As you age, your mitochondria become ever more damaged and dysfunctional, a process that causes further biochemical damage throughout your body, and is in fact an important component of aging.
cells entirely populated with damaged mitochondria start churning out large quantities of free radicals - through another, more forceful mechanism - into the body at large. That's a path to age-related degeneration and fatal conditions like atherosclerosis. The free radical theory of aging is based upon the harm done to tissues, structures and processes by these damaging biochemicals.
Can ongoing mitochondrial degeneration be slowed? Well, yes - calorie restriction appears to slow down every catalogued aspect of aging, and evidence suggests that regular exercise is just about as good for everything except extending maximum species longevity. But can we do better than this for failing mitochondria via new medical technologies?
I stumbled over recent research that suggests there are comparatively simple genetic changes that will slow the rate at which your mitochondria cause the damage that leads to aging:
Mitochondrial DNA (mtDNA) is highly susceptible to injury induced by reactive oxygen species (ROS). During aging, mutations of mtDNA accumulate to induce dysfunction of the respiratory chain, resulting in the enhanced ROS production. Therefore, age-dependent memory impairment may result from oxidative stress derived from the respiratory chain.
Mitochondrial transcription factor A (TFAM) is now known to have roles not only in the replication of mtDNA but also its maintenance. TFAM transgenic (TG) mice exhibited a prominent amelioration of an age-dependent accumulation of lipid peroxidation products and a decline in the activities of complexes I and IV in the brain.
In the aged TG mice, deficits of the motor learning memory, the working memory, and the hippocampal long-term potentiation (LTP) were also significantly improved. The expression level of interleukin-1beta (IL-1beta) and mtDNA damages, which were predominantly found in microglia, significantly decreased in the aged TG mice.
an overexpression of TFAM is therefore considered to ameliorate age-dependent impairment of the brain functions through the prevention of oxidative stress and mitochondrial dysfunctions in microglia.
Doing something about the decay of mitochondrial function has a number of evident benefits, as demonstrated above. But slowing things down is a second rate strategy at best - especially if it involves genetic engineering, a technology unlikely to be in widespread use for humans for another ten to twenty years. A slowing of damage does little for those who are already damaged and aged. What we really want to be capable of achieving is reversal of existing damage - to be able to restore old and damaged mitochondria to a pristine state.
This goal is unlikely to be any more expensive or time-consuming than engineering a slowing of mitochondrial decay, so it should be the first priority. If you look back in the Fight Aging! and Longevity Meme archives, you'll find mention of a range of potential technologies at varying stages of research: