Soluble amyloid β-protein dimers isolated from Alzheimer cortex directly induce Tau hyperphosphorylation and neuritic degeneration

• Published in: Proceedings of the National Academy of Sciences - PNAS Vol. 108; no. 14; pp. 5819 - 5824
• Main Authors: Jin, Ming, Shepardson, Nina, Yang, Ting, Chen, Gang, Walsh, Dominic, Selkoe, Dennis J., Petsko, Gregory A.
• Format: Journal Article
• Language: English
• Published: United States National Academy of Sciences 05.04.2011; National Acad Sciences
• Subjects: Alzheimer disease; Alzheimer Disease - physiopathology; Alzheimer's disease; Alzheimers disease; Amyloid; Amyloid beta-Peptides - metabolism; Amyloid beta-Peptides - pharmacology; Amyloids; Animals; Antibodies; Axons; beta -Amyloid; Biological Sciences; Blotting, Western; Brain; Chromatography, Gel; cognition; Cognitive ability; Cortex; Cytoskeleton; Deposits; Dimerization; Dimers; Dystrophy; Epitopes; Fibrils; Genetic Vectors - genetics; Hippocampus - cytology; Humans; Immunohistochemistry; Immunoprecipitation; Immunotherapy; In Situ Nick-End Labeling; Lentivirus; memory; Microscopy, Confocal; Microtubules; Microtubules - drug effects; Neurites; Neurites - drug effects; Neurites - pathology; Neurodegeneration; Neurodegenerative diseases; Neurons; Oligomers; peptides; Phosphorylation; Phosphorylation - drug effects; Rats; Rats, Sprague-Dawley; Tau protein; tau Proteins - metabolism

Alzheimer disease is a major cause of cognitive failure, and a pathogenically related but more subtle process accounts for many cases of mild memory symptoms in older humans. Insoluble fibrillar plaques of amyloid β-proteins (Aβ) and neurofibrillary deposits of hyperphosphorylated tau proteins are t...