A unifying hypothesis to explain the retardation of aging and tumorigenesis by caloric restriction
Oxidative damage is an ubiquitous, chronic process which is heavily dependent on oxidative metabolism. It is shown that repair is not 100% efficient and that PCD is an alternative mechanism which serves to selectively eliminate damaged cells from the healthy cell population. It is suggested that the upregulation of PCD through caloric restriction can effectively retard both aging and cancer.
Publication Name: The Journals of Gerontology, Series A
Mapping senescence genes
Human fibroblasts, certain nematodes, Werner syndrome and Alzheimer's disease have been successfully used as model systems for aging. Analysis of hybrids between immortal fibroblast lines showedat least four distinct complementation groups for indefinite division. Longer lived mutants of short-lived nematodes and fruit flies have also been selected to study the genes involved in aging.
Publication Name: Journals of Gerontology