It’s tempting, huh?

The problem, as I touched on above, is that rodents and humans do not use the same receptor to control innate immune activity. So Dr. Marshall would have to identify what the receptor is in mice that acts like the Vitamin D Receptor, while knowing quite well that their might not be an equivalent.

That’s the problem. Mice, particularly when it comes to their immune system, are incredibly different then humans. Since Marshall’s model for reversing inflammatory disease involves specific molecules of the human immune system he simply does not know if the same equivalents even exist in mice.

So he’d have to spend possibly years of research trying to correlate aspects of the rodent immune system with the human immune system and the work might not even result in fruitful consequences.

So it’s a rather large risk.

Have you read this article? It describes many of the ways that humans and rats differ. It should give you a better idea of how hard it would be to transfer the basic tenets of the MP from man to a rodent.

http://bacteriality.com/2007/11/07/mice/

Still, it’s great to hear your enthusiasm and thanks for posting.

Best,

Amy

So if Dr. Marshall were to re-direct all his efforts in the short term to achieving the MPrize, and in doing so prove once and for all his ideas hold water, do you not think the huge amount of extra funding that would undoubtedly ensue, along with the acceptance of his ideas by the scientific community, would make it all worthwhile?

With so many pathogens capable of inhabiting our surroundings and bodies it makes little sense to leave them out of the picture when it comes to understanding the processes that cause the human body to degrade.

Best,

Amy

“… Rather, most of the talks fit into the model of aging first invoked by de Grey at the inception of the Conference - a model in which the human body is thought of as a car …”

Unexamined outermost meta-models often determine/derail interpretation of data and whole experimental thrusts.

That endosymbiotic infections/processes are at the heart of the matter still eludes most, even 20+ years after Lynn Margulis put forward a detailed argument for the endosymbiotic origin of the mitochondria and endosymbiosis as a general mechanism - “Life did not take over the globe by combat, but by networking”.

Thanks to all of the MP research arm who attended the conference so as to just possibly broaden the horizons of other researchers.

Greg - The fact that the human VDR contains seven hydrogen bonds doesn’t necessarily make it better than the murine VDR which contains five. Dr. Marshall was just clarifying that the difference in bonds marks yet another way in which the murine VDR differs from the human VDR.

Should we go after the Mprize? It would take a lot of extra research on Dr. Marshall’s part. If you listen to his recent presentation, he says that about 90% of the microbiota found in man are found in rodents, so bacterial species are not necessarily interchangeable. Also, since the rat VDR fails to transcribe the beta-Defensin and cathelecidin AMPs, pathogens would have little evolutionary incentive to create ligands that would block the rodent VDR.

So while pathogens probably don’t create VDR blocking ligands in rodents, they may create ligands that block some other receptor that is more directly connected to murine innate immune function. However we don’t know what that receptor is at this point (to my knowledge). Even if we identify such a receptor, finding a capnine-like equivalent among the substances produced by rodent pathogens would be a difficult quest. It took luck and a lot of work for Dr. Marshall to identify capnine, and some might argue that if he’s going to spend time looking for more receptor blocking ligands he should continue to look for ones that impede the human immune response, since adding to his human model of chronic inflammatory disease is probably most important at the moment.

Still, if anyone out there likes to mess around with molecular software and is familiar with the Marshall Pathogenesis they definitely have a heads up on how to win the Mprize. Wouldn’t it be nice if Dr. Marshall could be cloned? Then we could tackle all these projects!

Best,

Amy

Yes, the murine vdr is different from a human vdr. I think enough time and energy has already been spent to do the murine life extension research. Not much would be needed at this point. Changing minds and bridging people together is well worth the effort. Dr. M and company are definitely blazing trails, but sometimes those trails are hanging by a thread and need to be further widened. If it means that we encourage others to look at ARF more closely, winning the prize could be very advantageous.