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March 14, 2009

SENS Anti-aging Progress


From Future Currents by Jeriaska: at the BIL unconference in February, 2009, Chief Science Officer Aubrey de Grey gave an overview of the research projects that the organization is now funding, their significance to SENS, and their potential to lead to accelerated progress towards the defeat of aging in 2009 and beyond.

There is a new Methuselah Foundation Undergraduate Research Initiative.

These are the four things that are really new projects in the SENS foundation.

1. A fantastic, originally Serbian immunologist called Janko Nikolich-Zubich, who is a prominent gerontologist and works in Tucson at the University of Arizona, has become very interested in the possibility of being more ambitious about repairing and rejuvenating the immune system than anyone has previously been. There are two major things that go wrong with the immune system during aging and they fall into two of seven categories that I always talk about. People have been exploring these things in isolation in a somewhat halfhearted sort of way for quite some time, but no one has had the balls to do them together.

I have managed to persuade Janko to do this. He is basically applying a combination therapy to mice whose immune systems are going downhill because of aging and seeing whether the immune systems can be really rejuvenated so that the mice are better at resisting infection, getting back to where they were in early adulthood. It is a reasonably long project, as is more or less any project involving the aging of mice, but it is already underway. It is being funded by the Methuselah Foundation and we are extremely happy about it.

2. Jan Vijg is a professor at Albert Einstein in New York and another very prominent gerontologist. He is another strong supporter of the general principle that I have been putting forward for the past two years. His main theme is the accumulation of nuclear mutations. (This is not mutations in our mitochondria, but mutations in our chromosomes.) He has for some time taken the view that the accumulation of non-specific mutations, mutations that randomly disable some aspect of the cell’s function, may actually be a major driving force in the rate of aging. I think he’s wrong. If I thought he was right, then I would be much more pessimistic about our ability to do much about aging anytime soon, because let’s face it, it’s pretty tricky to mend mutations in the nucleus. We are probably going to need molecular nanotechnology before we can do that.

I think we are lucky that actually the only thing that really matters as a consequence of nuclear mutations is cancer. As many of you who are familiar with my work will remember, I have a specific approach to dealing with cancer. My take is, if we can really get that working, then all the other things that the accumulation of nuclear mutations might cause will not actually matter for a long time—several times a currently normal lifespan. We can afford not to worry about that for a little while.

Jan, as I said, disagreed with me on this. He claims the mutations may matter in a normal lifespan, but he is such a damn good scientist and such a nice guy that he is doing an experiment that he did not want to do, and he’s doing it for me. Basically, he is having a look at the brain to see whether the brain accumulates what we like to call epimutations. These are not changes to the DNA sequence, but changes to the decorations of that sequence: things like methylation of histones, methylation of CpG dinucleotides. These are things that cause changes to which proteins are actually expressed from the genome, as opposed to which proteins could be expressed.

Jan found some years ago that in the brain actual bona fide mutations do not accumulate at all in mice during the whole of adulthood. They accumulate during growth, but after it the mouse gets to full size and nothing happens. Of course, if nothing is happening, then it cannot matter in aging. For this reason, it is very important to determine whether the same is true for epimutations. I think it probably will be, and he is having a go. If he finds that there is some change, then of course we have to find out whether there is enough change to actually matter. That is a whole other set of experiments.

That, again, is underway now. I should say that for both these projects, the people actually doing the work are not the professors, but the people working for the professors. In both cases we have an absolutely splendid person that each of these people have brought in. I am really happy that two accomplished and talented post-doctoral fellows are actually doing the experimental legwork here. I am delighted at how these projects have got going over the past few months since we started funding them. It really is happening.







3. Now, demography is not usually listed in my seven strands of what we need to deal with in order to defeat aging. However, as all of you know who have tried to talk to people who are not terribly persuaded that this would be a good idea, it is really important to think about the social consequences of defeating aging so as to be able to call the bluff of the idiots who actually say that aging is a good thing. Of course the biggest reservation that people normally have when you talk about defeating aging is “Oh dear, there will be lots of people, won’t there? That will be terrible.”

I have lots of fairly sarcastic answers to this, of course. However, it would be nice to actually have some data. What we have decided to do is create a really authoritative study, along with some software that can be used as the substrate for creating other studies, that will allow us to see what the demographic consequences would be of developing therapies that generally knocked aging on its head. This would be on the basis of various other permutations and assumptions, like how rapidly technology accommodates increasing population, how rapidly the birthrate declines, how rapidly these therapies spread around the world when they actually arrive, all those things.

The Gavrilovs, Natalia and Leonid, are professors in the University of Chicago. They are, again, very good supporters of this whole mission. They are some of the most pro-anti-aging, so to speak, demographers in the world, in marked contrast to other demographers. They are doing this work for us, and furthermore, it is not very expensive. It does not involve test tubes. I put this down on the bottom rather cheekily, because we have not strictly speaking signed the contract yet. We will probably do so next week.

4. Lenhard Rudolph is a professor in Ulm, a city in Germany. He is one of the experts in the manipulation of telomerase in mice, the enzyme that maintains the length of chromosomes. He has done some good work in this area over the years. In particular, he is the world’s leading specialist on the manipulation of mice with respect to the blood. Now, the blood is a tissue which is going to suffer if we do what I think we need to do in order to really defeat cancer. It is going to have side effects on the ability of stem cells in the blood to actually continue to work indefinitely.

The way that I propose we are going to get around that is by periodic replenishment of the bone marrow through the stem cells to the blood, but we need to determine that this is actually going to work. This is the world’s best person to do this experiment, and he is going to do it. I am pretty happy that all these things are happening, and it is mainly because of Peter Thiel. I bow down to his generosity.



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