神经元型一氧化氮合酶基因多态性与帕金森病左旋多巴诱导运动障碍的关系。

Association of a neuronal nitric oxide synthase gene polymorphism with levodopa-induced dyskinesia in Parkinson's disease.

机构信息

Department of Neurosciences and Behavioral Sciences, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil; Center for Research Support on Applied Neuroscience (NAPNA-USP), São Paulo, Brazil.

Department of Neurology, Federal University of São Paulo, São Paulo, SP, Brazil.

出版信息

Nitric Oxide. 2018 Apr 1;74:86-90. doi: 10.1016/j.niox.2017.06.004. Epub 2017 Jun 8.

DOI:10.1016/j.niox.2017.06.004

PMID:28602747

Abstract

BACKGROUND

Levodopa-induced dyskinesia (LID) is a common complication of advanced Parkinson's disease (PD). PD physiopathology is associated with dopaminergic and non-dopaminergic pathways, including the nitric oxide system. The present study aims to examine the association of a neuronal nitric oxide synthase gene (NOS1) single nucleotide polymorphism (rs2682826) with LID in PD patients.

METHODS AND RESULTS

We studied 186 PD patients using levodopa. The presence of LID was defined as a MDS-UPDRS Part IV score ≥1 on item 4.1. We tested for association between NOS1 rs2682826 and the presence, daily frequency, and functional impact of LID using regression models, adjusting for important covariates. There was no significant association between genotype and any of the LID-related variables examined.

CONCLUSIONS

Our results suggest that this NOS1 polymorphism does not contribute to LID susceptibility or severity. However, additional studies that include a comprehensive set of NOS1 variants will be needed to fully define the role of this gene in LID.

摘要

背景

左旋多巴诱导的运动障碍（LID）是晚期帕金森病（PD）的常见并发症。PD 的病理生理学与多巴胺能和非多巴胺能途径有关，包括一氧化氮系统。本研究旨在研究神经元型一氧化氮合酶基因（NOS1）单核苷酸多态性（rs2682826）与 PD 患者 LID 的关系。

方法和结果

我们使用左旋多巴研究了 186 名 PD 患者。LID 的存在定义为 MDS-UPDRS 第 IV 部分评分≥4.1 项。我们使用回归模型测试了 NOS1 rs2682826 与 LID 的存在、每日频率和功能影响之间的关系，并对重要的协变量进行了调整。基因型与任何检查的 LID 相关变量之间均无显著关联。