The role of GSK3 in Alzheimer disease

被引：60

作者：

Hernandez, Felix ^{[1
]}

Gomez de Barreda, Elena ^{[1
]}

Fuster-Matanzo, Almudena ^{[1
]}

Goni-Oliver, Paloma ^{[1
]}

Lucas, Jose J. ^{[1
]}

Avila, Jesus ^{[1
]}

机构：

[1] Univ Autonoma Madrid, CSIC, Ctr Biol Mol Severo Ochoa, E-28049 Madrid, Spain

来源：

BRAIN RESEARCH BULLETIN | 2009年 / 80卷 / 4-5期

关键词：

GSK3; Alzheimer disease; Tau protein; Dentate gyrus; GLYCOGEN-SYNTHASE KINASE-3; TRANSGENIC MICE; BETA-CATENIN; NEUROFIBRILLARY DEGENERATION; SIGNAL-TRANSDUCTION; EXTRACELLULAR TAU; NEURONAL CELLS; GSK-3-BETA; PATHWAY; NEURODEGENERATION;

D O I：

10.1016/j.brainresbull.2009.05.017

中图分类号：

Q189 [神经科学];

学科分类号：

071006 [神经生物学];

摘要：

Mutations in app, ps-1 and ps-2 genes result in the appearance of Familial Alzheimer disease (FAD). Although, in many cases, those mutations result in an increase of the amount of beta amyloid peptide, there is not a clear correlation between that amount and the time of the onset of the disease. Thus, other factors may explain how mutations in those genes result in the appearance of neurodegeneration. In this minireview we propose that GSK3 could be one of those factors. (C) 2009 Elsevier Inc. All rights reserved.

引用

页码：248 / 250

页数：3

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