Aging Reversed in Mice after Telomerase Treatment

Hugh Pickens writes: "The Guardian reports that scientists claim to be a step closer to reversing the aging process after experimental treatment developed by researchers at Harvard Medical School turned weak and feeble old mice into healthy animals by regenerating their aged bodies. "What we saw in these animals was not a slowing down or stabilization of the aging process. We saw a dramatic reversal – and that was unexpected," says Ronald DePinho, who led the study. The Harvard group focused on a process called telomere shortening where each time a cell divides, the telomeres are snipped shorter, until eventually they stop working and the cell dies or goes into a suspended state called "senescence". Researchers bred genetically manipulated mice that lacked an enzyme called telomerase that stops telomeres getting shorter causing the mice to age prematurely and suffer ailments, including a poor sense of smell, smaller brain size, infertility and damaged intestines and spleens. When the mice were given injections to reactivate the enzyme, it repaired the damaged tissues and reversed the signs of aging raising hope among scientists that it may be possible to achieve a similar feat in humans – or at least to slow down the aging process. "This could lead to strategies that enhance the regenerative potential of organs as individuals age and so increase their quality of life," added DePinho cautioning that "whether it serves to increase longevity is a question we are not yet in a position to answer.""

Inducing telomerase activity and cancer risk

[jcmurray]

Telomeres consistent of repetitive subunits of DNA at the ends of chromosomes, where they protect chromosomes from DNA damage. In aged humans, telomere shortening and DNA damage likely have occurred. Reintroducing telomerase activity in these individuals--where telomerase activity is low or absent in adults--may increase the risk of tumorigenesis by maintaining telomeres in cells with significant DNA damage, thereby avoiding DNA damage-induced cell death or senescence.

This may differ from the animal model