Considering the Data on Mitochondrial DNA Damage in Aging
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These researchers are concerned about the state of data for mitochondrial DNA damage in aging, suggesting that the research community doesn't in fact have enough data to demonstrate that work in mice is fully relevant to the human molecular biology of aging in this case:

A significant body of work, accumulated over the years, strongly suggests that damage in mitochondrial DNA (mtDNA) contributes to aging in humans. Contradictory results, however, are reported in the literature, with some studies failing to provide support to this hypothesis. With the purpose of further understanding the aging process, several models, among which mouse models, have been frequently used. Although important affinities are recognized between humans and mice, differences on what concerns physiological properties, disease pathogenesis as well as life-history exist between the two; the extent to which such differences limit the translation, from mice to humans, of insights on the association between mtDNA damage and aging remains to be established.

In this paper we revise the studies that analyze the association between patterns of mtDNA damage and aging, investigating putative alterations in mtDNA copy number as well as accumulation of deletions and of point mutations. Reports from the literature do not allow the establishment of a clear association between mtDNA copy number and age, either in humans or in mice. Further analysis, using a wide spectrum of tissues and a high number of individuals would be necessary to elucidate this pattern.

Likewise humans, mice demonstrated a clear pattern of age-dependent and tissue-specific accumulation of mtDNA deletions. Deletions increase with age, and the highest amount of deletions has been observed in brain tissues both in humans and mice. On the other hand, mtDNA point mutations accumulation has been clearly associated with age in humans, but not in mice. Although further studies, using the same methodologies and targeting a larger number of samples would be mandatory to draw definitive conclusions, the revision of the available data raises concerns on the ability of mouse models to mimic the mtDNA damage patterns of humans, a fact with implications not only for the study of the aging process, but also for investigations of other processes in which mtDNA dysfunction is a hallmark, such as neurodegeneration.



If this is true, does that leave us with telomere shorting as a cause of aging? Or perhaps its nothing more than the accumulation of lysosomol aggregates and glycolization cross-links. I still think mtDNA damage is the primary cause of aging.

Posted by: Abelard Lindsey at December 18, 2013 10:09 AM

I think it's a mistake to look at any particular thing as the 'primary cause' of aging in humans. Different types of problem are going to show up at different ages, and the age related issues that show up because of glucosepane are going to show up whether or not we fix mutation damage that causes cancer.

It seems like you're trying to look at aging as a pathology, caused primarily by a 'thing' - but from my standpoint, aging is merely a side effect of various kinds of breakdowns, wear and tear, and bad chemistry.

Posted by: Dennis Towne at December 18, 2013 3:37 PM
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