A recently published article on ScienceDaily talks about research done on human fibroblast cells to put to test the so-called mitochondrial theory of ageing, according to which—in a nutshell— the abnormal mitochondrial function observed in aged humans is due to accumulation of mutations in mitochondrial DNA; this specific aspect of ageing could in principle be dealt with by implementing MitoSENS.
The news is, though, that according to this experiment it seems that mitochondrial DNA mutations don’t play that big of a role in the decline of mitochondrial function as thought; the researchers had at their disposal cells from young and elderly humans, and they observed that while the so-called mitochondrial respiration was expectedly lower in older cells than in young ones, the amoung of mutations wasn’t significantly different. Additionally, the researchers found out that by means of epigenetic regulation of the genes regulating glycine production in mitochondria, they were able to restore the respiratory function in the elderly cells.
This would seem to make MitoSENS useless, since it is all about addressing mutation-caused problems, but it is to be said that, from what I recall of my reading of Ending Aging, these mutations are quite rare (1% of your cells) even in old age, so perhaps it comes as no surprise that the researchers didn’t find any significant difference; I have no say as to whether or not they play a role in ageing. That’s all I can guess: I would recommend you have a look at Fight Aging’s article about it, or perhaps even the relevant paper published by the Japanese team led by professor Jun-Ichi Hayashi.
The bottom line, though, is the usual: we need to do more research. We need to establish beyond reasonable doubt the causes of ageing if we want to defeat it. No anti-ageing science is carved in stone yet, but every tiny piece of the puzzle that we add to the picture gets us closer to the moment when ageing will be finally under medical control.