Telomeres are protective lengths of repetitive DNA at the end of chromosomes that shorten with each cell division. When a single telomere gets down to a critical length, it triggers a damage response that causes the cell to become quiescent. If enough cells in a tissue become quiescent or go into apoptosis, then the tissue suffers functionally—the main symptom of aging. Altering the shortening of telomeres could be a way of slowing down the overall aging process. Ronald DePinho and colleagues at the Dana-Farber Cancer Institute have shown that reactivation of endogenous telomerase in adult mice extends telomeres, reversing tissue atrophy (Nature, 469:102-6, 2011).
The Scientist: Is reactivating telomerase a potential way to increase human life span?
Preston Estep: Telomere attrition is not the only cause of senescence overall—that will vary from individual to individual. One process will be limiting in some individuals, and the big and unanswered question for ...
