Abstract
Aging is a primary risk factor for the progressive loss of function, disease onset, and increased vulnerability to negative health-related outcomes. These clinical manifestations arise in part from declines in mitochondrial, metabolic, and other processes considered to be hallmarks of aging. Collectively, these changes can be defined as age-associated cellular decline (AACD) and are often associated with fatigue, reduced strength, and low physical activity. This manuscript summarizes a recent Gerontological Society of America Annual Scientific Meeting symposium that explored mechanisms, clinical signs, and emerging cellular nutrition interventions for AACD. The session opened by highlighting results of an expert consensus that developed an initial framework to identify self-reported symptoms and observable signs of AACD in adults aged >50 years. Next, findings from the multi-ethnic molecular determinants of sarcopenia study were discussed, showing impaired mitochondrial bioenergetic capacity and NAD+ metabolism in skeletal muscle of older adults with sarcopenia. Lastly, recent clinical evidence was presented linking urolithin A, a natural mitophagy activator, to improved mitochondrial and cellular health. The virtual panel discussed how stimulation of mitochondrial function via biological pathways, such as mitophagy and NAD+ augmentation, could improve cellular function and muscle health, potentially impacting clinical signs of AACD and overall healthy aging.
Highlights
Geroscience has proposed that the underlying biological mechanisms of aging are central to the global increase in susceptibility to disease and disability that occurs with aging
Strong correlations have been revealed between biological mechanisms and some clinical phenotypes that are typical of aging, declines in autophagy, mitochondrial dysfunction, and cellular senescence [1]
Experts convened at the virtual 2020 Annual Scientific Meeting of the Gerontological Society of America to review recent developments to target the origins of cellular decline, understand the modifiable signs and risks of accelerated aging and cellular decline, discuss data showing how mitochondrial dysfunction in older adults impairs muscle bioenergetics and function, and share emerging evidence on nutritional interventions to mitigate age-related mitochondrial dysfunction and improve health
Summary
Geroscience has proposed that the underlying biological mechanisms of aging are central to the global increase in susceptibility to disease and disability that occurs with aging. Studying the common cellular declines and modifiable signs and risks serves to identify promising targets for future interventions aimed at slowing aging and preventing age-related clinical conditions. As muscle tissues have a high abundance of accessible mitochondria and are of clinical significance to overall altered mitochondrial morphology, special attention was given to the common changes in skeletal muscle—from mechanisms to symptoms and performance (Figure 1)—tightly linked to well-being as adults grow older [2]. This proceedings manuscript captures the key points of the presentations and panel/audience discussion
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