Although scientists don’t completely understand why our cells eventually stop dividing, many of them believe that the shrinking of protective DNA caps on the end of chromosomes called telomeres may be responsible. This is based on the fact that every time a cell divides, a bit of telomere is lost until it is no longer active in adult tissue. Ronald DePinho, a molecular biologist and director of the Belfer Institute of the Dana-Farber Cancer Institute along with colleagues, successfully turned a number of mice into younger versions of themselves by stimulating the regeneration of certain tissues. To do this they first genetically engineered mice to grow without telomerase and found that these mice aged prematurely and died at about 6 months; much earlier than the typical mouse that lives to about 3 years. In a second test, DePinho engineered the same type of mouse, but then added back a telomerase gene that became active when the mice received a certain drug. After reactivating the telomerase, the mice experienced almost total recovery of their fertility, livers, spleens, and brain neurons. The results indicate that cells don’t just die when their telomere runs out, but rather that they go into a dormant state from which they can be revived. “One could imagine applying this approach to humans,” DePinho states. By focusing the therapy on specific tissue types, DePinho believes telomerase may play an important role in cell regeneration, although many doubts still remain about whether such an intervention would actually slow aging, or even reverse it.