By Alan Ebringer

The target of this e-book is to publicise and produce to a much broader viewers the concept the reason for neurological ailments, particularly a number of sclerosis (MS) and “mad cow illness” often referred to as “bovine spongiform encephalopathy” are comparable via publicity to a standard microbe Acinetobacter that's present in human sinuses, on pores and skin and within the soil. infection is the reason for a neurological disorder in guy and in animals. increased degrees of antibodies to Acinetobacter were present in a number of sclerosis sufferers in addition to in ruminants who've been defined as struggling with “mad cow disorder” following publicity to infected feed vitamins. the general goal and scope of this e-book is to notify the viewers, the reader, that a number of sclerosis will be associated with a microbe Acinetobacter which includes molecular buildings reminiscent of myelin, the outer sheath masking of neurons.

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2012). 3 “Experimental Allergic Encephalomyelitis” as a Model of Multiple Sclerosis 23 The human diploid cell rabies vaccine was started in 1967 and produced from the attenuated Pitman-Moore strain of the virus. As the vaccine does not contain any brain antigens it does not lead to the complications initially discovered by Pasteur and colleagues. The question arises as to the origin of the complications following rabies immunization with extracts containing brain antigens. 3 “Experimental Allergic Encephalomyelitis” as an Animal Model of Multiple Sclerosis The disease complication occurring after rabies immunisation has to some extent been reproduced when injecting brain tissues into experimental animals.

Moreover, sporadic cases of scrapie infected sheep should have increased levels of antibodies to some of these microbes (Ebringer et al. 1998). 4. BSE is probably an autoimmune disease caused by bacteria which carry antigens resembling or showing molecular mimicry with brain tissues. 5. The BSE epidemic occurred as a result of producing animal feeds containing high concentrations of bacteria showing molecular mimicry with myelin and other brain antigens. 6. Experiments are required to determine if immune responses to these bacteria have occurred in BSE or scrapie affected animals.

The second assumption is being made here is that any pathological responses are due to the “scrapie” agent. The first assumption is clearly wrong, since we know since the time of Pasteur that brain homogenates produce “experimental allergic encephalomyelitis” (EAE). Homogenates from any organ will evoke an auto-immune disease. The second assumption is also wrong since the “scrapie” agent has not been identified. References 19 The “prion” molecule is anyway a self-molecule encoded by the DNA of the original animal or patient, therefore it is a self-molecule.

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