Mitochondrial DNA mutations and aging: A case closed?

Recent reports of premature aging in mutant mice with greatly increased rates of mitochondrial DNA mutagenesis (so-called 'mitochondrial mutator mice') appeared to confirm that accumulation of mtDNA mutations is a key mechanism of normal aging. Now, in a dramatic turnaround, a new study reports that levels of point mutations in tissues of aged normal mice are much lower than in the mutator mice, apparently ruling out a causal role in normal aging.