Effects of Stress and Stress Hormones on Amyloid-β Protein and Plaque Deposition

被引：104

作者：

Dong, Hongxin ^{[1
]}

Csernansky, John G. ^{[1
]}

机构：

[1] Northwestern Univ, Dept Psychiat & Behav Sci, Feinberg Sch Med, Chicago, IL 60611 USA

来源：

JOURNAL OF ALZHEIMERS DISEASE | 2009年 / 18卷 / 02期

基金：

美国国家卫生研究院;

关键词：

Alzheimer's disease; amyloid-beta; corticotrophin-releasing factor (CRF) and receptors (CRFRs); hypothalamic-pituitary-adrenal (HPA) axis; stress; Tg2576; mice; CORTICOTROPIN-RELEASING-FACTOR; PITUITARY-ADRENAL AXIS; FACTOR-LIKE IMMUNOREACTIVITY; BASAL CORTISOL-LEVELS; ALZHEIMERS-DISEASE; A-BETA; CEREBROVASCULAR-DISEASE; PSYCHOLOGICAL DISTRESS; SYNAPTIC PLASTICITY; RECEPTOR ANTAGONISM;

D O I：

10.3233/JAD-2009-1152

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Growing evidence indicates that physical and psychosocial stressors, in part acting through the hypothalamic-pituitary-adrenal (HPA) axis, may accelerate the process of Alzheimer's disease (AD). In this review, we summarize recent research related to the effects of stress and stress hormones on the various disease process elements associated with AD. Specifically, we focus on the relationships among chronic stressors, HPA axis activity, amyloid-beta protein, and amyloid-beta plaque deposition in mouse models of AD. The potential mechanisms by which stress and stress-related components, especially corticotrophin-releasing factor and its receptors, influence the pathogenesis of AD are discussed.

引用

页码：459 / 469

页数：11

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