Mutations in mitochondrial DNA have long been suspected as a culprit in aging. But whether these mutations are a cause or a result of aging has been debatable. In 2004, work from Nils-Göran Larsson's group at the Karolinska Institute suggested that mitochondrial mutations indeed promote aging, and a new debate has since arisen.
Larsson's group engineered mice to carry an error-prone mitochondrial DNA polymerase (Pol-g), and found that these mice accumulate mitochondrial mutations and age more quickly than normal mice.1 "The mice lost hair, got anemia, osteoporosis, and weight reduction," says Larsson. Lawrence Loeb, from the University of Washington, says that "until this paper came out it was just a correlation between mitochondrial DNA mutations and aging."
It is now known that the mutant mice also speak to the free-radical theory of aging. Larsson's group found that their mice don't accumulate more reactive oxygen species, suggesting their rapid aging isn't ...
