Abstract
Life span and decline of physiological functions in aged animals are regulated by interactions between genes and the environment. Genes have an important role in predisposing elderly individuals to several common and complex disorders caused by environmental risk factors. Recent completion of the Human and Animal Genome Project has opened a new era of studies to identify genes, which regulate the life span, rate of aging, and susceptibility to age-related diseases. Many gene mutations for increasing or decreasing the life span have been identified in model animals including worms, flies, and rodents, as well as in humans. It is of particular interest that mutations in glucose or insulin/insulin-like growth factor-1 signaling pathways consistently extend the life span by slowing the aging process and increasing stress resistance in these species. In addition, studies of mutant animals suggest that the reactive oxygen species in the mitochondria might be the main determinant of life spans. Human genetic disorders, which manifest accelerated aging or premature aging, suggest the importance of genes maintaining chromosomal stability. Genetic analysis of senescence-accelerated mouse strains (SAMP) indicate that several genes contribute to their short life spans. These findings suggest that the aging process may be controlled by many genes and might be decelerated by environment regulation of these genes. [Jpn J Physiol 54 Suppl:S31 (2004)]
