or tail evoked after similar direct stimulation. These declines in mobility appear irreversible during normal worm aging.
The development of sarcopenia in worms can be delayed by the age-1 mutation, which also extends the worm lifespan by 60 to 100% (Herndon et al., 2002). The age-1 mutation affects a phosphatidylinositol-3-phosphate kinase (PI3 kinase), which acts along with the daf-2 insulin/IGF-1 receptor and daf-16 FOXO family DNA-binding protein to control aging and life span of the worm. The ability of a single mutation to alter the development of sarcopenia provides a ready intervention to study the mechanisms involved. Other potential applications of C. elegans in sarcopenia research involve exploiting the small size and short lifespan of worms to develop genetic or pharmacologic screens to find new genes and compounds that prevent or delay sarcopenia.
There is a pressing need for new treatments for sarcopenia. Ideas generated by clinical studies or experiments in animals can serve as the basis for the design of new treatments. Experimental animals will need to serve as the initial test system with the goal of translating safe and effective treatments to clinical studies. Many of these treatments will ultimately be destined for trials in potentially frail older people. The age and comorbid illnesses in these subjects result in unique challenges (Ferrucci et al., 2004).
Sarcopenia is an unfortunate but normal aspect of the aging of the neuromuscular system of people and many other animal species. The loss of muscle strength that accompanies sarcopenia has important impacts on the health and functioning of people. Consequently there is a pressing need to better understand the clinical risk factors and cellular and molecular mechanisms involved to promote the development of new therapeutic approaches. Fortunately, the last several years have seen the development of new clinical and experimental resources to facilitate studies.
A current challenge in the field is to develop rigorous animal research in sarcopenia. Clinical research has provided support for a number of endocrine, nutritional, and inflammatory changes as being associated with the development of sarcopenia. As clinical studies based upon addressing some of these changes have shown only modest effects, there is a pressing need for animal research to prioritize the contribution that each change has on muscle mass and muscle strength. Further basic studies would then be able to elucidate the biochemical mechanisms underlying the effects with the ultimate goal of finding new targets for drug discovery. The development of the simple nematode C. elegans as a model system provides a new opportunity to study the development of sarcopenia at a genetic level.
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