A large number of point mutations in mitochondria -- the energy-producing units of the cell -- do not have a direct link to the ageing process in mice, according to a study to be published online in Nature Genetics. While such mutations have been shown to accumulate during ageing in mice and humans, this result contradicts the notion that such mutations are causal factors in the aging process.
The widely debated mitochondrial theory of ageing postulates that the lifelong accumulation of mitochondrial DNA mutations contributes to the decline of tissue function observed in ageing. Lawrence Loeb and colleagues used a new, highly sensitive approach to determine the rate of single base-pair mutations in mitochondrial DNA in normal ageing mice, and in so-called 'mitochondrial mutator mice', which have a 500-fold greater mutation burden than normal mice. While the authors found that normal mice have an 11-fold increase in mitochondrial point mutations with age, the mutator mice did not have any obvious features of accelerated ageing, suggesting that the more modest mutation burden in normal mice is not likely to be contributing to the ageing process. It is important to note that this study does not exclude the possibility that large deletions of mitochondrial DNA contribute to ageing. For example, large deletions in mitochondrial DNA have been correlated with the impairment of certain neurons in aged individuals and in individuals with Parkinson disease.
Lawrence Loeb (University of Washington, Seattle, WA, USA)
Abstract available online.
(C) Nature Genetics press release.
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