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Neurodegenerative Diseases

Presumably the same phenomenon is operative in AD and PD, although the neuronal damage is not as severe as seen in TSEs. This comparison brings up the idea that all neurodegenerative diseases are potentially infectious, with the focus on the amyloid deposits themselves by extension of the prion replicating protein theory. However, the UPR response and disruption of autophagy are known to occur after the buildup of misfolded amyloid proteins associated with intracellular viruses and bacteria. This phenomenon is operative in plant virus infection. Furthermore, there are problems with the concept of replicating prion amyloid in TSEs, since there is convincing evidence of consistent involvement of spiroplasma, a wallless bacterium, in TSE-affected brains and eyes. Thus Spiroplasma spp. are candidate causal agents in CJD and the animal TSEs. Recognition of conventional bacterial or viral involvement in the pathogenesis of the neurodegenerative diseases could lead to new diagnostic and therapeutic approaches. This treatise encourages a more balanced research and funding approach to investigating the exciting possibility of the infectious nature of AD. Frank O. Bastian, Cross-Roads in Research on Neurodegenerative Diseases
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Last date updated on June, 2014

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