Coordinating both hands is something most people take for granted. Everyday activities such as buttoning a shirt, preparing a meal, driving, or using a knife and fork all depend on the brain’s ability to precisely control movements on both sides of the body. As people age, however, these tasks often become more difficult, especially when they require both hands to perform different movements at the same time.

A research paper published in Volume 18 of Aging titled “Age-specific relationship between the modulation of brain dynamics in response to task demands and bimanual performance,” investigated how aging affects the brain’s ability to adapt to increasingly complex hand-coordination tasks. The study was led by first author Sara Magalhães Ferreira from Hasselt University, with corresponding author Koen Cuypers from Hasselt University and KU Leuven.

Full blog - https://aging-us.org/2026/07/brain-flexibility-is-linked-to-hand-coordination-during-aging/

DOI - https://doi.org/10.18632/aging.206363

Corresponding author - Koen Cuypers - [email protected]

Abstract video - https://www.youtube.com/watch?v=3TbcGFCZV9s

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Keywords - aging, bimanual coordination, Bimanual Tracking Task, BOLD variability, task modulation

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BUFFALO, NY — July 21, 2026 — A new #research paper was #published in Volume 18 of Aging on July 6, 2026, titled “Inhibition of peroxisomal protein PRX-11 promotes longevity in Caenorhabditis elegans via enhancements to mitochondria.”

The study was authored by Yash Flora, Dhriti Shastri, Kathryn R. DeLeo, and K. Adam Bohnert from the Department of Biological Sciences, Louisiana State University.

Aging is accompanied by the gradual decline of many cellular structures that help maintain healthy tissues and organs. Among these are peroxisomes, which play essential roles in breaking down toxic molecules and metabolizing lipids, and mitochondria, which generate most of the cell’s energy. Although these organelles work closely together, little has been known about how changes in one influence the aging of the other. This new study reveals that preserving peroxisomes helps maintain healthier mitochondria and extends lifespan in the nematode Caenorhabditis elegans, providing new insight into how communication between cellular organelles influences aging.

In this study, the researchers investigated the function of PRX-11, a peroxisomal protein involved in peroxisome division. Previous work from the group showed that reducing PRX-11 activity prevents the age-related degradation of peroxisomes through a process known as pexophagy and increases lifespan. The new study explored why preserving peroxisomes produces these beneficial effects and found that maintaining peroxisomes also preserves mitochondrial health during aging.

The researchers found that animals with reduced PRX-11 activity retained long, interconnected mitochondrial networks that resembled those seen in young adults, whereas normal aging was associated with progressive mitochondrial fragmentation. These preserved mitochondria also accumulated less calcium, generated lower levels of oxidative stress, maintained higher ATP-to-ADP ratios, and were associated with improved locomotor function in older animals. Together, these findings indicate that preventing age-related peroxisome loss supports multiple aspects of mitochondrial function during aging.

Full press release - https://www.aging-us.com/news-room/preserving-peroxisomes-helps-maintain-mitochondrial-health-and-extend-lifespan-in-c-elegans

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

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

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

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

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Each month, we will highlight a paper published in Aging chosen as the “Editors’ Choice.” These selections are handpicked by our editors and accompanied by a brief summary, showcasing research with significant impact and novel insights in aging and age-related diseases.

Cellular senescence is a hallmark of aging and age-related disease, yet the diverse mechanisms that trigger this cellular state remain incompletely understood. The review recently published in Volume 18 of Aging, titled “The multifaceted inducers of cellular senescence,” examines the many intrinsic and extrinsic stimuli that induce senescence, including DNA damage, oxidative and mitochondrial stress, telomere attrition, oncogene activation, cell–cell fusion, and developmental signals. The authors, Hilah Gal and Valery Krizhanovsky, explain how these distinct pathways converge on a stable cell-cycle arrest. By highlighting the complexity and heterogeneity of senescent cells, the authors provide valuable insights that may guide the development of future therapies targeting senescence to promote healthy aging and combat age-related diseases.

DOI - https://doi.org/10.18632/aging.206391

Corresponding author - Valery Krizhanovsky - [email protected]

Abstract video - https://www.youtube.com/watch?v=5Y7R_8GQ1gk

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Keywords - aging, cell senescence

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BUFFALO, NY — July 16, 2026 — A new #research paper was #published in Volume 18 of Aging on July 1, 2026, titled “Senescent cells accumulate lipid droplets.”

The study was led by first author Noa Rachmian-Cooper and corresponding author Valery Krizhanovsky from the Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.

Cellular senescence is a natural biological process in which damaged or stressed cells permanently stop dividing while remaining metabolically active. Although senescence helps suppress tumor formation and supports normal processes such as tissue repair and development, senescent cells accumulate with age and contribute to chronic inflammation and numerous age-related diseases, including cancer, cardiovascular disease, and Alzheimer’s disease. While many of the biological effects of senescent cells have been linked to inflammatory signaling, much less has been understood about the metabolic changes that accompany senescence.

In this study, the researchers investigated how cellular metabolism changes during senescence, with a particular focus on lipid metabolism. Using comprehensive metabolic profiling of human fibroblasts, they discovered that senescent cells accumulate high levels of triacylglycerols—the major precursors of lipid droplets—alongside increased glycolytic activity. Additional laboratory experiments confirmed that senescent cells contain significantly more lipid droplets than actively dividing cells.

Full press release - https://www.aging-us.com/news-room/senescent-cells-found-to-accumulate-lipid-droplets-across-aging-and-alzheimers-disease

DOI - https://doi.org/10.18632/aging.206390

Corresponding author - Valery Krizhanovsky - [email protected]

Abstract video - https://www.youtube.com/watch?v=GZbhY3wtGGI

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Keywords - aging, senescence, lipid droplets, metabolism, Alzheimer’s disease

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BUFFALO, NY — July 13, 2026 — A new #review was #published in Volume 18 of Aging on June 26, 2026, titled “Hormonal dimorphism in sarcopenia disease.”

The review was led by first author Romain Menard and corresponding author Romain Madelaine from the MDI Biological Laboratory, Kathryn W. Davis Center for Regenerative Biology and Aging, Bar Harbor, Maine, USA.

Sarcopenia—the progressive loss of skeletal muscle mass, strength, and physical function with aging—is one of the leading causes of frailty and disability in older adults. Although the condition affects millions of people worldwide and has been recognized as a disease by the World Health Organization since 2016, treatment options remain largely limited to exercise and nutritional interventions, with no approved medications specifically targeting the disease. Growing evidence now suggests that one reason for this limited success is that sarcopenia develops through distinct biological mechanisms in women and men.

In this comprehensive review, the authors examine how biological sex influences the hormonal mechanisms underlying muscle aging. They focus on three peptide hormones—apelin, insulin, and oxytocin—and describe how age-related changes in these interconnected signaling networks contribute to muscle decline through distinct biological pathways in women and men.

According to the review, women often experience an abrupt decline in muscle health during menopause as estrogen levels fall rapidly. This hormonal transition disrupts apelin signaling, accelerates insulin resistance, reduces oxytocin-mediated muscle regeneration, and impairs the function of satellite cells, the muscle stem cells responsible for repair and regeneration. In contrast, men generally undergo a slower, more gradual decline in muscle function that parallels progressive reductions in testosterone, resulting in different patterns of hormonal dysregulation and disease progression.

The review also highlights the central roles of apelin, insulin, and oxytocin in maintaining healthy skeletal muscle. Together, these hormones regulate muscle metabolism, glucose utilization, mitochondrial function, protein homeostasis, inflammation, and satellite-cell activity through overlapping signaling pathways. Disruption of this hormonal network during aging is proposed to contribute to impaired muscle repair, reduced metabolic function, chronic inflammation, and progressive muscle loss.

Full press release - https://aging-us.net/2026/07/13/sex-specific-hormones-could-hold-the-key-to-better-sarcopenia-treatments/

DOI - https://doi.org/10.18632/aging.206392

Corresponding author - Romain Madelaine - [email protected]

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Keywords - aging, sarcopenia, hormonal dimorphism, muscle aging, sex-stratified medicine, sexual dimorphism

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In this episode of the Longevity & Aging Series (S4, E4), Dr. Maria Blasco of the Spanish National Cancer Centre (CNIO) joins host Dr. Yuan Zhao to discuss the research paper she co-authored in Volume 18 of Aging, titled “Cross species activity of TERT human telomerase component.”

Interview video - https://www.youtube.com/watch?v=DHeysGp9oPg

DOI - https://doi.org/10.18632/aging.206372

Corresponding author - Maria A. Blasco - [email protected]

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

About Dr. Yuan Zhao: https://www.qmul.ac.uk/sbbs/staff/yuan-zhao.html

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Keywords - aging, telomeres, telomerase

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BUFFALO, NY — July 7, 2026 — A new #review was #published in Volume 18 of Aging on June 22, 2026, titled “The multifaceted inducers of cellular senescence.”

The review was led by first author Hilah Gal and corresponding author Valery Krizhanovsky from the Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.

Cellular senescence is a fundamental biological process in which damaged or stressed cells permanently stop dividing while remaining metabolically active. This response plays an essential role in suppressing tumor formation, supporting embryonic development, facilitating wound healing, and maintaining tissue integrity. However, as people age, senescent cells accumulate because they are no longer efficiently cleared by the immune system. Their persistence contributes to chronic inflammation, tissue dysfunction, cancer, and many age-related diseases.

In this comprehensive review, the authors examine the diverse biological stimuli that trigger cellular senescence and describe how seemingly different stimuli ultimately converge on common molecular pathways that establish stable growth arrest. Rather than viewing senescence as a single process, the review emphasizes its remarkable biological diversity and the importance of understanding how different initiating events shape distinct senescent cell phenotypes.

The review discusses several major biological inducers of cellular senescence. One of the best-established mechanisms is telomere attrition, in which repeated cell division gradually shortens chromosome ends until they trigger a persistent DNA damage response. Other important stimuli include direct DNA damage caused by ionizing radiation, ultraviolet light, chemotherapy, and oxidative injury, all of which activate cellular pathways that permanently halt proliferation.

Full press release - https://aging-us.net/2026/07/07/multiple-biological-triggers-shape-cellular-senescence-in-aging-and-disease/

DOI - https://doi.org/10.18632/aging.206391

Corresponding author - Valery Krizhanovsky - [email protected]

Abstract video - https://www.youtube.com/watch?v=5Y7R_8GQ1gk

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Keywords - aging, cell senescence

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As people live longer, maintaining good health is becoming just as important as extending lifespan. While chronological age simply reflects the number of years a person has lived, biological age measures how well the body is functioning and may better predict future health. Researchers have increasingly focused on lifestyle factors that may slow biological aging, and diet has emerged as one of the most promising.

A research paper published in Volume 18 of Aging titled “Plant-based dietary patterns are associated with slower epigenetic aging,” investigated whether diets emphasizing plant foods are associated with slower biological aging as measured by DNA methylation-based epigenetic clocks.

Full blog post - https://aging-us.org/2026/07/plant-based-dietary-patterns-are-associated-with-slower-biological-aging/

DOI - https://doi.org/10.18632/aging.206362

Corresponding author - Hyunju Kim - [email protected]

Abstract video - https://www.youtube.com/watch?v=FcJ7oEZ-KFk

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Keywords - aging, plant-based diets, DNA methylation, epigenetic aging, all-cause mortality, middle-aged adults

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BUFFALO, NY — July 6, 2026 — A new systematic #review was #published in Volume 18 of Aging on June 18, 2026, titled “Life expectancy and causes of death in classical laminopathic progeroid syndromes: systematic review with individual-patient data synthesis.”

The study was led by co-first authors Carlos López-Vila, Manuel García-Cordeiro, and Luís Estévez-Martínez from the University of Santiago de Compostela, and corresponding author David Araújo-Vilar from the University of Santiago de Compostela and the University Clinical Hospital of Santiago de Compostela, Spain.

Classical laminopathic progeroid syndromes are among the rarest inherited disorders known. Caused by mutations affecting the LMNA gene or the ZMPSTE24 enzyme, these conditions lead to premature aging, severe multisystem disease, and markedly shortened life expectancy. Although Hutchinson-Gilford progeria syndrome (HGPS), mandibuloacral dysplasia (MAD), and restrictive dermopathy (RD) all belong to this group, reliable information about survival and causes of death for each disorder has remained limited because most published reports describe only individual patients or small case series.

In this study, researchers performed a comprehensive systematic review and individual-patient data analysis to date of classical laminopathic progeroid syndromes. Following PRISMA guidelines, they analyzed data from 169 published studies together with two additional genetically confirmed institutional cases, creating a cohort of 158 genetically confirmed patients for the primary survival analysis. By examining individual patient records rather than pooled summaries, the investigators were able to compare survival patterns and causes of death across each disease subtype with greater precision.

Full press release - https://aging-us.net/2026/07/06/comprehensive-individual-patient-analysis-clarifies-life-expectancy-across-rare-progeria-disorders/

DOI - https://doi.org/10.18632/aging.206389

Corresponding author - David Araújo-Vilar - [email protected]

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Keywords - aging, progeria, Lamin A/C (LMNA), ZMPSTE24, survival, cause of death

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BUFFALO, NY — July 1, 2026 — A new #review was #published in Volume 18 of Aging on June 11, 2026, titled “Age-related dysfunctions of the neuroendocrine axes in nonhuman primates with depression-like and anxious behavior.”

The review, dedicated to the late Dr. Mikhail (Misha) Blagosklonny, was written by Nadezhda D. Goncharova from the Kurchatov Complex of Medical Primatology, National Research Center “Kurchatov Institute,” Adler, Sochi, Russian Federation.

As people grow older, their risk of developing stress-related disorders—including depression, metabolic disease, cardiovascular disease, cognitive decline, and neurodegenerative conditions—increases substantially. However, not everyone ages in the same way. Some individuals appear more resilient to stress, while others develop endocrine and metabolic disturbances that may accelerate aging and disease. Understanding the biological mechanisms behind these differences could help identify people at greater risk and support more personalized approaches to healthy aging.

In this review, the author summarizes decades of experimental research investigating how aging affects two major neuroendocrine systems—the hypothalamic-pituitary-adrenal (HPA) axis and the hypothalamic-pituitary-thyroid (HPT) axis—in nonhuman primates displaying either typical adaptive behavior or depression-like and anxiety-like behavior. Because rhesus monkeys closely resemble humans in their physiology, endocrine function, and behavior, they provide a valuable translational model for studying age-related changes that are difficult to examine in people.

The research shows that older monkeys with depression-like and anxiety-like behavior develop more pronounced dysfunction of the HPA axis than animals with standard behavior. These animals exhibited impaired negative feedback regulation, higher evening and nighttime cortisol levels, increased responses to acute stress, and greater activation of stress-related hormonal pathways. Together, these findings suggest impaired regulation of stress responses during aging.

The review also describes important age-related alterations in thyroid function. Older animals with depression-like and anxiety-like behavior showed lower thyroxine secretion, diminished thyroid responsiveness to hormonal stimulation, and evidence of impaired thyroid gland function. These endocrine changes were accompanied by greater insulin resistance, altered triglyceride metabolism, and reduced insulin secretion in overweight animals, indicating that stress-related neuroendocrine dysfunction may extend well beyond the brain.

Importantly, the findings suggest that behavioral characteristics may influence how endocrine systems age. Rather than experiencing identical biological changes over time, individuals with greater vulnerability to stress may develop more severe hormonal disturbances that contribute to age-related disease.

Full press - https://aging-us.net/2026/07/01/nonhuman-primate-research-reveals-how-aging-stress-and-behavior-may-interact-to-increase-disease-risk/

DOI - https://doi.org/10.18632/aging.206388

Corresponding author - Nadezhda D. Goncharova - [email protected] (ORCID id: 0000-0002-2720-9846)

Abstract video - https://www.youtube.com/watch?v=yj8zvthBiA4

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