Adam Ford (Director of H+) interviewed Aubrey.
1. There is work to make mitochondrial mutations harmless by placing the mitochondrial DNA into the cell nucleus (this ensures the necessary mitochondrial functions continue even if the mitochondria are damaged.)
2. They have identified enzymes that can break down the
This is INTRAcellular junk, not EXTRAcellular junk -- ie, it's damaged material that accumulates /inside/ cells, not outside of them.
3. They are working on telomeres. Alternative lengthening of telomeres is used in ten percent of cancers.
Work with Plenty of other sources of funding
RepleniSENS is to replace loss of cells. This would help for Parkisons disease and spinal cord damage. There is work on stem cells and there are some clinical trials now. Some trials are working and it appears to be a matter of time before it works spectacularly well on a reliable basis. There is many companies and researchers working on stem cells so SENS does not need to address it.
The extracellular garbage in the brain are being addressed. SENS is funding a project for addressing extracellular garbage in other parts of the body.
Divide and Conquer Approach
SENS targets seven areas of aging damage. SENS approach is to target each of the seven pieces but there should not be any expectation of significant life extension until all seven areas are being addressed quite well. There are other simpler approaches which are showing some benefit (rapamycin and calorie restriction.) Each of the seven strands of SENS work (other than mitochondrial mutations) has a disease or diseases associated with that area. This means that the work in that area can be justified as addressing those diseases for regulatory approval.
Clarification from SENS Science Writer Michael Rae
"Each of the seven strands of SENS work (other than mitochondrial mutations) has a disease or diseases associated with that area. This means that the work in that area can be justified as addressing those diseases for regulatory approval."
Having listened to the relevant section of the interview I can understand why Adam (or whoever wrote the summary) would have misunderstood the point, by dint of overextrapolation. Aubrey said (correctly) that the various kinds of damage targeted by SENS are also know to cause *age-related* disease, whereas the links between (age-related) mitochondrial mutations and such diseases remain a matter of debate. However, it is quite certain that /some/ mitochondrial mutations cause /some/ diseases: to wit, *inherited* (rather than age-related) mitochondrial mutations cause many very terrible inherited diseases, though most of them occur in very few people. The good news, for both these patients and for aging, is that the "allotopic expression"/mitoSENS approach to making these mutations irrelevant will work for both, so again, there is in principle a way to get regulatory approval for their use by using it to target a specific disease. (In fact, because these inherited mitochondrial diseases are so rare, it may even be easier, at least on the regulatory front, to advance mitoSENS into clinical trials than it is to do so with the other therapies, because special provisioins are made to ease the regulatory burdens for therapies targeting such so-called "orphan diseases."
Aubrey never explains the latter, but it isn't correct (fortunately), and he didn't say, that mt mutations don't cause known, discrete, FDA-recognized diseases.
10 to 20 year outlook not that good
Chances for significant life extension over the next ten to 20 years are quite low according to Aubrey. The 2 year per decade increase of life expectancy sources (reduced smoking and improved infant health) are running down. When regenerative medicine gets more mature and capable then this trend will reverse and life extension will accelerate again.
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