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Nature Genetics 39, 445 - 446 (2007)
doi:10.1038/ng0407-445
Mitochondrial DNA mutations and aging: a case closed?
Konstantin Khrapko1 & Jan Vijg2
- Konstantin Khrapko is in the Gerontology Division, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA. e-mail: khrapko@hms.harvard.edu
- Jan Vijg is in the Buck Institute for Age Research, 8001 Redwood Blvd., Novato, California 94945, USA. e-mail: jvijg@buckinstitute.org
Abstract
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.
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