Last week, I had the chance to attend the Edmonton Aging Symposium, a public conference put together by Methuselah Foundation volunteer Kevin Perrott in Alberta, Canada. I can sum up only selected aspects of the meeting here, and apologize to the presenters whose work I could not include. The reader shall be referred to the abstract book, and the conference videos which will shortly be announced on this blog.
The opening talk was by Huber Warner, well known for his outspoken criticism of SENS as a whole, and less well known for his financial support of selected SENS projects. Warner set out to discuss the relationship between “time, damage and aging”, but did not make it beyond the limited, albeit interesting example of DNA damage in our cells’ nuclei and mitochondria. As most of the symposium was neatly organized according to types of age-related damage, it would have been useful to have a general introduction to “time, damage and aging” covering all the “big seven” damage-types at this stage, but we had to wait for this until de Grey took over later in the day. Warner did set the stage for subsequent presenters in the most heated one of these fields, namely the contribution of mitochondrial DNA mutations to the aging process of certain gene-targeted mice. In the words of presenter Konstantin Khrapko: “When the prevailing opinion about the role of mitochondrial mutation in aging changes more than twice within your funding period, it is pretty stressful”. We at the Methuselah Foundation of course hope that the stress exerted by mitochondrial mutations on hard-working gerontologists can soon be relieved by doing away with them (the mutations, not the gerontologists), and we recently got to work towards that end.
Interestingly, the introductory session was completed by Janet Fast, a sociologist, who cited Canadian retirees’ leisure behavior to argue that the aged aren’t damaged after all. However, as far as one can tell from the fact that none of the world’s best and brightest gerontologists and bioengineers present packed their things and went home, she cannot have been very convincing. I think that while the work to prevent discrimination of the aged on grounds of their impaired physical function or “ageism” is certainly important, it can become dangerous to take it as far as to deny that such impaired function exists, progresses, and ultimately becomes terminal.
Progress has been solid and steady in the other fields pertaining to the removal of age-related damage according to the SENS proposals: Too few cells, and too many cells, and the three types of junk (inside cells, between cells and protein crosslinks). The cellular work featured Conboy and Conboy from Berkeley, pioneers in investigating the role of how an aged bodily environment dictates the aging various stem cell types, and presented excellent data with implications on how one might go about shielding the stem cells from this influence. This might one day allow the stem cells in an aged person to ignore the body’s calls to stop regenerating, and effectively remedy the “too few cells” problem. Geoff Goldspink discussed how regenerating muscle cells might be helped along further with growth factors, and how professional athletes and the industry behind them have become very interested in supporting this work.
On the other hand, Judith Campisi (Buck Institute) attempted to get rid of unwanted cells (“too many“), and reported on overcoming matrix metalloproteinases, an important mechanism by which such senescent cells can defend themselves against immune cells attempting to clear them out.
In the field of age-related storage diseases (“junk“), atherosclerosis researcher Jay Jerome explained the need for enzyme therapies to resolve arterial plaques, and Rittmann showed how his Methuselah Foundation-funded work to clone suitable enzymes from environmental microbes has made excellent progress over the past year.
Cynthia Lemere explained how a vaccine against extracellular beta-amyloid to resolve Alzheimer’s disease plaques suffered a severe setback in 2001, when a clinical trial had to be shut down due to severe side-effects. She introduced several good ideas how to prevent this, and which have shown promise in mice. Efforts to bring these into the clinic are well underway.
And finally, another conference highlight I would like to mention in conclusion was the presentation of an autopsy of a supercentenarian (someone who died older than 110 years of age) validated by the supercentenarian research foundation, by Steve Coles and Doros Platika. We saw photos of a 115 year old brain preparation with no trace of plaque deposition or neurodegeneration, and an aorta with as much atherosclerosis as a newborn baby. Pre-medical textbooks teach that both types of lesions should be prevalent in just about everybody, half a century earlier. For those of us with more commonplace genomes, it is not a question of whether we get these lesions, but how fast they progress towards diseases. We wish the Supercentenarian Research Foundation the best of luck in discovering the basis of this biomedical miracle.
In sum, I think we are all indebted to graduate student and Methuselah Foundation volunteer Kevin Perrott for putting together this excellent conference. Normally this type of thing is done by committees of senior researchers, and I find it truly amazing that a single motivated student single-handedly pulled one of that I honestly think was far above what you get in the field on average. It is an honor and a pleasure to work with the excellent volunteers at the Methuselah Foundation such as Kevin.