Studies at the Dana-Farber Cancer Institute and Harvard Medical School in Boston showed that mice engineered to lack the enzyme, called telomerase, became prematurely decrepit, an article published by the journal Nature reported. When the enzyme was replaced, the mice recovered their health, the researchers said.
Reawakening the enzyme in cells in which it has stopped working might slow normal human aging, Ronald DePinho, a cancer geneticist at the Dana-Farber institute, says.
"This has implications for thinking about telomerase as a serious anti-aging intervention," he says.
Other scientists, however, note that mice lacking telomerase are a poor stand-in for the normal aging process, and that increasing telomerase in humans could have the potential to promote tumor growth.
"Telomere rejuvenation is potentially very dangerous unless you make sure that it does not stimulate cancer," David Harrison, who researches ageing at the Jackson Laboratory in Bar Harbor, Maine, says.
"They are not studying normal aging, but aging in mice made grossly abnormal," he says of the Dana-Farber research.
DePinho acknowledges there is more to aging than shortened telomeres, as the ends of chromosomes are called -- particularly late in life -- but argues that telomerase therapy could one day be combined with other therapies that target the biochemical pathways of aging.
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