High measurement reliabilities were obtained. Asymmetries in brain structures were not affected by aging in either sex. Our results are generally consistent with the few published studies on sex differences in brain aging and suggest that, for at least some structures, aging effects may be more apparent in men than women. The neurobiological bases and functional correlates of these sex differences require further investigation. It has been proposed that one mechanism for nerve and muscle dysfunction with age involves the mitochondria.
Mitochondria contain the only DNA outside the nucleus in mammalian cells.
However, the role of these mutations in the aging process is uncertain unless a mechanism can be identified that would lead to a biochemical defect. In muscle tissue from normal elderly subjects we show that there are muscle fibers with very low activity of cytochrome c oxidase, suggestive of a mtDNA defect. In addition, different mtDNA mutations are present in different fibers, which explains why there is a low overall incidence of an individual mutation in tissues from elderly subjects. These studies show a direct age-related correlation between a biochemical and genetic defect in normal human tissues and that mtDNA abnormalities are involved in the aging process in human muscle. Here, we show that the human telomeric protein TRF2 plays a key role in the protective activity of telomeres.