Hopefully you know the story behind mitochondrial DNA, free radicals and the accumulating damage to our biological machinery that we call "aging." If not, a summary of the modern mitochondrial free radical theory of aging can be found back in the Fight Aging! archives, and a more detailed version in the book "Ending Aging: The Rejuvenation Breakthroughs That Could Reverse Human Aging in Our Lifetime".

The very short summary: mitochondria inside your cells produce fuel to power cellular machinery, but side-effects of that process tend to damage the DNA the mitochondria carry within them - quite separate from the DNA in the cell nucleus, and much more fragile. An accumulation of damaged mitochondria over the years leads to more free radicals in the body, which in turn cause all sorts of varied destruction to molecular machinery and important molecules. That contributes to, and some would say is the dominant cause of, aging and age-related disease.

The best way to deal with all this? Either replace all the mitochondrial DNA with fresh undamaged versions every few decades, a feat demonstrated in mice a few years ago via protofection, or make the damage to mitochondrial DNA irrelevant by blocking its ability to generate more free radicals. This latter approach is used by Methuselah Foundation funded researchers, amongst others, and is a part of the Strategies for Engineered Negligible Senescence.

So, with the background out of the way, I can now point out some interesting research via FuturePundit. It seems that not all human mitochondrial DNA (mtDNA for short) is created equal: some leads to a more rapid accumulation of age-related damage than others. Perhaps not in all tissue in the body, and perhaps not of great enough relative significance to spend a lot of resources investigating, but take a look and see what you think based on this evidence:

Genetic variation in the DNA of mitochondria - the "power plants" of cells - contributes to a person’s risk of developing age-related macular degeneration (AMD) ... Variation in the mitochondrial genome reflects human migrations and different environmental exposures. Changes in the mitochondrial DNA can alter the efficiency of energy generation and lead to over-production of "reactive oxygen species" - free radicals that can damage the cell. "By identifying genetic changes associated with the mitochondria, our results lend additional confirmatory evidence for the role of oxidative stress in AMD. This supports study of interventions that attempt to bolster our antioxidant defenses."

The interesting question: if you're going to use protofection to replace your mitochondrial DNA every few decades, is it worthwhile to replace it with the best of breed, most efficient human mitochondrial DNA? Since you're wiping the slate clean every time regardless, and the normal course of human life suggests that 30 years is a fine length of time to be carrying a set of mitochondrial DNA without replacement, the answer might be "no," unless the additional cost is very small.

Looking at research priorities, identifying best of breed mitochondrial DNA, or manipulating our mitochondrial DNA to look more like it via some form of gene therapy, is clearly nowhere near as important or impactful as wholesale replacement and repair of all our mitochondrial DNA.