CJD, regardless of the version, is a disease that is caused by what? A lack of copper or an over abundance of it or lack or overabundance of Manganese? The arguments are legion and the research is growing as Randy mentioned. Having said that, the fact remains that numerous governments around the world and their collective scientists have already identified and agree that the feeding of ruminant extracted protein back to other ruminants that have been carriers of PrPsc, is the proimary cause of Bovine infection with BSE. There is also an emerging school of thought that is researching the effect of metals of proteins (PrPc) and how they can mutate into PrPsc. One thing to consider also is the fact that after numerous controlled experiments conducted by MAFF and other research houses in the UK which has shown that in animal exposures, where infection has been documented after oral feed, transmission was so irregullar that the question arose as to whether the true portal was the gastrointestinal tract itself or through areas of mucosal abrasions. In some patients, the portal route of entry may have been through bad teeth. Ulcerations of the lips, gums and intestinal lesions may have played a huge role in the transmission since it is known that the disease develops with a significantly shorter incubation period where such ulcerations have been present. Now to throw an interesting fact into the current argument or generally accepted thinking as to how PrPsc is transmitted from cattle to humans, it is important to note the following facts: In the UK, at the height of the BSE crisis, researchers had, up to then, regarded the holes (vacuoles) in the neurons [brain/swiss cheese effect] as being of major interest and importance for diagnostic purposes, with all other indicators being either ignored or not of equal value for the purposes of identification of the disease. The precise significance of vacuoles, their numbers and distribution is, as yet, puzzling and troublesome. In spite of the many advances in knowledge made in recent years, there is still much uncertainty as to what actually constitutes a hole in a nerve cell when viewed through a light microscope. The differences between normal and infected tissues can be minimal, making recognition and identification of the vacuoles extremely difficult. The spongiform change in natural scrapie, as well as being variable in its appearance, is never as extensive as it is in experimental scrapie. The vacuoles result from the damage caused by the infection, the agent can incubate without their formation and therefore, the presence or absence of vacuoles is not a reliable indicator of infection. In the case of all the cattle in the UK that were clinically diagnosed as infected with BSE and slaughtered due to their infection, over 20% [32,000 or more] were found to have no evidence of vacuoles in their brains and were therefore, not officially included as BSE victims in the statistics. Whether this means that these animals were free of BSE or that their histological examination had failed to detect the disease in uncertain. The same reservations apply in human CJD cases. CJD is not regarded as confirmed in the nearly 50% of clinically diagnosed cases where, although all the typical symptoms of CJD are present, no vacuoles are seen. They are also excluded from official records, leaving unanswered questions as to how so much reliance can be given to a clinical diagnosis in human cases based upon the presence or absence of vacuoles? THere are many questions surrounding diagnostic techniques and the steady progression of science will hopefully provide the answers. This, along with other reasons, is why we have developed our urine test, to try to provide alternative and proven methods of early detection and positive identification of the PrPsc in humans and animals.
:lol: 