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Voigtländer T, Klöppel S, Birner P, Jarius C, Flicker H, Verghese-Nikolakaki S, Sklaviadis T, Guentchev M, Budka H. Marked increase of neuronal prion protein immunoreactivity in Alzheimer's disease and human prion diseases. Acta Neuropathol. 2001 May;101(5):417-23. PubMed.
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University of Texas at San Antonio
Pathogenic versus Pathology Voigtlander and colleagues provide compelling supporting evidence for the notion that PrP is a neuroprotectant. Therefore, PrP, like amyloid-beta protein precursor/amyloid-beta in Alzheimer disease (AD), alpha-synuclein in Parkinson disease, neurofilament protein in amyotrophic lateral sclerosis and huntingtin in Huntington's disease, serves a protective function and therefore, as one might predict, the greater the stress, the higher the level of protectant necessary (otherwise neurons drop like flies). High levels of such protectants characterize these diseases, so much so, in fact, that pathologists use them to diagnose disease. It is such a travesty that most scientists confuse "pathology" and "pathogenic"; only the latter is causative. - Mark A. Smith and George Perry, Institute of Pathology, Case Western Reserve University
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