The SENS Foundation will be hosting the SENS5 conference in Cambridge, England at the end of August. Registration is open, and this note arrived in my in-box today:

I am writing to inform you that June 15th is the deadline for discounted registration and abstract submission for the fifth Strategies for Engineered Negligible Senescence (SENS) conference ... The conference program features 33 confirmed speakers so far, all of them world leaders in their field. As with previous SENS conferences, the emphasis of this meeting is on "applied gerontology" - the design and implementation of biomedical interventions that may, jointly, constitute a comprehensive panel of rejuvenation therapies, sufficient to restore middle-aged or older laboratory animals (and, in due course, humans) to the physical and mental robustness of young adults.

I notice that Caleb Finch will be giving the SENS Lecture, entitled "Regenerative medicine for aging: a new paradigm worth trying" - now there's an example of progress in winning over the mainstream of aging research to the SENS approach of repair rather than slowing down aging. In this context, "regenerative medicine" means SENS; SENS Foundation founder Aubrey de Grey uses the term more expansively than the general public and media, who use it only in reference to stem cell therapies.

The SENS Foundation also recently issued a research report (in PDF format) for the first ten months of last year, with a year end report to follow. You should find it interesting to see funding amounts listed for the varying strands of SENS research, as well as insight into exactly what the researchers are up to at present:

I'm delighted to be able to share with you our research report, prepared for the first 10 months of 2010, by Tanya Jones (our Director of Research Operations), working with our researchers and my CSO Team. I thought it would be of interest to our supporters, and serve as a precursor to our 2010 Year End Report, which is currently under production as part of our finalizing our 2010 accounts.

...

SENS Foundation conducts intramural research in its Research Center in Mountain View, California. The primary focus of our intramural work is LysoSENS - investigating novel lysosomal hydrolases against intracellular aggregates that impair cell function - and we recently produced a detailed and comprehensive LysoSENS planning document in collaboration with our extramural project at Rice University.

We have also arranged for research in the MitoSENS strand - obviating mitochondrial DNA deletions - to be conducted at the Research Center, following the negotiation of a transfer agreement with Dr Corral-Debrinski covering materials produced, and used in, previous successful work by her group. Dr Matthew "Oki" O'Connor joined us in September to initiate this project.

The relative amounts devoted to each project clearly illustrate that the Foundation's primary focus at this time is the LysoSENS project, and I can guess at some of the strategic reasoning there. Much money and many connections with industry might be gained through success in the LysoSENS platform. Not just aging, but many diseases could be effectively treated in their late stages through progress in bioremediation of this sort, and that means that big pharma and big biotech would be very interested in licensing agreements - which in turn would assist the Foundation in greatly expanding its purview and influence.

It is, however, frustrating to see far less funding devoted to MitoSENS, the project aimed at removing the contribution of mitochondrial DNA damage to aging. Everyone has an opinion, and mine (for what it's worth, which isn't all that much in this case, and nor should it be) is that mitochondrial repair would make a better primary focus. Irrespective of the methodology chosen, it seems clear that the research community as a whole is frustratingly close to something that will work to completely reverse mitochondrial damage, whether it is through allotopic expression as advocated by the SENS Foundation or periodic whole-body replacement of mitochondrial DNA as demonstrated in mice some years ago.

Yet the funds going towards mitochondrial repair - both here and generally - are in no way proportionate to the degree to which the research community believes mitochondrial DNA damage to be a cause of aging and longevity.

The advice I give myself on this issue is the same as I'll give to anyone else in the same position: if you believe that too little funding is devoted to any given research goal, then get out there and do something about it. Earn money and donate it, and persuade others to do the same. After all, that's exactly what Aubrey de Grey did in order to arrive at his present position: helping to direct a Foundation of his own creation where enthusiastic people are now writing annual reports on their progress towards engineering the end of aging.