[Aging--from the molecule to the organism]

Age-related changes at the molecular, cellular and organ level, as well as at the organism level are heterogeneous with respect to their timing and intensity. Theories on aging are numerous, but for none is there yet any strong, convincing evidence, particularly in regard to whether or not age-changes are programmed or are due to accumulations of random changes in constituent cells. Recent studies indicate, however, that DNA damage and repair may be central to cellular senescence, e.g., there is a direct relationship between the repair capacity and the maximum life span of a given species. The limited division potential of normal human diploid fibroblast cells in vitro is well documented and has been established as a model for cellular aging. Thus, fibroblasts taken from young individuals have a greater total doubling capacity as compared to fibroblasts derived from older individuals. Aging of the brain, heart, liver, and locomotory system are discussed. Within the context of organism aging the multimorbidity, chronic diseases, as well as some peculiarities of pharmacokinetics are also discussed.