摘要: Modern gerontology is faced with a major paradox. On the one hand, we have evolutionary biologists who concluded that modulation of longevity and senescence under highly polygenic controls, multiple mechanisms are likely to be involved, much pathology unfolds stochastic in origin. Let us refer members this camp as “complificationists.” other some point three lines evidence seem challenge view. They believe aging may produced by small number mechanisms, perhaps even single mechanism, such oxidative damage macromolecules. “simplificationists.” emphasize exceedingly well documented observations calorically restricted rodents substantially greater life spans than their fed brethren do. also experiments nematodes (Caenorhabditis elegans) fruit flies (Drosophila melanogaster). In both organisms, simple genetic manipulation, including gene mutations, lead substantial increments span. For case man, they research on Werner syndrome, recessive progeroid syndrome caused mutation helicase gene. Homozygotes exhibit an acceleration aspects senescent phenotype, four geriatric disorders associated human (arteriosclerosis, cancer, diabetes mellitus osteoporosis).