The role of Wnt signaling and its interaction with diverse mechanisms of cellular apoptosis in the pathophysiology of bipolar disorder

被引:14
|
作者
Hu, Li Wen [1 ]
Kawamoto, Elisa Mitiko [2 ]
Brietzke, Elisa [1 ]
Scavone, Cristoforo [2 ]
Lafer, Beny [1 ]
机构
[1] Univ Sao Paulo, Dept Psychiat, Sch Med, Bipolar Disorder Res Program, BR-01060970 Sao Paulo, Brazil
[2] Univ Sao Paulo, Dept Pharmacol, Inst Biomed Sci, BR-01060970 Sao Paulo, Brazil
基金
巴西圣保罗研究基金会;
关键词
Bipolar disorder; GSK3; beta; Inflammation; Neuroplasticity; Wnt; GLYCOGEN-SYNTHASE KINASE-3-BETA; SUBGENUAL PREFRONTAL CORTEX; NEUROTROPHIC FACTOR; OXIDATIVE STRESS; BETA-CATENIN; TRANSDUCTION PATHWAYS; EUTHYMIC PATIENTS; MOOD STABILIZERS; DECREASED LEVELS; GENE-EXPRESSION;
D O I
10.1016/j.pnpbp.2010.08.031
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
The neurobiology of Bipolar Disorder (BD) is not completely understood, although abnormalities in neuroplasticity and control of apoptosis have been considered as central events in its pathophysiology. The molecules of the Wnt family comprise a class of proteins that control essential developmental processes such as embryonic patterning, cell growth, migration, and differentiation with their actions largely exerted by modulating gene transcription. The Wnt signaling pathway has interface with some mediators with a well documented action in neuroplasticity and regulation of cell surviving. In addition, mood stabilizers such as lithium and valproate may have their neuroprotective properties in part mediated by the Wnt pathway. This article is an overview of how the Wnt signaling cascade might be involved in the pathogenesis of BD and also in details of intracellular events related to this pathway. Further studies of Wnt signaling may lead to a better comprehension of the neuroprotective actions of mood stabilizers and contribute to improving the therapeutics of BD. (C) 2010 Elsevier Inc. All rights reserved.
引用
收藏
页码:11 / 17
页数:7
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