Roles of brain-derived neurotrophic factor/tropomyosin-related kinase B (BDNF/TrkB) signalling in Alzheimer's disease

被引：89

作者：

Zhang, Fang ^{[1
]}

Kang, Zhilong ^{[1
]}

Li, Wen ^{[1
]}

Xiao, Zhicheng ^{[1
,2
]}

Zhou, Xinfu ^{[1
,3
]}

机构：

[1] Kunming Med Univ, Inst Mol & Clin Med, Kunming 650500, Peoples R China

[2] Monash Univ, Monash Immunol & Stem Cell Labs, Clayton, Vic, Australia

[3] Flinders Univ S Australia, Dept Human Physiol, Adelaide, SA 5001, Australia

来源：

JOURNAL OF CLINICAL NEUROSCIENCE | 2012年 / 19卷 / 07期

关键词：

Alzheimer's disease (AD); Amyloid-beta (A beta); Cognition; Tau; Tropomyosin-related kinase B (TrkB); AMYLOID PRECURSOR PROTEIN; LONG-TERM POTENTIATION; NEUROBLASTOMA-CELLS; SYNAPTIC PLASTICITY; PARIETAL CORTEX; TRKB RECEPTORS; BDNF; MEMORY; HIPPOCAMPUS; NEURONS;

D O I：

10.1016/j.jocn.2011.12.022

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

Alzheimer's disease (AD) is one of the most common causes of dementia in the elderly. It is characterized by extracellular deposition of the neurotoxic peptide, amyloid-beta (A beta) peptide fibrils, and is accompanied by extensive loss of neurons in the brains of affected individuals. However, the pathogenesis of AD is not fully understood. The aim of this review is to discuss the possible role of brain-derived neurotrophic factor (BDNF)/tropomyosin-related kinase B (TrkB) signalling in the development of AD, focusing on BDNF/TrkB signalling in the production of A beta, tau hyperphosphorylation and cognition decline, and exploring new possibilities for AD intervention. (C) 2012 Elsevier Ltd. All rights reserved.

引用

页码：946 / 949

页数：4

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