Glycogen synthase kinase 3β and Alzheimer's disease:: pathophysiological and therapeutic significance

被引：147

作者：

Balaraman, Y.

Limaye, A. R.

Levey, A. I.

Srinivasan, S.

机构：

[1] Emory Univ, Div Digest Dis, Atlanta, GA 30322 USA

[2] Emory Univ, Dept Neurol, Sch Med, Atlanta, GA 30322 USA

来源：

CELLULAR AND MOLECULAR LIFE SCIENCES | 2006年 / 63卷 / 11期

关键词：

Alzheimer's disease; glycogen synthase kinase 3 beta; amyloid precursor protein; presenilins; tau; beta-amyloid; neuronal apoptosis; lithium;

D O I：

10.1007/s00018-005-5597-y

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Alzheimer's disease (AD) is a neurodegenerative disorder associated with cognitive and behavioral dysfunction and is the leading cause of dementia in the elderly. Several studies have implicated molecular and cellular signaling cascades involving the serine-threonine kinase, glycogen synthase kinase beta(GSK-3 beta) in the pathogenesis of AD. GSK-3 beta may play an important role in the formation of neurofibrillary tangles and senile plaques, the two classical pathological hallmarks of AD. In this review, we discuss the interaction between GSK-3 beta and several key molecules involved in AD, including the presenilins, amyloid precursor protein, tau, and beta-amyloid. We identify the signal transduction pathways involved in the pathogenesis of AD, including Wnt, Notch, and the PI3 kinase/Akt pathway. These may be potential therapeutic targets in AD.

引用

页码：1226 / 1235

页数：10

共 116 条

[1] Lithium protects cultured neurons against β-amyloid-induced neurodegeneration [J].