Telomeres are protective endcaps of DNA, which shorten each time cells divide. Telomere shortening has been linked to the aging process. Ronald A. DePinho, from Harvard Medical School (Massachusetts, USA), and colleagues engineered mice with short telomeres and inactive telomerase to mimic aging.  The team then switched telomerase back on, and after four weeks, atrophied tissue had regenerated in several organs, new brain cells were developing, and the mice were living longer. The researchers report that: “Telomerase reactivation in such late generation transcriptase-oestrogen receptor (TERT-ER) mice extends telomeres, reduces DNA damage signalling and associated cellular checkpoint responses, allows resumption of proliferation in quiescent cultures, and eliminates degenerative phenotypes across multiple organs.” Writing that: “Accumulating evidence implicating telomere damage as a driver of age-associated organ decline and disease risk ,” the team submits that: “The marked reversal of systemic degenerative phenotypes in adult mice observed here support the development of regenerative strategies designed to restore telomere integrity.”