The genetics of aging has made substantial strides in the past decade. This
progress has been confined primarily to model organisms, such as filamento
us fungi, yeast, nematodes, fruit flies, and mice, in which some thirty-fiv
e genes that determine life span have been cloned. These genes encode a wid
e array of cellular functions, indicating that there must be multiple mecha
nisms of aging. Nevertheless, some generalizations are already beginning to
emerge. Pt is now clear that there are at least four broad physiological p
rocesses that play a role in aging: metabolic control, resistance to stress
, gene dysregulation, and genetic stability. The first two of these at leas
t are common themes that connect aging in yeast, nematodes, and fruit flies
, and this convergence extends to caloric restriction, which postpones sene
scence and increases life span in rodents. Many of the human homologs of th
e longevity genes found in model organisms have been identified. This will
lead to their use as candidate human longevity genes in population genetic
studies. The urgency for such studies is great: The population is graying,
and this research holds the promise of improvement in the quality of the la
ter years of life.