Aubrey de Grey's mother died in May 2011. He was her only child. He inherited roughly $16.5 million. He assigned $13 million to SENS. His donation will be spent over a period of about five years, and it roughly doubles the budget they had previously, from $2 million annually to $4 million. The number one external donor remains Peter Thiel. Additionally, another internet entrepreneur, Jason Hope, has recently begun to contribute comparable sums.
Readers can donate to SENS life extension through the repair of damage caused by aging at this link
Aubrey has great confidence that our outreach efforts will bear fruit in that time. His hope is that five years from now we will be big enough that the expiry of my donation will go relatively unnoticed.
Aging is not a risk factor for disease. Aging is the CAUSE of the diseases of old age, and we need to start saying so.
Life Extension Foundation interviewed Aubrey and got an update on SENS research
Q - Which of your SENS strategies would success achieve the most additional healthy years?
AdG: No one strategy would achieve very much on its own - certainly not as much as ten years, probably not even five.
Q: Which of the SENS strategies has the best prospect for success first?
AdG: A couple of the strategies are already in clinical trials for some relevant conditions - stem cells for various things, including Parkinson’s disease, and vaccination against extracellular debris for Alzheimer’s.
Q: Which of the SENS strategies would be the most difficult to achieve?
AdG: I think it’s pretty clear that the approaches for defeating cancer and for obviating mitochondrial mutations are the hardest, because they will both involve gene therapy, something we’re not at all good at yet. Out of those two, I would say that the OncoSENS (the elimination of telomerase enzyme) is the harder, because it is much more complex and also because it involves gene targeting rather than just insertional gene therapy.
Q: Will you make a general statement about the goal of SENS research?
AdG: SENS is based on the appreciation that there is a continuum between (a) the initially harmless, progressively accumulating damage that accumulates in the body as a side-effect of its normal operation and (b) the pathologies that emerge when the amount of that damage exceeds what the body is set up to tolerate. We want to treat (remove or obviate) the damage and thereby prevent the pathology.
Q: How difficult would it be to eliminate lipofuscin (the cellular junk that particularly accumulates in neurons and heart muscle cells) compared to eliminating 7KC (an oxidized derivative of cholesterol that accumulates in atherosclerotic plaques) or A2E (a substance accumulating in the retina with age that causes macular degeneration and blindness) as a lysoSENS project? How much difference do you think elimination of lipofuscin would make in terms of rejuvenation?
AdG: This is a big question right now. We have a PhD student in our funded group at Rice University who is working on lipofuscin, but he is just starting. Lipofuscin is indeed harder, but what makes it harder is not the aging-versus-disease distinction but simply the nature of the substance. Lipofuscin is very heterogeneous in its molecular composition, and moreover it is mainly made of proteins, so it is hard to distinguish from material that we don’t want to break down. I should note in passing that the material whose accumulation causes macular degeneration is often called lipofuscin but really should not be, because the only thing it has in common with bonafide lipofuscin is its subcellular location (the lysosome) and its fluorescence properties: its molecular composition is entirely different.
Q: In the 2011 report of the SENS Foundation, progress on mitoSENS (making copies of mitochondrial DNA in the nucleus to protect them from free-radicals generated by mitochondria) was restricted to 5 of the 13 protein-encoding mitochondrial genes. How confident are you that all 13 such genes can be copied into the nucleus in the foreseeable future? Are some of those genes more important than others, or are you simply going after the easier targets?
AdG: We’re pretty confident. Some of the genes we’ve chosen to work on first are easy targets in the sense that other researchers have demonstrated some success with them already; other genes are chosen more because success would be high-impact, in that it would allow more clear-cut assays of efficacy. In the end, all 13 are equally important.
Q: You have been demonstrating an increased appreciation for the role of neurofibrillary tangles (tangled aggregates of tau protein) as a potential cause and treatment target resulting in the cognitive decline of Alzheimer’s disease. Are you planning any SENS Foundation projects to remove tangled tau to better prevent Alzheimer’s disease than simply removing amyloid? Would this be distinct from LysoSENS (elimination of intracellular junk by more powerful enzymes in lysosomes)?
AdG: I’ve always said that (tau) tangles are likely to be just as important as (amyloid) plaques in Alzheimer’s disease, and indeed that cell loss must also be addressed. Absolutely we want to remove tangles. Tangles are an unusual type of intracellular aggregate in that they are not normally eliminated by lysosomes, but they are still a target of LysoSENS because we believe that they are the visible manifestation of a “traffic jam” caused by lysosomal dysfunction, which is itself caused by other molecules, maybe the same ones that cause atherosclerosis. (This suspicion arises from, among other things, the fact that apoE genotype is the most significant genetic contributor to risk of both Alzheimer’s disease and atherosclerosis.) At the moment we have no project in this area but we are in detailed conversations with people focused on it.
LE: Is AmyloSENS (elimination of extracellular junk, mainly amyloid) now primarily focused on transthyretin amyloid, rather than the amyloid plaques believed to cause Alzheimer’s disease? (Transthyretin is a form of amyloid that accumulates outside of the brain, especially in the heart, and has been found to be the frequent cause of death of persons over 110 years of age.)
AdG: Yes, our only AmyloSENS project at present (a collaboration between labs at Harvard and at University of Texas, Houston) is focused on transthyretin amyloid. We are leaving the research on Alzheimer’s disease amyloid to the many well-funded groups that already have it in their sights. The other main amyloid identified as having a role in Alzheimer’s disease is islet amyloid in the pancreas, and we may get into that area soon.
LE: SENS Foundation has been investigating the possibility that mutation and epimutation (changes in gene expression rather than alterations of the genes themselves) may be deleterious in ways other than cancer. If that proves to be true, what strategies do you envisage to address that problem?
AdG: Our current work is focused on epimutations; we feel that the work of experts in the field of the genetics of aging (Jan Vijg’s group at the Albert Einstein College of Medicine in particular) has already shown really conclusively that mutations accumulate far too slowly in most tissues (notably the brain) during adulthood to have any chance of contributing to age-related ill-health. If epimutations don’t come out the same way, we will need to look at ways to mildly accelerate cell turnover, combined with autologous stem cell therapy, which uses one’s own stem cells for cellular therapy. But that’s awfully hard, so let’s hope we don’t need to go there!
If you liked this article, please give it a quick review on ycombinator or StumbleUpon. Thanks