Mitochondria are the cell's power plants, important in the operation of metabolism, how that metabolism determines life span, and many age-related diseases. As described in the mitochondrial free radical theory of aging, a small number of mitochondrial genes are known to be crucial to its operation as the cell's power plant. Damage to those genes is a natural consequence of the operation of a mitochondrion, and leads to a Rube Goldberg sequence of events in which is a healthy cell is turned into a damaged cell that spews forth damaging biochemicals into your body. As those errant cells accumulate, their actions collectively give rise to many of the unwelcome forms of change and damage that come with age: systems failing, organs shutting down, and important biochemical processes running awry because their component molecules are corrupted.
Given all this, we can see that the ability to replace genes in mitochondrial DNA is a foundation for methods of repairing and eliminating this contribution to the aging process. The course of human life suggests that such a working technology would only have to be applied once every few decades.
Of all the branches of potential longevity science, replacement of mitochondrial DNA is one of the most advanced (beyond stem cell research and regenerative medicine of course, which benefits from a far larger research community and funding base). Replacement of all mitochondrial DNA was demonstrated in mice through protofection in 2005, and moving mitochondrial genes into the cell nucleus as an alternative to direct replacement was demonstrated in mice in 2008. That second option is not as simple as you might think in an age of genetic science: copying the gene into the nucleus is a straightforward use of established technology, but that done you still have to manipulate the cell into transporting the proteins produced by that gene back into the mitochondria without breakage. Fortunately, this breakthrough was made, so full steam ahead there.
But back to the straight replacement of entire damaged mitochondrial genomes. Here is a recent report of this goal achieved in primates, though this is a pre-embryonic manipulation performed on a single cell rather than a global change in all the cells of an adult. The point of interest is that it worked and the resulting offspring seem fine; it provides further evidence for the safety of replacing all of a human's mitochondrial DNA (mtDNA):
Mutations in mtDNA contribute to a diverse range of currently incurable human diseases and disorders. To establish preclinical models for new therapeutic approaches, we demonstrate here that the mitochondrial genome can be efficiently replaced in mature non-human primate oocytes (Macaca mulatta) by spindle-chromosomal complex transfer from one egg to an enucleated, mitochondrial-replete egg. The reconstructed oocytes with the mitochondrial replacement were capable of supporting normal fertilization, embryo development and produced healthy offspring.
The underlying technologies are within a few years of completion by the look of it. At that point the real issue becomes one of regulation; the FDA does not permit treatments for aging or changes that happen with aging that have not been lobbied into a designation as an official disease. So any significant progress towards therapies aimed at repairing mitochondrial damage of aging will have to be made outside the regulatory systems of the largest markets. With this science - and many other fields of medicine - so very far ahead of what regulators permit, the breaking point at which large for-profit development groups abandon the system to operate in more permissive regions has to arrive at some near future date.
Tachibana, M., Sparman, M., Sritanaudomchai, H., Ma, H., Clepper, L., Woodward, J., Li, Y., Ramsey, C., Kolotushkina, O., & Mitalipov, S. (2009). Mitochondrial gene replacement in primate offspring and embryonic stem cells Nature DOI: 10.1038/nature08368