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首页> 外文期刊>Journal of neurology >Autonomic failure in Parkinson's disease is associated with striatal dopamine deficiencies
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Autonomic failure in Parkinson's disease is associated with striatal dopamine deficiencies

机译:帕金森病的自主主义失败与纹状体多巴胺缺乏有关

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Autonomic dysfunction is a common non-motor symptom in Parkinson's disease (PD). Dopamine and serotonin are known to play a role in autonomic regulation, and, therefore, PD-related degeneration of serotonergic and dopaminergic neurons in these regions may be associated with autonomic dysfunction. We sought to clarify the association between extrastriatal serotonergic and striatal dopaminergic degeneration and the severity of autonomic symptoms, including gastrointestinal, pupillomotor, thermoregulatory, cardiovascular, and urinary dysfunction. We performed hierarchical multiple regression analyses to determine the relationships between (extra)striatal serotonergic and dopaminergic degeneration and autonomic dysfunction in 310 patients with PD. We used [I-123]FP-CIT SPECT binding to presynaptic serotonin (SERT) and dopamine (DAT) transporters as a measure of the integrity of these neurotransmitter systems, and the SCOPA-AUT (Scales for Outcomes in Parkinson's Disease-Autonomic) questionnaire to evaluate the perceived severity of autonomic dysfunction. Motor symptom severity, medication status, and sex were added to the model as covariates. Additional analyses were also performed using five subdomains of the SCOPA-AUT: cardiovascular, gastrointestinal, urinary, thermoregulatory, and pupillomotor symptoms. We found that autonomic symptoms were most significantly related to lower [I-123]FP-CIT binding ratios in the right caudate nucleus and were mainly driven by gastrointestinal and cardiovascular dysfunction. These results provide a first look into the modest role of dopaminergic projections towards the caudate nucleus in the pathophysiology of autonomic dysfunction in PD, but the underlying mechanism warrants further investigation.
机译:自主功能障碍是帕金森病(PD)的常见非运动症状。已知多巴胺和血清素在自主语控中发挥作用,因此,这些地区中的血清onergic和多巴胺能神经元的PD相关退化可能与自主功能障碍有关。我们试图澄清群体血清奈良能和纹状体多巴胺能退化和自主主义症状的严重程度之间的关联,包括胃肠道,瞳孔,热调节,心血管和尿辨率功能障碍。我们进行了分层多元回归分析,以确定Pd 310例患者的(额外)纹状体血清onOrotonergic和多巴胺能变性和自主神经功能障碍之间的关系。我们使用[I-123] FP-CIT SPECT与突触前血清素(SERT)和多巴胺(DAT)转运蛋白结合,作为这些神经递质系统的完整性,以及SCOPA-AUT(帕金森病 - 自主主义结果的尺度)调查问卷评估自主功能障碍的感知严重程度。作为协变者将电机症状严重程度,药物状态和性别添加到模型中。还使用SCOPA-AUT的五个亚域进行了额外的分析:心血管,胃肠道,泌尿,疗法和瞳孔受体症状。我们发现,自主主义症状最显着与尾部核核的较低[I-123] FP-CIT结合率有关,主要由胃肠道和心血管功能障碍驱动。这些结果提供了首先研究多巴胺能突起对PD中自主神经功能障碍病理生理病理学的尾状核的适度作用,但底层机制需要进一步调查。

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