The dendritic hypothesis for Alzheimer's disease pathophysiology

被引：83

作者：

Cochran, J. Nicholas

Hall, Alicia M.

Roberson, Erik D. ^{[1
]}

机构：

[1] Univ Alabama Birmingham, Dept Neurol, Ctr Neurodegenerat & Expt Therapeut, Birmingham, AL 35294 USA

来源：

BRAIN RESEARCH BULLETIN | 2014年 / 103卷

关键词：

Postsynaptic; Spine; Amyloid; Tau; Fyn; Calcium; A-BETA OLIGOMERS; CELLULAR PRION PROTEIN; LONG-TERM POTENTIATION; NICOTINIC ACETYLCHOLINE-RECEPTORS; TARGETED REPLACEMENT MICE; REGION-SPECIFIC STABILITY; AMYLOID-BETA; CALCIUM-CHANNEL; TAU-PROTEIN; ENDOGENOUS TAU;

D O I：

10.1016/j.brainresbull.2013.12.004

中图分类号：

Q189 [神经科学];

学科分类号：

071006 [神经生物学];

摘要：

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 A beta, 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. This article is part of a special issue Dendrites and Disease. (C) 2013. Elsevier Inc. All rights reserved.

引用

页码：18 / 28

页数：11

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