Saul Posted May 25, 2017 Report Share Posted May 25, 2017 Dear ALL, Dr. Sinclair was the principle speaker at the annual UR Conference on aging today! He has been our guest, and a principle speaker, at CR Society meetings, and needs no introduction to long time members of the Society. Some of what he talked about is not published yet, so I can't discuss some details; but I'll summarize a small part of it: He presented, and seems to favor, the "epigenetic theory of aging": this notes that, with aging, there are changes occurring in the epigenome -- he was concentrating (in his talk) mostly on groups adhering to chromosomes (phosphorolation, methylation, etc.). He has done experiments on mice, in which he cut chromosomes, and repaired them, repeatedly, very carefully. The usual chemical tests showed that the genes of these modified mice were identical to their litermates. But, tests showed changes in their epigenome. The modified mice performed identically to their litermates; equally intelligent, active, etc. But they aged faster. After 6 or so months, they resembled 12 month old mice. A molecule with the acronym NMN (which stimulates NAD+, which among other things seems to improve chromosomal repair) appears to help improve the aging rate of these epigenetically modified mice. Phase I testing of the use of NMN in possible treatment of some human ailments is hoped to be underway soon. During the question period, I asked Dr. Sinclair if the maximal lifespan of the modified mice differed from untreated mice. He said that this was the case, in the tiny experiment that he has so far made -- 15 modified, 15 control mice: The modified mice had significantly lower maximal lifespan -- but he intends to repeat the experiment, with a much larger cohort. One other attendee asked questions about calorie restrction. Perhaps more information is available at the Department of Biology website of the UR. -- Saul Link to comment Share on other sites More sharing options...
Michael R Posted May 25, 2017 Report Share Posted May 25, 2017 Wait: Dr. Spindler, or Dr. Sinclair? Or both? Who was talking about what? You make it sound like they were both talking about the same experiment — were they? EDIT: Based on this program, it was Sinclair only — right? Link to comment Share on other sites More sharing options...
Saul Posted May 25, 2017 Author Report Share Posted May 25, 2017 Yuk! Of course! You're right! I kept changing the name back and forth! Michael, could you please edit my title, changing Spindler to Sinclair? I don't have that power; I've been trying to do it since posting. -- Saul Link to comment Share on other sites More sharing options...
Saul Posted May 25, 2017 Author Report Share Posted May 25, 2017 If I remember correctly, Spindler is in California, not Harvard. -- Also Link to comment Share on other sites More sharing options...
Michael R Posted May 25, 2017 Report Share Posted May 25, 2017 Michael, could you please edit my title, changing Spindler to Sinclair? I don't have that power; I've been trying to do it since posting. Done. I've also struck out the bit about him having presented at previous CR Conferences (that is indeed Spindler, and not Sinclair), and fixed "MNM" to "NMN." If I remember correctly, Spindler is in California, not Harvard. Yup: UC Riverside. Link to comment Share on other sites More sharing options...
Saul Posted May 25, 2017 Author Report Share Posted May 25, 2017 Thanks Michael; I was going to change the "MNM" to "NMN"; but was happy to see that you'd already done that. -- Saul Link to comment Share on other sites More sharing options...
Saul Posted May 26, 2017 Author Report Share Posted May 26, 2017 Here's something that I sent to a fellow CRONnie here in Rochester (but not at UR): Sinclair gave a nice talk; he discussed mice in which he cut chromosomes and repaired them multiple times. The resulting mice had perfect genomes -- but there epigenomic data (mostly measured by groups attached to the chromosomes -- such as phosphorulation, etc. -- were very different. The modified mice behaved normally, and were as healthy as the untouched, control mice -- but 6 months later, they resembled normal mice that were 12 months older. Sinclair compared the genome to digital data -- but the epigenome to analog data. He explained that defects in the genome can be repaired (e.g., by existing molecular machinery in the cell), but when the epigenome is damaged, it can't be fixed, any more than a scratched LP (analog data). Fascinating and interesting. -- Saul Link to comment Share on other sites More sharing options...
Guest Aaron Posted June 12, 2017 Report Share Posted June 12, 2017 What does this say about boosting NAD+ as a means to support DNA repair? That it can possibly shorten one's lifespan? Link to comment Share on other sites More sharing options...
Saul Posted June 14, 2017 Author Report Share Posted June 14, 2017 Hi Aaron! My reading would be the opposite about lifespan -- NMN, according to Dr. Sinclair (and I believe him), boosts NAD+, which again does support DNA repair. And Dr. Sinclair's preliminary work with a small number of rodents suggests that this might INCREASE healthspan, average lifespan and maximal lifespan. One might ask: "Why not just boost NAD+ instead of NMN?" No one asked that question at Dr. Sinclair's talk. My guess: Perhaps it's well known to those in molecular biology (which I am not) that that's totally impractical for some reason. Perhaps NMN is a much more stable molecule (I would guess so. I think that NAD+ is involved in the electron transport cycle in mitochondria, and might be a transitory product that is probably unstable. But others, such as Michael and Al, will know much more about this than I do.) IMO, It might be nice to invite Dr. Sinclair to present a talk at the next meeting of the CR Society. -- Saul Link to comment Share on other sites More sharing options...
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