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ARS Home » Northeast Area » Boston, Massachusetts » Jean Mayer Human Nutrition Research Center On Aging » Research » Publications at this Location » Publication #390493
Research Project: Nutrition, Sarcopenia, Physical Function, and Skeletal Muscle Capacity During Aging

Location: Jean Mayer Human Nutrition Research Center On Aging

Title: Nutritional mediators of cellular decline and mitochondrial dysfunction in older adults

Author
item GURALNIK, JACK - University Of Maryland School Of Medicine
item FEIGE, JEROME - Nestle Research & Development
item SINGH, ANURAG - Amazentis Sa
item FIELDING, ROGER - Jean Mayer Human Nutrition Research Center On Aging At Tufts University

Submitted to: Geriatrics
Publication Type: Review Article
Publication Acceptance Date: 4/2/2021
Publication Date: 4/6/2021
Citation: Guralnik, J.M., Feige, J.N., Singh, A., Fielding, R.A. 2021. Nutritional mediators of cellular decline and mitochondrial dysfunction in older adults. Geriatrics. 6(2):37. https://doi.org/10.3390/geriatrics6020037.
DOI: https://doi.org/10.3390/geriatrics6020037

Interpretive Summary:

Technical 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.