People who attend SENS conferences are the demographic that is the most receptive to cryonics of any identifiable group I have yet found. They are mostly scientists interested in intervening in the aging process.
great progress has been made in starting research programs on each of the SENS strategies, and by 2012 research on all the strategies is expected to be in progress.
In addition to my oral presentation on cryonics I also had a poster. Scientific conferences usually have poster sessions where scientists present research, reviews, or ideas in the form of a poster. Poster presenters stand by their posters at scheduled times to discuss their work on a one-to-one basis with individuals rather than to an audience. My poster dealt with challenging the concept of biological age and denying the possibility of a biomarker of aging that could determine biological age. I contended that biological age and biomarkers of aging assume a singular underlying aging process, which I denied on the grounds that aging is multiple forms of damage.
His view on biomarkers is an interesting one; you might look back in the Fight Aging! archives for a background on the search for biomarkers of aging - there are a good number of posts on the topic, and it's an area of research that has some importance to the future pace of progress. Absent good biomarkers, it's going to be hard to rapidly tell the difference between a working rejuvenation therapy and a non-working rejuvenation therapy - and time is in short supply.
I did want to draw you attention to a point from Best that I disagree with. He says:
I consider gene therapy to be an essential tool for the ultimate implementation of SENS, and a deficiency of SENS that there is so little attention paid to this technology. I don't see how SENS can be implemented by any means other than genetic re-programming. LysoSENS, for example, would require new genes to create new, more effective enzymes for the lysosomes. MitoSENS would require all mitochondrial proteins be made in the nucleus and imported into the mitochondria.
For mitochondrial repair, agreed, all of the most plausible paths look like gene therapy. The problem that MitoSENS seeks to solve is the accumulation of damage to mitochondrial DNA, and so that DNA either needs to be protected, repaired, or replaced. Fair enough. But I think there will be a wide range of other practical mechanisms for the delivery of necessary enzymes to lysosomes as a part of the LysoSENS program. Recent years have made it clear that biotechnologies other than gene therapy can target small molecules to specific cells and even specific portions of a cell, such as by hijacking normal protein targeting mechanisms or through carefully designed nanocarrier structures. I would agree that an ultimate implementation would be one that is always on - an unambigiously beneficial genetic change to allow lysosomes to digest what is presently indigestible and which will be passed on to future generations. But it seems far more likely that initial implementations will be periodic clinical treatments - injections and infusions - designed to flush the body's lysosomes with enzymes for a short period of time, and thereby clean them out. This would seem to be sufficient, given that we humans manage three decades of life at the outset without the obvious degenerations of aging starting to show up.