aging/

Reddit - https://www.reddit.com/user/AgingUS/

Pinterest - https://www.pinterest.com/AgingUS/

YouTube - https://www.youtube.com/@Aging-US

Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc

BUFFALO, NY — October 6, 2026 — A new #research paper was recently #published in Volume 18 of Aging, titled “Spatially fractionated mini-GRID radiotherapy differentially modulates radiation-induced senescence in murine glioma and normal cells.”

The study found that spatially fractionated mini-GRID radiotherapy reduced several features of radiation-induced cellular senescence in two glioma cell lines while maintaining an antiproliferative effect comparable to conventional radiotherapy. In non-tumor cell models, however, the two radiation approaches produced similar senescence responses.

The research was led by equal-contributing first authors M. Isabel Acuña and Miguel Ángel Prados, both affiliated with the University of Santiago de Compostela. Corresponding authors Manuel Collado and Yolanda Prezado are also affiliated with the University of Santiago de Compostela. Collado is additionally affiliated with the National Centre for Biotechnology (CNB-CSIC), while Prezado is additionally affiliated with the Oportunius Program of the Galician Agency of Innovation (GAIN), Xunta de Galicia.

Radiotherapy remains a cornerstone of cancer treatment, but it can also push surviving cells into senescence, a state of persistent cell-cycle arrest. Senescent cells can develop a senescence-associated secretory phenotype (SASP), releasing inflammatory and other signaling molecules that affect surrounding tissues and the tumor microenvironment. Although senescence can restrict tumor-cell proliferation, persistent therapy-induced senescence may also contribute to inflammation, treatment resistance and other adverse effects.

Spatially fractionated radiotherapy (SFRT) differs from conventional radiotherapy by delivering radiation in a deliberately non-uniform pattern, creating high-dose “peaks” separated by lower-dose “valleys.” The researchers investigated whether mini-GRID, a form of SFRT, produces different senescence responses from conventional uniform irradiation.

The study compared the two approaches in F98 and RG2 rat glioma cells, immortalized rat astrocytes and primary mouse embryonic fibroblasts. Cells received single radiation doses ranging from 5 to 20 Gy and were evaluated seven days later using morphological, biochemical and molecular measures of senescence.

Full press release - https://www.aging-us.com/news-room/mini-grid-radiotherapy-reduces-senescence-while-preserving-growth-inhibition-in-glioma-cells

DOI - https://doi.org/10.18632/aging.206410

Corresponding authors - Manuel Collado - [email protected], and Yolanda Prezado - [email protected]

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

Sign up for free Altmetric alerts about this article -

https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206410

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

Keywords - aging, cellular senescence, spatially fractionated radiotherapy, mini-GRID radiotherapy, conventional radiotherapy, cancer cells

To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at:

Bluesky - https://bsky.app/profile/aging-us.bsky.social

ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589

X - https://twitter.com/AgingJrnl

Facebook - https://www.facebook.com/AgingUS/

Instagram - https://www.instagram.com/agingjrnl/

LinkedIn - https://www.linkedin.com/company/aging/

Reddit - https://www.reddit.com/user/AgingUS/

Pinterest - https://www.pinterest.com/AgingUS/

YouTube - https://www.youtube.com/@Aging-US

Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc

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.

To learn more about the journal, please visit www.Aging-US.com​​ and connect with us on social media at:

Bluesky - bsky.app/profile/aging-us.bsky.social

ResearchGate - www.researchgate.net/journal/Aging-1945-4589

X - twitter.com/AgingJrnl

Facebook - www.facebook.com/AgingUS/

Instagram - www.instagram.com/agingjrnl/

LinkedIn - www.linkedin.com/company/aging/

Reddit - www.reddit.com/user/AgingUS/

Pinterest - www.pinterest.com/AgingUS/

YouTube - www.youtube.com/@Aging-US

Spotify - open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc

For media inquiries, please contact [email protected].

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

Sign up for free Altmetric alerts about this article -

https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206417

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

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

To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at:

Bluesky - https://bsky.app/profile/aging-us.bsky.social

ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589

X - https://twitter.com/AgingJrnl

Facebook - https://www.facebook.com/AgingUS/

Instagram - https://www.instagram.com/agingjrnl/

LinkedIn - https://www.linkedin.com/company/aging/

Reddit - https://www.reddit.com/user/AgingUS/

Pinterest - https://www.pinterest.com/AgingUS/

YouTube - https://www.youtube.com/@Aging-US

Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc

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

Sign up for free Altmetric alerts about this article -

https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206365

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

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

To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at:

Bluesky - https://bsky.app/profile/aging-us.bsky.social

ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589

X - https://twitter.com/AgingJrnl

Facebook - https://www.facebook.com/AgingUS/

Instagram - https://www.instagram.com/agingjrnl/

LinkedIn - https://www.linkedin.com/company/aging/

Reddit - https://www.reddit.com/user/AgingUS/

Pinterest - https://www.pinterest.com/AgingUS/

YouTube - https://www.youtube.com/@Aging-US

Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc

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

Sign up for free Altmetric alerts about this article -

https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206396

Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts

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

To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at:

Bluesky - https://bsky.app/profile/aging-us.bsky.social

ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589

X - https://twitter.com/AgingJrnl

Facebook - https://www.facebook.com/AgingUS/

Instagram - https://www.instagram.com/agingjrnl/

LinkedIn - https://www.linkedin.com/company/aging/

Reddit - https://www.reddit.com/user/AgingUS/

Pinterest - https://www.pinterest.com/AgingUS/

YouTube - https://www.youtube.com/@Aging-US

Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc