Biogerontologist Aubrey de Grey gave lectures at Stanford Thursday evening and Friday morning. de Grey laid out his argument for life extension research at the first talk. My brief summary:

• There are seven changes at the cellular level that accumulate and eventually cause pathology.
• No new such changes have been discovered in over twenty years despite massively increased capability to study organisms at the cellular level in that time; seven is probably it.
• All seven changes should be repairable at the cellular level.
• Repair damange below levels that cuase pathology, goodbye aging.
• If an individual lives through the first breakthrough that extends lifespan by decades they will probably survive through the next, and the next… Hello, indefinite lifespan.
• Aging and death are barbaric and must be stopped.

de Grey calls the second to last point “escape velocity” and presented at least two arguments for it:

• Once a breakthrough is made, science progresses in a relatively straightforward and rapid fashion for awhile.
• Other primates’ aging is very similar to humans’, only at least twice as fast. There is time to discover and cure any new disease of extended life before any humans get it.

The second talk, apparently more intended for biologists, was a repeat of the first to a disappointing extent. I was prepared to understand very little, but de Grey only spoke for awhile on one of his proposed solutions to one of the seven types of damage–extracellular junk. The solution takes a cue from bioremediation: find microbes that break down the extracellular junk. Where? Human remains of course. From Appropriating microbial catabolism: a proposal to treat and prevent neurodegeneration:

Soil microbes display astonishing catabolic diversity, something exploited for decades in the bioremediation industry. Environments enriched in human remains impose selective pressure on the microbial population to evolve the ability to degrade any recalcitrant, energy-rich human material. Thus, microbes may exist that can degrade these lysosomal toxins. If so, it should be possible to isolate the genes responsible and modify them for therapeutic activity in the mammalian lysosome.

Neat idea. Later de Grey said that this idea is the easiest to explain to non-specialists and that the others that he has personally worked on would have required far longer to introduce than the hour lecture format allowed.

de Grey is attempting to jump start anti-aging interventions with the Methuselah Mouse Prize[s] for extending the lifespan of mice, inspired by the X Prize. His “engineering” approach sounds good to me and I wholly endorse the goal of defeating aging. I will donate more once more information is provided about the participating scientists and their mice–not much is available at this point.

There are four (unfortunately not real money) claims related to the M Prize. Three directly concern the prize:

Methuselah Mouse Postponement. Predicting a 2929 day old mouse by 2010/01/01. The current record is 1819 days.

Methuselah Mouse Post up 1 yr. Says there’s a 2/3 chance of a 2284 day old mouse by 2012/11/01. That doesn’t seem to jibe with MMPost above (time to short MMPost I think). [Correction 20060102: I misread the claim. As of 20050612 it predicted a 2284 day old mouse on 2010/02/01, which still didn’t jibe with MMPost, though the discrepancy was not as bad as I thought]

Methuselah Mouse Reversal<2015. The wording of this claim could be better (the current prize holder is for 1551 days, the claim would pay 1 if 3102 day old mice were obtained by 2015/01/01). Last trade at .67, predicting a 2590 day old mouse with anti-aging interventions only begun late in life within 10 years.

Immortality in mammal by 2015. Not really immortality, but three times a species’s maximum life span as of 1996. Possibly the world’s oldest mouse in 1996 was just shy of four years. If so, this claim would predict a less than one in five chance of a 4380 day old mouse by 2015/12/31. (Another mammilian species could meet this claim.)

It would be very interesting to see versions of the above claims conditioned on the M Prize reaching some fundraising goal.