Soluble amyloid β-protein dimers isolated from Alzheimer cortex directly induce Tau hyperphosphorylation and neuritic degeneration - Jin, Ming; Shepardson, Nina; Yang, Ting; Chen, Gang; Walsh, Dominic; Selkoe, Dennis J.; Petsko, Gregory A. (Proceedings of the National Academy of Sciences - PNAS, 2011)
Keywords: 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