Recent research has shown that inserting a gene for the protein component of 
telomerase into senescent human cells reextends their telomeres to lengths 
typical of young cells, and the cells then display all the other identifiable 
characteristics of young, healthy cells. This advance not only suggests that 
telomeres are the central timing mechanism for cellular aging, but also 
demonstrates that such a mechanism can be reset, extending the replicative life 
span of such cells and resulting in markers of gene expression typical of 
"younger" (ie, early passage) cells without the hallmarks of malignant 
transformation. It is now possible to explore the fundamental cellular 
mechanisms underlying human aging, clarifying the role played by replicative 
senescence. By implication, we may soon be able to determine the extent to which 
the major causes of death and disability in aging populations in developed 
countries-cancer, atherosclerosis, osteoarthritis, macular degeneration, and 
Alzheimer dementia--are attributable to such fundamental mechanisms. If they are 
amenable to prevention or treatment by alteration of cellular senescence, the 
clinical implications have few historic precedents.