Etiology Versus Pathogenesis: The Causes of Post-Translational Modifications of Host-Specified Brain Proteins to Amyloid Configuration
Since amyloid is deposited as neurofibrillary tangles, plaques, and vascular amyloid in brains of all the very aged (> 90 years), and this amyloid is biochemically the same as that in Alzheimer’s disease, Down’s syndrome, and Guamanian amyotrophic lateral sclerosis/Parkinsonism-dementia (ALS/PD), we know that no abnormal hereditable gene is necessary for such deposition. By isolating the gene for the precursor to this amyloid we are surely tracking pathogenesis of normal aging. Alzheimer’s disease, Down’s syndrome, and Guamanian ALS/PD. The same applies to isolating the gene for the normal host precursor protein for the much different amyloid of the scrapie-associated fibrils of unconventional viruses (scrapie-kuru-Creutzfeldt-Jakob disease) and the amyloid plaques of these diseases.
KeywordsCrystallization Dementia Polypeptide Fibril Colchicine
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