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What is this cuprizone???
http://www.saanendoah.com/madcowdisease.html
A Case for the Role of Copper Deficiency
in "Mad-Cow" Disease and
Human Creutzfeldt-Jakob Disease
By
William H. Dresher, Ph.D., P.E.,
Geoffrey Greetham, Ph.D., F.I.M. and Brenda J. Harrison, Ph.D.
http://innovations.copper.org/december01/Mad-Cow.html
It is used in experiments to induce demyelination...
It is involved in Mad Cows disease... which according to some is cause by a copper deficiency in their foods????
http://www.markpurdey.com/science_ecosystems8.htm
"The issue of copper depletion / disruption as a TSE causal prerequisite which was first raised in the academic literature in my paper that reported the data from my 1995 - 1998 analytical studies of the food chains where sporadic TSEs were clustering around the world.
In this paper I combined the knowledge already brought to us by Hornshaw / Brown et al with that of my own environmental data, to hypothesise that the displacement or loss of copper from the prion protein molecule in conjunction with the substitution by a rogue replacement metal - e.g.; manganese or silver, etc - caused the malformed protease resistant form of prion protein to develop ( e.g. the abnormal form that is seen in the brains of TSE victims).
Whilst someone had proposed copper toxicity as a cause for TSE, nobody had proposed copper loss as a prerequisite before, which I found strange since the chemical cuprizone had been repeatedly used by the Compton labs during the 1970s to induce a chemical scrapie in mice ( albeit non-transmissible, since, according to my theory, there was no additional rogue metal microcrystal prerequisite involved in these tests that would have rendered the scrapie transmissible;). I guess that the researchers did not see the possible aetiological relevance of the fact that cuprizone is a copper chelator. This naturally interested me when I started to observe rock bottom levels copper in all of the TSE cluster foodchains I was visiting and sampling around the world ( e.g.; where the TSE affected populations were self sufficient off their local foodchain ), and led to me generating this theory of copper loss from the prion protein.
Brown et al, then tested my hypothesis of high manganese / low copper in cell cultures and got a positive result. He produced the protease resistant prion using my hypothesis - and this elevated my theory several rungs up the ladder of respectability amongst the non political quarters of the purist scientific community. For no research team had ever produced protease resistant prion protein before - as a de novo transformation. This deserved a lot more academic attention than it actually received..."