Rethinking the Mitochondrial Theory of Aging

An interesting paper here, proposing that changes in gene expression have as much or more to do with rising levels of free radical damage with age than simple damage to mitochondrial DNA (mtDNA): "The Mitochondrial Theory of Aging postulates that accumulation of mtDNA mutations and mitochondrial dysfunction are responsible for generating aging phenotypes and limiting lifespan. Although widely accepted, this theory remains unproven because the evidence supporting it, while substantial, is largely correlative. Furthermore, recent experimental results in mice with accelerated rates of mtDNA mutagenesis have challenged the traditional formulation of the Mitochondrial Theory, perhaps warranting a reevaluation of some of its core principles. In this perspective, we summarize recent work suggesting that both the quantity and the quality of mitochondrial gene expression play a much greater role in the aging process than previously appreciated. We speculate that this form of mitochondrial dysfunction may operate independently or in concert with mtDNA mutations to promote age-related pathology and limit lifespan." Non-functional gene expression has the same effective result as a damaged gene - the proteins produced from the blueprint of that gene, essential to cellular machinery, are no longer made inside that cell.

Link: http://www.ncbi.nlm.nih.gov/pubmed/17603300

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