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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.[1]

References

  1. Mitochondrial DNA mutations and aging: a case closed? Khrapko, K., Vijg, J. Nat. Genet. (2007) [Pubmed]
 
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