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amedstudent131 karma

Thanks for replying! The seeding theory is the exact same as the Alzheimer's seed theory. I worked in protein chemistry research before medical school, and did some work with A-beta. It seems that the processes are amazingly similar, but PrPTSE seems to be a much more potent neurotoxin (especially judging by the pathology of spongiform encephalopathies. Nasty brain slices, those).

In the refolding model, is there any indication as to what the cellular change is that lowers the energy barrier? I would have guessed aging (increased natural cellular damage due to free radicals and such), but vCJD has been known to kill people as young as 28. What kind of variables do you play with to induce transformation?

Also, what do you think about eating wild venison knowing that elk and deer also have prion encephalopathies?

amedstudent131 karma

I've learned about prion diseases from a medical standpoint, but I'm still unclear on how the PrPSC protein catalyzes the conversion of normal PrP into PrPSC. It's all been pretty vague, and we've been told to just accept it. How does it work?