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To browse Academia. The mitochondrial theory of ageing proposes that the lifetime accumulation of mutations in mitochondrial DNA leads to the progressive loss of cellular viability, via some combination of bioenergy insufficiency, enhanced production of reactive oxygen species ROS and apoptosis.
It has also been suggested that this could entrain a vicious cycle of ROS damage and mutagenesis. Mitochondrial DNA mutations do indeed accumulate with age, albeit to a very low level.
Debate rages as to whether this could have any physiological significance, even if mitotic segregation is substantial. However, in stem cells, where mtDNA copy number may be relatively low, and the number of rounds of cell division high, segregation of mutants could result in eventual loss of precisely those cells that provide the body with the repair capacity needed to stave off functional decline and eventual death.
Until recently, our ability to evaluate the role of mtDNA mutations in ageing was based purely on correlative data. However, the introduction of germline mutations into the nuclear genome which affect the mtDNA replication apparatus has allowed us to manipulate the mitochondrial genome experimentally, and provide a more formal test of the hypothesis.
