The scientists developed a strain of mice with a mutation in a gene called p66, thought to inhibit tumor formation. Not only did they not develop cancer, the mutants lived an average of 30 percent longer than their unaltered neighbors. It’s a long way from an extra few months for a mouse to Old Testament-like life spans for humans. But, says Pier Paolo Pandolfi, a geneticist at the Memorial Sloan-Kettering Cancer Center in New York who developed the mice, “this is a tremendous insight into the aging process.”
The p66 protein appears to affect how cells cope with a kind of chemical damage called oxidative stress, which is associated with aging. The protein may act as an on-off switch for cellular repair mechanisms; disrupting its gene would jam the switch on, causing cells to resist damage more vigorously as it occurs. It might also work by instructing injured cells to self-destruct, a common biological strategy to prevent damaged cells from becoming cancerous. Knocking the gene out would make the system more forgiving, allowing damaged cells–and the organs they make up–to survive longer.
Leonard Guarente, a molecular biologist who studies aging at MIT, says that controlling oxidative stress probably won’t lead to longer human lives–“there are too many other things that can get you.” But now scientists have a target for drugs that could combat the symptoms of aging, from wrinkled skin and failing eyesight to neurodegenerative diseases like Parkinson’s and Alzheimer’s. Mickey Mouse, who turned 71 this month, still seems awfully perky. His cousins in the lab may help us to figure out his secret.
