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帕金森病:靶向炎症能否成为一种有效的神经保护策略?

Parkinson's Disease: Can Targeting Inflammation Be an Effective Neuroprotective Strategy?

作者信息

Gundersen Vidar

机构信息

Section for Movement Disorders, Department of Neurology, Oslo University Hospital, Oslo, Norway.

出版信息

Front Neurosci. 2021 Feb 25;14:580311. doi: 10.3389/fnins.2020.580311. eCollection 2020.

Abstract

The reason why dopamine neurons die in Parkinson's disease remains largely unknown. Emerging evidence points to a role for brain inflammation in neurodegeneration. Essential questions are whether brain inflammation happens sufficiently early so that interfering with this process can be expected to slow down neuronal death and whether the contribution from inflammation is large enough so that anti-inflammatory agents can be expected to work. Here I discuss data from human PD studies indicating that brain inflammation is an early event in PD. I also discuss the role of T-lymphocytes and peripheral inflammation for neurodegeneration. I critically discuss the failure of clinical trials targeting inflammation in PD.

摘要

多巴胺神经元在帕金森病中死亡的原因在很大程度上仍然未知。新出现的证据表明脑部炎症在神经退行性变中起作用。关键问题在于脑部炎症是否足够早地发生,以至于干扰这一过程有望减缓神经元死亡,以及炎症的作用是否足够大,以至于有望通过抗炎药物发挥作用。在此,我讨论来自人类帕金森病研究的数据,这些数据表明脑部炎症是帕金森病中的一个早期事件。我还讨论了T淋巴细胞和外周炎症在神经退行性变中的作用。我批判性地讨论了针对帕金森病炎症的临床试验的失败。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e43f/7946840/e7a16c522340/fnins-14-580311-g001.jpg

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