Abstract
Work, initially in Caenorhabditis elegans and then more recently in fruit flies and mice, has suggested that anti-aging mutations extend life span by simultaneous activation of pathways that protect cells from multiple forms of injury. This "multiplex stress resistance" theory suggests a number of new avenues for investigation of the genetic and cellular controls that influence organismic longevity within and among species, and that might lead to the development of pharmaceuticals that retard the aging process and, therefore, the entire panoply of age-dependent diseases and disabilities.