Aging-US

BUFFALO, NY — October 28, 2026 — A new #research paper was #published in Volume 18 of Aging on October 6, 2026, titled “Body composition, but not morphological masculinity, is associated with biological aging markers in middle-aged men.” The study found that masculine physical characteristics were not independently associated with biological aging markers in middle-aged men. Instead, body composition, particularly fat-free mass percentage and body fat distribution, showed stronger relationships with inflammation and growth hormone levels. However, these associations disappeared after adjusting for adiposity, suggesting that body fat may help explain the observed relationships. The research was led by first and corresponding author Agnieszka Żelaźniewicz, affiliated with the University of Wroclaw. Aging involves changes in hormonal regulation, immune function, metabolism and body composition. In men, testosterone influences the development of masculine physical characteristics, muscle mass and reproductive function. However, its relationship with biological aging remains unclear, with evidence suggesting both potentially beneficial and harmful effects depending on physiological conditions. Some evolutionary theories propose that greater investment in reproductive characteristics may come at the expense of long-term bodily maintenance. According to the limited soma hypothesis, resources devoted to reproductive competition could reduce those available for cellular repair and maintenance, potentially accelerating aging. Traits such as broad shoulders, muscularity, facial proportions and physical strength are influenced to varying degrees by androgen signaling. If developing and maintaining these characteristics carries long-term physiological costs, men with more pronounced masculine traits might be expected to show signs of accelerated biological aging. DOI - https://doi.org/10.18632/aging.206427 Corresponding author - Agnieszka Żelaźniewicz - [email protected] Abstract video - https://www.youtube.com/watch?v=jQa9XRsvrIU Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206427 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, androgen signaling, inflammaging, endocrine aging, klotho, life-history trade-offs 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 [email protected]

Aging is shaped not only by changes in DNA and metabolism but also by the gradual accumulation of proteins that cells struggle to remove. One striking example is Progerin, an abnormal form of lamin A that accumulates at the nuclear periphery in Hutchinson-Gilford Progeria Syndrome, or HGPS. A new study shows that expressing this human protein in budding yeast reproduces several aging-related cellular defects and creates a simple experimental system for studying how toxic proteins accumulate and affect lifespan. A research paper published in Volume 18 of Aging titled “Modeling premature aging in yeast via the expression of Progerin,” developed a yeast model in which human Progerin and its normal counterpart, lamin A, were expressed as fluorescent fusion proteins. The study was led by first author Zachery R. Belak of the University of Saskatchewan, with corresponding author Troy AA. Harkness, affiliated with the University of Saskatchewan and the University of Alberta. The researchers found that Progerin localized to the yeast nuclear membrane, slowed cellular growth, shortened chronological lifespan, increased genomic instability, and was preferentially retained in older mother cells. Together, these findings suggest that yeast can reproduce several cellular consequences associated with Progerin accumulation despite lacking the conventional nuclear lamina found in human cells. Full blog post - https://aging-us.org/2026/10/progerin-expression-creates-a-yeast-model-of-premature-aging/ DOI - https://doi.org/10.18632/aging.206367 Corresponding author - Troy AA. Harkness - [email protected] Abstract video - https://www.youtube.com/watch?v=VYQKAJjgIb8 Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206367 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, Hutchinson-Gilford Progeria Syndrome, yeast, Progerin, Lamin A, premature aging 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 [email protected]

BUFFALO, NY — October 22, 2026 — A new #research paper was #published in Volume 18 of Aging on September 23, 2026, titled “Hypomagnetic fields modulate lifespan, physical ability and mitochondrial metabolism in a Pink1 model of neurodegeneration.” The study found that exposure to extremely weak magnetic fields increased survival in a fruit fly model of Parkinson’s disease while unexpectedly worsening movement ability. The researchers also identified changes in mitochondrial metabolism and free radical production, suggesting that magnetic field strength may influence aging-related biological processes differently depending on an organism’s genetic background. The research was led by first author Jacob Reed and corresponding author Lisa Chakrabarti, both affiliated with the University of Nottingham. Parkinson’s disease is a progressive neurodegenerative disorder associated with the loss of dopamine-producing neurons, impaired movement and mitochondrial dysfunction. Mitochondria generate much of the energy required for cellular function, and defects in their maintenance can contribute to oxidative stress and neuronal damage. Understanding how environmental conditions influence mitochondrial activity may therefore provide insights into neurodegeneration. The researchers investigated hypomagnetic fields (HMFs), environments in which magnetic field strength is substantially lower than Earth's natural geomagnetic field. Earth's magnetic field typically ranges from 25 to 60 microtesla (μT), while hypomagnetic conditions are generally defined as fields below 5 μT. Although magnetic fields have been studied in relation to animal navigation and cellular metabolism, their influence on neurodegenerative disease remains poorly understood. The study used Drosophila melanogaster, commonly known as the fruit fly, including a genetically modified strain lacking functional Pink1. This gene plays an important role in mitochondrial quality control through the PINK1/Parkin pathway, which helps identify and remove damaged mitochondria. Loss of Pink1 function produces several features resembling early-onset Parkinson’s disease, including impaired movement, mitochondrial dysfunction and reduced lifespan. Full press release - https://www.aging-us.com/news-room/hypomagnetic-fields-extend-survival-but-reduce-mobility-in-a-fly-model-of-parkinsons-disease DOI - https://doi.org/10.18632/aging.206424 Corresponding author - Lisa Chakrabarti - [email protected] Abstract video - https://www.youtube.com/watch?v=em8W24_6wSI Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206424 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, hypomagnetic field, diamond quantum sensing, mitochondria, drosophila melanogaster, Parkinson’s disease 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 [email protected]

BUFFALO, NY — October 20, 2026 — A new #review was #published in Volume 18 of Aging on September 19, 2026, titled “mTOR signaling in aging: from causality to geroprotective interventions and hallmark-level outcomes.” The review examines how the mechanistic target of rapamycin (mTOR) signaling pathway influences aging, longevity and age-related diseases. Drawing on evidence from molecular research, animal experiments and human studies, it highlights mTOR as a central regulator of cellular metabolism, stress adaptation and tissue maintenance. The evidence reviewed suggests that carefully controlled modulation of mTOR signaling could support future strategies for healthy aging, although its long-term benefits in humans remain unproven. The review was authored by Natalia Bobok, Chief Scientific Officer at INSTYTUTUM AG, Zug, Switzerland. Aging involves interconnected biological changes, including mitochondrial dysfunction, cellular senescence, impaired protein maintenance and declining regenerative capacity. The mTOR pathway helps coordinate many of these processes by responding to nutrient availability, growth factors and cellular stress. However, while excessive mTOR activity has been associated with age-related dysfunction, completely suppressing the pathway may interfere with essential functions such as tissue repair, metabolism and immune regulation. The review synthesizes evidence from 265 publications and organizes the findings into three major areas: the biological role of mTOR in aging, interventions that influence its activity, and its interactions with the hallmarks of aging and age-related diseases. This framework emphasizes that mTOR operates as a dynamic signaling network rather than a single molecular switch. Full press release - https://www.aging-us.com/news-room/mtor-signaling-emerges-as-a-key-regulator-of-aging-highlighting-need-for-targeted-interventions DOI - https://doi.org/10.18632/aging.206423 Corresponding author - Natalia Bobok - [email protected] Abstract video - https://www.youtube.com/watch?v=d5Ogq6Myfis Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206423 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, mTOR signaling, mTORC1, mTORC2, geroprotective interventions, hallmarks of aging 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 [email protected]

Aging Editorial Board member Dr. Irina Conboy and Dr. Zachery Robinson from the Department of Bioengineering and QB3 Institute at the University of California, Berkeley, present their findings in the research paper, “Selective targeting of cancer and senescence via shared metabolic shifts extends lifespan of old mice.” DOI - https://doi.org/10.18632/aging.206399 Corresponding author - Irina M. Conboy - [email protected] Video presentation - https://www.youtube.com/watch?v=tke71MaAays Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206399 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, senescence, cancer, metabolic shift, ATP 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 [email protected]