Point Mutations, Mitochondria and Aging

A little science from sci.life-extension to start the week off on the right foot:

Increasing evidence suggests that mitochondrial function declines during aging in various tissues and in a wide range of organisms. This correlates with an age-dependent large accumulation of specific point mutations in the mtDNA control region that was reported recently in human fibroblast and the skeletal muscle. However, it is rather rare to evaluate aging-related mtDNA mutations in other model animal systems. In this study, we analyzed mtDNA control regions of brain, skeletal muscle, heart, and other tissues from aged mice, in search of specific point mutations.
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This may suggest that that humans have a better or tighter copy number control. Deletion mutations and clonal expansions occur in in human cells with relaxed copy number control but apparently not normally as in mice . If this is in fact true then this could presumably account for the longer lifespans and decreased ROS of humans in relation to mice.

The commentary is of course speculative (if well informed), but it is always good to see more work being done on mitochondria in the context of aging. Unlike many other areas of aging science, some groups are making headway on the required groundwork for repairing age-related damage in mitochondria.