As regular readers already know, damage to your mitochondrial DNA is important to the aging process. It is the first step in a chain of events that leads to dysfunctional mitochondria, damaged tissues, and processes run awry in the body. You might want to follow that link and read the introduction if this is new to you.
Some effects of accumulated mitochondrial damage are more direct than others: in age-related retinal disease for example.
Mitochondria are central to retinal cell function and survival. There is increasing evidence to support an association between mitochondrial dysfunction and a number of retinal pathologies including age-related macular degeneration (AMD), diabetic retinopathy and glaucoma.
The past decade has highlighted mitochondrial genomic instability as an important factor in mitochondrial impairment culminating in age-related changes and age-related pathology. This represents a combination of the susceptibility of mitochondrial DNA (mtDNA) to oxidative damage ... This random cumulative mtDNA damage leads to cellular heteroplasmy and, if the damage affects a sufficient proportion of mitochondria within a given cell, results in loss of cell function and greater susceptibility to stress.
mtDNA damage is increased in the neural retina and RPE with aging and appears to be greatest in AMD. It thus appears that the mitochondrial genome as a weak link in the antioxidant defenses of retinal cells and that deficits in mitochondrial DNA (mtDNA) repair pathways are important contributors to the pathogenesis of retinal degeneration. Specifically targeting mitochondria with pharmacological agents able to protect against oxidative stress or promote repair of mtDNA damage may offer potential alternatives for the treatment of retinal degenerations such as AMD.
The dysfunctional regulatory regime for medical research in most developed nations ensures that significant funding is only available for applications of science to named diseases. Much of the limited groundwork presently taking place to develop a way to repair mitochondrial DNA is actually aimed at specific gene defects associated with specific forms of hereditary blindness, for example. This is the perverse result of the incentives in place: potentially revolutionary science is corralled and herded down alleys of limited application. No developer will invest in a revolution when the government prevents them from selling the results of their labor - and for every example you hear about, a hundred take place in silence. The real cost is what you don't see - researchers working towards what is possible rather than what is permitted.