Purdey published a paper proposing that: Manganese could, in the presence of copper deficiency in the animal or human, substitute for copper in the prion protein, thus producing the abnormal prion found in the brains of spongiform encephelopathy disease victims.
This was a hypothesis based on his field work in the areas where clusters of mad cow and CJD were occurring and where, he observed, all these areas had unusually low levels of copper in the soil and unusually high levels of manganese in either the soil or the atmosphere.
Purdey reports that, “David Brown ran the necessary cell-culture experiments, in which he introduced manganese into copper-depleted prion protein cell cultures.”
Behold the mutated prion
Amazingly, his experiments produced the key deformation of the prion protein which the earlier tests using organophosphate (OP) insecticides like the Phosmet (Purdey initially suspected as the cause of mad cow disease at the Institute of Psychiatry) had failed to create. These experiments represented the first time that malformed prion protein had been created experimentally as a de novo transformation.
So it appears that these experiments definitively answered the key question of where this abnormal prion came from in the first place, something I have not heard the advocates of the conventional theory do with any clarity.Proliberty Idaho Observer: Mad Cow disease: Is it really Manganese Madness?