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肿瘤坏死因子-α作为双相情感障碍的分子靶点。

TNF-alpha as a molecular target in bipolar disorder.

作者信息

Brietzke Elisa, Kapczinski Flávio

机构信息

Bipolar Disorder Program and Molecular Psychiatry Unit, Hospital de Clínicas de Porto Alegre, Federal University of Rio Grande do Sul. Porto Alegre, Brazil.

出版信息

Prog Neuropsychopharmacol Biol Psychiatry. 2008 Aug 1;32(6):1355-61. doi: 10.1016/j.pnpbp.2008.01.006. Epub 2008 Jan 16.

Abstract

The pathophysiology of bipolar disorder (BD) is poorly understood. An emerging body of evidence points to impairments in neuroplasticity, cell resilience and neuronal survival as the main neuropathological correlates of BD. It has been suggested that inflammatory cytokines, particularly TNF-alpha may play a critical role in this process. In the present review we examine the evidence suggesting that TNF-alpha regulates apoptotic cascades which may be related to neuronal and glial loss in BD. Current evidence suggests that an increase in serum levels of TNF-alpha takes place during manic and depressive episodes. The present article reviews the therapeutic implications of TNF-alpha signaling pathways involvement in the pathophysiology of BD.

摘要

双相情感障碍(BD)的病理生理学仍未得到充分理解。越来越多的证据表明,神经可塑性、细胞弹性和神经元存活受损是BD主要的神经病理学相关因素。有人提出,炎性细胞因子,尤其是肿瘤坏死因子-α(TNF-α)可能在此过程中起关键作用。在本综述中,我们研究了表明TNF-α调节凋亡级联反应的证据,这可能与BD中的神经元和神经胶质细胞丢失有关。目前的证据表明,在躁狂和抑郁发作期间,血清TNF-α水平会升高。本文综述了TNF-α信号通路参与BD病理生理学的治疗意义。

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