作者: Alex E. Roher , Yu-Min Kuo , Alexander A. Roher , Mark R. Emmerling , Warren J. Goux
DOI: 10.1007/978-94-017-1007-7_9
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摘要: Substantial evidence demonstrates that amyloid deposition in the cerebral vasculature plays a major role pathophysiology of Alzheimer’s disease. Chemical and immunohistochemical analyses have demonstrated Aβ40 Aβ42 peptides are present vascular deposits with preponderance former peptide. The accumulation cerebrovascular leads to obliteration capillary lumen destruction arterial myocytes resulting hypoperfusion loss control blood flow. Post-translational modifications such as racemization, isomerization, cyclization, oxidation N-terminal degradation largely contribute insolubility proteolytic resistance exhibited by Aβ filaments. strong association other proteins, carbohydrates lipids results additional stability. There appears be positive correlation between magnitude dosage apolipoprotein E4.