Research

摘要

Loss of telomeres, the protective tips on the ends of chromosomes, causes tissue atrophy and other damage. A growing body of evidence points to telomere defects as a driver of age-associated organ decline and disease. Ronald DePinho and colleagues now show that reactivation of endogenous telomerase in mice extends telomeres, reduces DNA-damage signalling, allows resumption of proliferation in quiescent cultures and eliminates degenerative phenotypes in many organs, including the brain.