Research Article: One size may not fit all: anti-aging therapies and sarcopenia

Date Published: December 16, 2011

Publisher: Impact Journals LLC

Author(s): Tyesha N. Burks, Ronald D. Cohn.

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Abstract

Sarcopenia refers to age-related loss of muscle mass and function. Several age-related changes occur in skeletal muscle including a decrease in myofiber size and number and a diminished ability of satellite cells to activate and proliferate upon injury leading to impaired muscle remodeling. Although the molecular mechanisms underlying sarcopenia are unknown, it is tempting to hypothesize that interplay between biological and environmental factors cooperate in a positive feedback cycle contributing to the progression of sarcopenia. Indeed many essential biological mechanisms such as apoptosis and autophagy and critical signaling pathways involved in skeletal muscle homeostasis are altered during aging and have been linked to loss of muscle mass. Moreover, the environmental effects of the sedentary lifestyle of older people further promote and contribute the loss of muscle mass. There are currently no widely accepted therapeutic strategies to halt or reverse the progression of sarcopenia. Caloric restriction has been shown to be beneficial as a sarcopenia and aging antagonist. Such results have made the search for caloric restriction mimetics (CRM) a priority. However given the mechanisms of action, some of the currently investigated CRMs may not combat sarcopenia. Thus, sarcopenia may represent a unique phenotypic feature of aging that requires specific and individually tailored therapeutic strategies.

Partial Text

Aging is a multi-factorial process affecting every organ of the body. In the past, aging research has primarily focused on neurodegeneration and loss of bone mass. Not much attention has been given to sarcopenia until recently. Sarcopenia refers to the physiological loss of skeletal muscle mass and function during aging [1]. Several age-related changes occur in skeletal muscle including a decrease in myofiber size and number and a diminished ability of satellite cells to activate and proliferate upon injury leading to impaired muscle remodeling [2, 3]. The progressive loss of muscle mass poses health risks for older adults that lead to a decrease in physical activity and a rise in the incidence of falls and related fractures. Rehabilitation time is often prolonged after injury, which in turn extends the duration of bed rest resulting in disuse atrophy, an additional variable that is exaggerated in the aging population [4-6] thus interfering with a successful recovery.

Sarcopenia is a devastating condition that can lead to disability, increased morbidity and mortality. The age-related modulation of a variety of signaling pathways together with environmental constraints imposed on elderly patients accelerate its progression. The etiology of sarcopenia is linked to a variety of pathogenic mechanisms and it is therefore challenging to identify targeted therapies. The only currently existing management for sarcopenia consists of nutritional supplementation and an exercise regimen, albeit with only mild beneficial effects. However, all geriatric patients cannot benefit from this treatment. Because normal muscle mass and strength are required to perform daily activities, it is imperative to identify pharmacological compounds that can prevent or slow the progression of sarcopenia.

 

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