Understanding the relationship between GSK-3 and Alzheimer's disease: a focus on how GSK-3 can modulate synaptic plasticity processes

被引:1
作者
Medina, Miguel [1 ]
Avila, Jesus [1 ,2 ]
机构
[1] Ctr Invest Biomed Red Enfermedades Neurodegenerat, Madrid 28041, Spain
[2] Ctr Biol Mol Severo Ochoa CSIC UAM, Madrid 28049, Spain
关键词
Alzheimer's; dementia; GSK-3; long-term depression; long-term potentiation; memory; neurodegeneration; synaptic plasticity; GLYCOGEN-SYNTHASE KINASE-3; BETA PRECURSOR PROTEIN; LONG-TERM POTENTIATION; TAU-PROTEIN; IN-VIVO; TRANSGENIC MICE; AMYLOID PATHOLOGY; NEURONAL POLARITY; SIGNALING PATHWAY; EXTRACELLULAR TAU;
D O I
10.1586/ERN.13.39
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Originally discovered because of its role in the regulation of glucose metabolism, GSK-3 is now widely recognized as a crucial player in many cellular functions. Control of GSK-3 activity occurs by complex mechanisms that are each dependent upon specific signaling pathways. Furthermore, GSK-3 dysfunction has been linked to a number of pathologies, including Alzheimer's disease (AD). In particular, the involvement of GSK-3 in several key pathophysiological pathways leading to AD and neurodegenerative diseases has placed this enzyme in a central position in this disorder. In this article, the authors will specifically focus on the role of this enzyme as a key regulator of synaptic plasticity and how alterations in the GSK-3 synaptic functions may be a major factor in AD and other neurodegenerative disorders.
引用
收藏
页码:495 / 503
页数:9
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