I'm somewhat late in directing your attention to the science reports from the third conference on Strategies for Engineered Negligible Senescence, but here they are. In my defence, I did mention them in Monday's Longevity Meme newsletter - one of many good reasons to subscribe.
We'll start with a look at the range of research presented on repair or damage prevention for mitochondrial DNA, one root cause of aging. You'll find an outline of the process by which damage to the mitochondria in a small portion of cells can lead to significant accumulated biochemical damage throughout the body back in the Fight Aging! archives.
Dr. Samit Adhya of the Division of Molecular and Human Genetics at the Indian Institute of Chemical Biology is pursuing yet another innovative approach. He proposes to dispense with the need for mitochondrial DNA altogether, by instead providing the mitochondrial protein-making machinery directly with the "working instructions" (messenger RNA) that it normally receives in the form of a transcribed copy taken from the mitochondrial DNA originals. This would allow the mitochondria to continue their protein production even if the mitochondrial DNA were completely destroyed: they would still have their marching orders, even if the general himself were incommunicado. Dr. Adhya is accomplishing this goal by borrowing a trick used by a single-celled organism called Leishmania tropica. This organism, unlike mammals, generates another kind of RNA in the main cell body, and uses a specialized protein to move it into the mitochondria. Dr. Adhya reasoned that he could bind copies of our own RNA to the same protein and use it to deliver both kinds of RNA into mammalian mitochondria, bypassing the need for a DNA original. Very clever.
Kinetoplastid protozoa, including Leishmania, have evolved specialized systems for importing nucleus-encoded tRNAs into mitochondria. We found that the Leishmania RNA import complex (RIC) could enter human cells [where] it induced import of endogenous cytosolic tRNAs [and] restored mitochondrial function.
Last year, Dr. Cui electrified the world when he showed that the [cancer-fighting abilities of a new strain of mice] were caused by a particular subset of their immune cells -- members of a class of white blood cell known as neutrophil granulocytes. These cells are from the innate immune system, meaning that they don't have to "learn" to identify a narrowly-defined enemy, but are constantly on the lookout for broadly-defined "foreign" cells. They are a kind of phagocytic cells, surrounding, engulfing, and digesting their targets when they find them.
Dr. Cui tested the ability of these cells to fight off cancer by transfusing them into normal mice with cancers. Surprisingly, the simple transfusion of the cancer-fighting immune cells from the resistant mice effectively transfered the same remarkable protection to the normal mice. And even more excitingly, the treatment didn't just prevent cancers from forming, but actually fought off existing cancer: when researchers transfused the anti-cancer white blood cells into normal mice with existing skin tumors, the tumors regressed completely in a matter of weeks. Moreover, a single dose of the cancer-fighting immune cells gave the normal animals a cancer immunity that often lasted for the rest of their lives.
At SENS3, Dr. Cui presented the next logical step in his research: work demonstrating the existence of, and characterizing, high-potency cancer-killing granulocytes in humans.
You might have seen overly excited press articles on this research turning up in recent days - journalists have a way of mangling information on timelines into something much more sensational than is in fact the case. Dr. Cui's work is important, and an impressive technology demonstration, but still pre-trial and one of dozens of just as effective demonstrated means to kill cancer. We should be so lucky to be spoiled for choice when the cancer with our name on it arrives.
Lastly, I should point out the post-conference blogging taking place at the Frontier Channel - starting with the author, Aubrey de Grey and Michael Rae in the Anchor Pub, discussing advocacy for healthy life extension:
I had my first conversation with Michael Rae. We talked about Christopher Sykes' recently-widely-net-viewed documentary "Do you want to live forever?", which focuses on Aubrey. Michael had said in a Methuselah Foundation forum post that he intensely dislikes it. I wanted to know why.
I thought its excellent production values and on-balance pro-Aubreyness overcame its cartoonishness, contrived melodrama, shallowness, and emphasis on sex and sentiment. Combining heads with Michael I'm not sure whether or not its existence is a net favor.
I think what Joe Layboy takes away from the film is "there's this weirdo genius dude who thinks he can make us live forever and what's next on the telly?"
Vastly preferable would be to make Joe Layboy incredibly mad that we're all going to die and only 1 in 1,234,567 people are doing anything about it.
Our best minds haven't yet succeeded in inciting riots. The first great documentarian of our movement might figure out how.
Inciting quiet, focused riots of research and support for healthy life extension is indeed a worthy goal for the advocates - and we haven't yet hit on the key to amazing growth or instant understanding and support. I suspect that, like most successful movements in history, this is going to require a number of years and hard work by a great many people.
That said, that work is underway. Progress is definitely being made; the sales and reviews of Ending Aging, the attendance at SENS conferences, positive media attention week after week and funds raised by the Methuselah Foundation for research are all good yardsticks. We can and will raise a research community and gathering of supporters to match that presently focused on cancer - these are the early days in a growth trend, and the best time to jump in and help out.