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5-羟色胺能系统参与帕金森病左旋多巴诱导的运动障碍。

Serotonergic involvement in levodopa-induced dyskinesias in Parkinson's disease.

机构信息

Van Cleef Roet Centre for Nervous Diseases, 4th Floor, Monash University, Alfred Hospital, 89 Commercial Road, Melbourne, Victoria 3004, Australia.

出版信息

J Clin Neurosci. 2012 Mar;19(3):343-8. doi: 10.1016/j.jocn.2011.09.008. Epub 2012 Jan 16.

Abstract

Levodopa-induced dyskinesias (LID) represent a substantial barrier to effective symptomatic management of Parkinson's disease, but current treatment options for this debilitating side effect are limited, despite an increasing understanding of their pathophysiology from animal models. Increasing evidence suggests that serotonin neurons have a pivotal role in the induction and maintenance of dyskinesias, and provide a promising target for anti-dyskinetic therapies. Here, we review the evidence for serotonergic involvement in dyskinesias from animal and human data, and highlight some of the translational gaps which may explain why the success of serotonin autoreceptor agonists as anti-dyskinetic agents in experimental models has failed to be replicated in clinical trials.

摘要

左旋多巴诱导的运动障碍(LID)是有效治疗帕金森病症状的主要障碍,但尽管从动物模型中对其病理生理学有了更深入的了解,针对这种使人衰弱的副作用的治疗选择仍然有限。越来越多的证据表明,5-羟色胺神经元在运动障碍的诱导和维持中起着关键作用,为抗运动障碍治疗提供了一个有前途的靶点。在这里,我们回顾了来自动物和人类数据的 5-羟色胺能参与运动障碍的证据,并强调了一些可能解释为什么 5-羟色胺自身受体激动剂作为抗运动障碍药物在实验模型中取得成功而在临床试验中未能复制的转化差距。

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