A herd of mitochondria exist in every cell, each with their own copies of mitochondrial DNA. Mitochondria replicate like bacteria, and mitochondrial dynamics are complex and reactive. So counting mitochondria, such as by measuring levels of mitochondrial DNA, doesn't necessarily tell us anything about cause and effect. If we see this measure declining with aging, but not in long-lived individuals, that really only says that we might want to look more closely at the role of mitochondria in aging. Long-lived individuals are long-lived precisely because they have less damage and fewer age-related changes in their biochemistry:
Mitochondrial DNA (mtDNA) content plays an important role in energy production and sustaining normal physiological function. A decline in the mtDNA content and subsequent dysfunction cause various senile diseases, with decreasing mtDNA content observed in the elderly individuals with age-related diseases. In contrast, the oldest old individuals, for example, centenarians, have a delayed or reduced prevalence of these diseases, suggesting centenarians may have a different pattern of the mtDNA content, enabling them to keep normal mitochondrial functions to help delay or escape senile diseases.
To test this hypothesis, a total of 961 subjects, consisting of 424 longevity subjects and 537 younger control subjects from Hainan and Sichuan provinces of China, were recruited for this study. The mtDNA content was found to be inversely associated with age among the age of group 40-70 years. Surprisingly, no reduction of mtDNA content was observed in nonagenarians and centenarians; instead, these oldest old showed a significant increase than the elderly people aged between 50 and 70 years. The results suggest the higher mtDNA content may convey a beneficial effect to the longevity of people through assuring sufficient energy supply.