The study of a rare genetic disease that speeds up the aging process may lead scientists to ways to extend human lifespans. Erasmus Medical Center geneticists Jan Hoeijmaker and his colleagues examined DNA from a boy who suffered from XPF-progeroid syndrome, a condition that caused him to die of "old age" at just 15. From Scientific American:
The teen's illness… when replicated in mice, allowed an international team of researchers to answer a fundamental question in the science of aging: Do we get old due to the accumulation of damage over our lifetimes or due to the genetic blueprint we inherit?
"What we say is [that] both are valid and that, in particular, damage to DNA contributes to aging," says Jan Hoeijmakers, a geneticist at the Erasmus Medical Center in Rotterdam, the Netherlands, and lead author of the study, which comprised teams from four different institutions in Europe and the U.S. "Damage accumulates … but it is modulated by your genetic makeup. If you have better repair and/or slower metabolism, you age slower…"
The researchers compared the activity of thousands of genes in the liver of a 15-day-old mutant mouse to those in a normal mouse who lived two and a half years. The result? "The rapidly aging mice switched their activity from growth to maintenance and repair, up-regulating cellular defenses and down-regulating respiration and metabolism," Hoeijmakers says. "This also occurs upon natural aging, and if you [could] switch to this 'survival' mode early in life, you would live longer."
