Open access paper: http://dx.doi.org/10.1038/srep10434

Read the paper, not the publicity materials in this case - they are more than usually misleading.

In the past researchers have shown that reprogramming adult cells to create induced pluripotent stem cells sweeps away some specific forms of damage observed in old cells. In particular it seems to clean up damaged mitochondria, which is of considerable interest given the role of mitochondrial DNA damage in aging. It is possible that this has some connection to the aggressive cleanup that takes place in early stage embryos, stripping out damage inherited from parental cells. There may be the basis for a future therapy somewhere in here, but is also possible that finding out how to apply this sort of process in isolation to adult cells safely is going to be very hard, and the end result impractical in comparison to other technologies: if induced pluripotency as it currently stands somehow happened to many of your cells, you would certainly die.

I've linked to the open access paper above rather than the publicity materials because I think that the latter are misleading as to what was accomplished and the significance of the research. The researchers theorize that the ability to restore mitochondrial function, and then break it again when you take the induced pluripotent stem cells and redifferentiate them back into ordinary cells, means that mitochondrial DNA damage is not a primary source of harm, but rather something under the influence of the state of nuclear DNA and thus some other cell process. For example, perhaps epigenetic changes in nuclear DNA are mediating the pace of replication-induced DNA damage in mitochondria.

All in all it is interesting work, and programmed aging supporters, who theorize that aging is largely caused by epigenetic changes, will no doubt find it encouraging, though I think that at this stage there are other possible interpretations of what is taking place here. For example, in how reprogramming restores function and how that function is lost again: one could proposed clearance and damage mechanisms rather than direct regulation mechanisms. The researchers are in most circumstances looking at mitochondrial function (via oxygen consumption rates) rather than at mitochondrial DNA damage, which greatly muddies the water. The two do not have a straightforward relationship, and there are any number of simple drug treatments that can tinker with the results of measures of mitochondrial function without touching the issue of damage. I'd like to see the same work done again with mitochondrial DNA damage assessments at each stage and each intervention, and also animal studies rather than just cell line studies in the case of the interventions in ordinary aged cells - which seems to be where this research group is heading in any case.

Aubrey de Grey commented to me that:

It has long been very obvious that mito dysfunction in the elderly is hardly at all caused by mutations (since they are too rare) and rather, by elimination, almost entirely by “deliberate” (i.e. regulated) nuclear gene expression changes, occurring as an adaptation to other things that are going wrong. That’s not to say that mito mutations are harmless though, not at all - but that their harm is via other means, such as my “reductive hotspot hypothesis” from 1998. There is one interesting result in the paper, namely that glycine supplementation partly rejuvenates mito function - but I don’t think the authors believe that the result is robust, because they have relegated it to one sentence at the end of the results and one supplementary figure.