Evolution theory indicates that investment in mechanisms of somatic ma
intenance and repair is likely to be limited, suggesting that aging ma
y result from the accumulation of unrepaired somatic defects. An impor
tant corollary of this hypothesis is that multiple mechanisms of aging
operate in parallel. We describe a recently developed ''network theor
y of aging'' that integrates the contributions of defective mitochondr
ia, aberrant proteins, and free radicals in the aging process and that
includes the protective effects of antioxidant enzymes and proteolyti
c scavengers. Possibilities for further extension of the theory and it
s role in prediction and simulation of experimental results are discus
sed. (C) 1997 Elsevier Science Inc.