title: The dendritic hypothesis for Alzheimer's disease pathophysiology.
abstract: Converging evidence indicates that processes occurring in and around neuronal dendrites are central to the pathogenesis of Alzheimer's disease. These data support the concept of a "dendritic hypothesis" of AD, closely related to the existing synaptic hypothesis. Here we detail dendritic neuropathology in the disease and examine how Aβ, tau, and AD genetic risk factors affect dendritic structure and function. Finally, we consider potential mechanisms by which these key drivers could affect dendritic integrity and disease progression. These dendritic mechanisms serve as a framework for therapeutic target identification and for efforts to develop disease-modifying therapeutics for Alzheimer's disease.
authors: Center for Neurodegeneration and Experimental Therapeutics, Departments of Neurology and Neurobiology, University of Alabama at Birmingham, Birmingham, AL 35294, United States.
authors: J Nicholas
authors: JN
authors: Cochran
authors: Center for Neurodegeneration and Experimental Therapeutics, Departments of Neurology and Neurobiology, University of Alabama at Birmingham, Birmingham, AL 35294, United States.
authors: Alicia M
authors: AM
authors: Hall
authors: Center for Neurodegeneration and Experimental Therapeutics, Departments of Neurology and Neurobiology, University of Alabama at Birmingham, Birmingham, AL 35294, United States. Electronic address: eroberson@uab.edu.
authors: Erik D
authors: ED
authors: Roberson
mesh_terms: D000544:Alzheimer Disease / Q000473:pathology* / Q000503:physiopathology*; D016229:Amyloid beta-Peptides / Q000378:metabolism; D000818:Animals; D003712:Dendrites / Q000502:physiology* / Q000648:ultrastructure*; D006801:Humans; D016501:Neurites / Q000648:ultrastructure; D024801:Tauopathies / Q000473:pathology
chemical_list: D016229:Amyloid beta-Peptides
keywords: Amyloid; Calcium; Fyn; Postsynaptic; Spine; Tau