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Abstract
There is now substantial evidence, in some cases compelling and in others fairly preliminary, that mouse lifespan can be extended by 3 dietary interventions (Miller et al. 2005; Sun, Sadighi Akha, Miller, & Harper, 2009; Weindruch & Sohal, 1997), by mutations in numerous genes (Ladiges et al., 2009), and by multiple drugs including rapamycin (Harrison et al., 2009). There are also provocative reports of genetic or nongenetic interventions that seem to convey health benefits to mice without clear improvement in lifespan. These new methods for postponing ill health and/or death provide valuable tools for asking questions, at the level of cell biology and organismic physiology, about the factors that control the rate of aging in mammals and the pathways that link aging to diseases and to death. This research area may also someday be seen as an early step toward the development of preventive medicines that postpone a wide range of human maladies by retarding the common factor, aging, that underlies them.
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