Synaptotoxicity in Alzheimer's Disease Involved a Dysregulation of Actin Cytoskeleton Dynamics through Cofilin 1 Phosphorylation - Rush, Travis; Martinez-Hernandez, Jose; Dollmeyer, Marc; Frandemiche, Marie Lise; Borel, Eve; Boisseau, Sylvie; Jacquier-Sarlin, Muriel; Buisson, Alain (The Journal of neuroscience, 2018)
Keywords: Actin; Actins - metabolism; Adult; Aged; Aged, 80 and over; Alzheimer Disease - metabolism; Alzheimer Disease - pathology; Alzheimer's disease; Amyloid; Animals; Calcium; Calcium imaging; Cells, Cultured; Cofilin; Cofilin 1 - metabolism; Cognitive ability; Cytoskeleton; Cytoskeleton - metabolism; Cytoskeleton - pathology; Dendritic plasticity; Dendritic spines; Dendritic structure; Female; Fluorescence; Fluorescence recovery after photobleaching; Humans; Impairment; Inhibitors; Kinases; Long-term potentiation; Male; Mice; Mice, Inbred C57BL; Mice, Transgenic; Middle Aged; Molecular modelling; Mutants; Neurodegenerative diseases; Neurons; Oligomers; Pathophysiology; Patients; Phosphorylation; Phosphorylation - physiology; Photobleaching; Postsynaptic density; Presenilin 1; Protein kinase; Proteins; Rocks; Rods; Spine; Stabilization; Synapses; Synapses - metabolism; Synapses - pathology; Synaptic plasticity; Synaptic strength; Synaptosomes; Therapeutic applications; α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors; actin; cofilin; amyloid-β oligomers; Alzheimer's disease; fasudil; Rho-associated protein