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炎症与帕金森病发病机制。

Inflammation and Parkinson's disease pathogenesis.

机构信息

Department of Neurology, Pathology and Cell Biology, Columbia University, New York, New York, USA.

出版信息

Mov Disord. 2010;25 Suppl 1:S55-7. doi: 10.1002/mds.22638.

Abstract

Inflammation is a neuropathological feature of parkinsonian brains and also in experimental models of the disease. It is believed that activated glial cells, which compose the majority of this inflammatory response contribute to the neurodegenerative process through the production of toxic molecules. Therapeutic strategies geared toward reducing inflammation and inhibiting the production of these glial-derived toxic molecules may be a promising neuroprotective strategy for the treatment of Parkinson's disease and related conditions.

摘要

炎症是帕金森病患者大脑的神经病理学特征,也是该疾病实验模型中的特征。人们认为,构成这种炎症反应主要部分的活化神经胶质细胞通过产生毒性分子,促成了神经退行性过程。针对减轻炎症和抑制这些源自神经胶质的毒性分子产生的治疗策略,可能是治疗帕金森病和相关疾病的一种很有前途的神经保护策略。

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