GSK-3β, a pivotal kinase in Alzheimer disease

被引：472

作者：

Llorens-Martin, Maria ^{[1
,2
]}

Jurado, Jeronimo ^{[1
,2
]}

Hernandez, Felix ^{[1
,2
,3
]}

Avila, Jesus ^{[1
,2
]}

机构：

[1] Univ Autonoma Madrid, Consejo Super Invest Cient, Ctr Biol Mol Severo Ochoa, E-28049 Madrid, Spain

[2] Inst Salud Carlos III, Ctr Invest Biomed Red Enfermedades Neurodegenerat, Madrid, Spain

[3] Univ Autonoma Madrid, Fac Biol, E-28049 Madrid, Spain

来源：

FRONTIERS IN MOLECULAR NEUROSCIENCE | 2014年 / 7卷

关键词：

GSK-3; beta; Alzheimer disease; kinase; neurodegeneration; tau proteins; GLYCOGEN-SYNTHASE KINASE-3; CYCLIN-DEPENDENT KINASE-5; RABBIT SKELETAL-MUSCLE; HIPPOCAMPUS IN-VIVO; TAU-PROTEIN; TRANSGENIC MICE; A-BETA; SYNAPSE ELIMINATION; SIGNALING PATHWAY; PHOSPHORYLATION SITES;

D O I：

10.3389/fnmol.2014.00046

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Alzheimer disease (AD) is the most common form of age-related dementia. The etiology of AD is considered to be multifactorial as only a negligible percentage of cases have a familial or genetic origin. Glycogen synthase kinase-3 (GSK-3) is regarded as a critical molecular link between the two histopathological hallmarks of the disease, namely senile plagues and neurofibrillary tangles. In this review, we summarize current data regarding the involvement of this kinase in several aspects of AD development and progression, as well as key observations highlighting GSK-3 as one of the most relevant targets for AD treatment.

引用

页数：11

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