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Our ability to define the causes of aging could enable targeted interventions to extend healthspan. Classical evolutionary models based on individual age have provided critical insights into empirical trajectories of aging; however, gaps remain. We argue that technological advances in data capture, resolution, and scale, present a rich opportunity to shed light on heterogeneity in patterns of aging. Computational and data analysis advances have produced expanded theoretical models that explicitly address details of the underlying biology, introducing variables and dynamics that go beyond ‘age’ itself. We argue that by incorporating richer biological detail to create more integrative predictive models, we can gain insight into expected future distributions of aging within populations, and better understand the molecular and demographic context in which selection has given rise to variability in aging. We provide an overview of existing models that address heterogeneity, and outline future directions and applications that would advance this key area in aging and biomedical research.

Ageing of the immune system, or immunosenescence, contributes to the morbidity and mortality of the elderly 1 , 2 . To define the contribution of immune system ageing to organism ageing, here we selectively deleted Ercc1 , which encodes a crucial DNA repair protein 3 , 4 , in mouse haematopoietic cells to increase the burden of endogenous DNA damage and thereby senescence 5 – 7 in the immune system only. We show that Vav-iCre +/− ;Ercc1 −/fl mice were healthy into adulthood, then displayed premature onset of immunosenescence characterized by attrition and senescence of specific immune cell populations and impaired immune function, similar to changes that occur during ageing in wild-type mice 8 – 10 . Notably, non-lymphoid organs also showed increased senescence and damage, which suggests that senescent, aged immune cells can promote systemic ageing. The transplantation of splenocytes from Vav-iCre +/− ;Ercc1 −/fl or aged wild-type mice into young mice induced senescence in trans , whereas the transplantation of young immune cells attenuated senescence. The treatment of Vav-iCre +/− ;Ercc1 −/fl mice with rapamycin reduced markers of senescence in immune cells and improved immune function 11 , 12 . These data demonstrate that an aged, senescent immune system has a causal role in driving systemic ageing and therefore represents a key therapeutic target to extend healthy ageing. An aged, senescent immune system has a causal role in driving systemic ageing, and the targeting of senescent immune cells with senolytic drugs has the potential to suppress morbidities associated with old age.

For several decades, understanding ageing and the processes that limit lifespan have challenged biologists. Thirty years ago, the biology of ageing gained unprecedented scientific credibility through the identification of gene variants that extend the lifespan of multicellular model organisms. Here we summarize the milestones that mark this scientific triumph, discuss different ageing pathways and processes, and suggest that ageing research is entering a new era that has unique medical, commercial and societal implications. We argue that this era marks an inflection point, not only in ageing research but also for all biological research that affects the human healthspan. The milestones that mark the advances in ageing research, the medical, commercial and societal implications of ageing and the different ageing pathways and processes that are associated with ageing are discussed.

[...]there was a thinner myelin sheath around the optic nerve in cKO mutants, which resulted in more nodes of Ranvier but reduced nerve conduction velocity. [...]when the authors used a tamoxifen-inducible cKO model to deplete oligodendrocyte ankyrin G in 2-month-old animals, there were no consistent deficits in PNJ formation or animal behavior. From whole-brain translatomic profiling of inducible cKO mutants, the authors observed a significant increase in expression of cytoskeletal genes such as Ank2 (which encodes ankyrin B).

Background Active aging empowers older adults to maintain physical, social, and psychological well-being as they age, enabling them to participate in social activities according to their preferences and capabilities. However, many older adults face communication and social skills challenges, necessitating interventions to minimize social communication barriers and promote active aging. Despite the importance of communication and social skills in active aging, further studies are essential to explore older adults’ perspectives and develop strategies that support active aging and address potential barriers. Therefore, this study aimed to investigate the effect of communication and social skills training on the active aging of older adults. Methods This quasi-experimental trial with randomized allocation study involved 80 older adults from two daycare centers in southeastern Iran in 2024. Participants were randomly assigned to either a control or an intervention group. The intervention group received an eight-session communication and social skills training program, conducted twice a week for two hours in groups of 20. Both groups completed the Iranian Active Aging Measurement Instrument before and one month after the intervention. Results The mean ages of participants in the intervention and control groups were 68.94 ± 7.27 and 67.13 ± 5.09 years, respectively. Training in communication and social skills led to a significant increase in the total score of active aging (98.18 ± 17.77) and its dimensions (mindfulness, active insight, physical-functional dynamics, interactionism, role-playing, and social participation) during the post-test stage compared to the pre-test (148.97 ± 13.19), (t = -25.87, p  < 0.001) and the control group (1.101 ± 8.18), (t = 1.35, p  = 0.18). Conclusion This study contributes valuable evidence supporting psychosocial interventions for active aging. To advance this field, further research should focus on the long-term impact, cultural adaptability, and multimodal strategies that comprehensively address physical, cognitive, and social domains.

People in developed countries are living longer and, just as the aged population around the world is steadily growing, the number of adults eighty-five and older in the United States is projected to quadruple to twenty-one million people by 2050. The aging of our population has huge implications for baby boomers and their children, and has generated a greater interest in the causes and effects of aging. Our Aging Bodies provides a clear, scientifically based explanation of what happens to all the major organ systems and bodily processes-such as the cardiovascular and digestive systems-as people age. The first section is an overview of secondary aging-changes that occur with age that are related to disease and the environment-and include the effect of such things as diet, humor, and exercise. Readers will also learn about primary aging-intrinsic changes that occur with the aging of specific organs and body systems (including the prostate, the heart, the digestive system, and the brain). Throughout the book, Gary F. Merrill weaves in personal anecdotes and stories that help clarify and reinforce the facts and principles of the underlying scientific processes and explanations. Our Aging Bodies is accessible to a general reader interested in the aging phenomenon, or baby boomers wanting to be more informed when seeing their doctor and discussing changes to their bodies as they age.

The global population of individuals over the age of 65 is growing at an unprecedented rate and is expected to reach 1.6 billion by 2050. Most older individuals are affected by multiple chronic diseases, leading to complex drug treatments and increased risk of physical and cognitive disability. Improving or preserving the health and quality of life of these individuals is challenging due to a lack of well‐established clinical guidelines. Physicians are often forced to engage in cycles of “trial and error” that are centered on palliative treatment of symptoms rather than the root cause, often resulting in dubious outcomes. Recently, geroscience challenged this view, proposing that the underlying biological mechanisms of aging are central to the global increase in susceptibility to disease and disability that occurs with aging. In fact, strong correlations have recently been revealed between health dimensions and phenotypes that are typical of aging, especially with autophagy, mitochondrial function, cellular senescence, and DNA methylation. Current research focuses on measuring the pace of aging to identify individuals who are “aging faster” to test and develop interventions that could prevent or delay the progression of multimorbidity and disability with aging. Understanding how the underlying biological mechanisms of aging connect to and impact longitudinal changes in health trajectories offers a unique opportunity to identify resilience mechanisms, their dynamic changes, and their impact on stress responses. Harnessing how to evoke and control resilience mechanisms in individuals with successful aging could lead to writing a new chapter in human medicine. Finding a reference metric for the rate of biological aging is key to understanding the molecular nature of the aging process. Defining and validating this metric in humans opens the door to a new kind of medicine that will overcome the limitation of current disease definitions. We will then be able to approach health in a global perspective and bring life course preventative measures to the center of attention.

È stato inoltre osservato che gli eventi avversi auto-riportati si sono verificati con minore frequenza nel gruppo VNP. Vaporized nicotine products for smoking cessation among people experiencing social disadvantage: a randomized clinical trial. Secondo Thomas McDade, antropologo biologico alla Northwestern University di Chicago, «nelle società non industrializzate, l’infiammazione è attivata in modo molto diverso, spesso da una maggiore esposizione precoce a fattori ambientali che modulano il sistema immunitario in senso protettivo». A Common Assumption About Aging May Be Wrong, Study Suggests.

Abstract For more than 50 years, under the leadership of four editors and two publishers, The International Journal of Aging and Human Development (IJAHD) has featured multidisciplinary scholarship related to aging processes and older adults. With the publication of eight issues a year and over 1000 pages of scientific content, the IJAHD places emphasis upon psychological and social studies of aging and the aged. However, the Journal also publishes research that integrates observations from other disciplines that illuminate the “human” side of gerontology. A more recent focus includes midlife development, as well. About half (47%) of the publications in the IJAHD are from international colleagues. IJAHD is delighted to support new investigators as they navigate dissemination. This presentation will discuss tips for both international and US-based scholars for ensuring timely reviews and positive decisions for manuscript submissions, including such areas as key words, suggesting unbiased reviewers, formatting, writing mechanics, clearly-articulated methods, and a sound theoretical basis.