A large number of mutations have now been identified that extend the life span of simple model organisms such as yeast, nematodes, and fruit flies. Many cause a doubling or more of mean and maximum life span. Most can be organized into a few broad categories: mutations that blunt the insulin/IGF-1 signaling pathway, reduce mitochondrial activity and/or oxidative byproducts of energy production, increase stress resistance, and optimize genome maintenance (11,15,159,160).
Because many of these mutations act in conserved pathways, analogous mutations have been studied in mammals, principally mice. A consistent finding in mice is that, whereas some mutations do indeed extend longevity, for the most part, the life span extensions are much more modest and rarely exceed a 40% increase. It is beyond the scope of this chapter to review all the mouse models of extended longevity that have been created and studies, but a few are discussed below.
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