Clinical Neurosciences, Department of Clinical Medicine, Faculty of Medicine, University of Turku, Turku, Finland.
Neurocenter, Turku University Hospital, Turku, Finland.
Mov Disord. 2021 Aug;36(8):1781-1791. doi: 10.1002/mds.28632. Epub 2021 May 6.
Dopamine receptors are abundant along the central nigrostriatal tract and are expressed as 5 subtypes in two receptor families. In PD, compensatory changes in dopamine receptors emerge as a consequence of the loss of dopamine nerve terminals or dopaminergic pharmacotherapy. We performed a systematic review and meta-analysis of the available PET and single-photon emission computed tomography studies that have investigated dopamine receptors in PD, PSP and MSA. The inclusion criteria were studies including human PET or single-photon emission computed tomography imaging; dopamine receptor tracers (D1-like or D2-like) and idiopathic PD, PSP, or MSA patients compared with healthy controls. The 67 included D2-like studies had 1925 patients. Data were insufficient for an analysis of D1-like studies. PD patients had higher striatal binding early in the disease, but after a disease duration of 4.36 years, PD patients had lower binding values than healthy controls. Striatal D2R binding was highest in unmedicated early PD patients and in the striatum contralateral to the predominant motor symptoms. PSP and MSA-P patients had lower striatal D2R binding than PD patients (14.2% and 21.8%, respectively). There is initial upregulation of striatal D2Rs in PD, which downregulate on average 4 years after motor symptom onset, possibly because of agonist-induced effects. The consistent upregulation of D2Rs in the PD striatum contralateral to the predominant motor symptoms indicates that receptor changes are driven by neurodegeneration and loss of striatal neuropil. Both PSP and MSA patients have clearly lower striatal D2R binding values than PD patients, which offers an opportunity for differential diagnostics. © 2021 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.
多巴胺受体在中央黑质纹状体束中大量存在，并在两个受体家族中表达为 5 种亚型。在 PD 中，多巴胺神经末梢的丧失或多巴胺药物治疗会导致多巴胺受体代偿性改变。我们对已发表的研究 PD、PSP 和 MSA 中多巴胺受体的 PET 和单光子发射计算机断层扫描研究进行了系统评价和荟萃分析。纳入标准为包括人类 PET 或单光子发射计算机断层扫描成像的研究；多巴胺受体示踪剂（D1 样或 D2 样）和特发性 PD、PSP 或 MSA 患者与健康对照组相比。纳入的 67 项 D2 样研究中有 1925 名患者。数据不足以分析 D1 样研究。PD 患者在疾病早期纹状体结合较高，但在疾病持续 4.36 年后，PD 患者的结合值低于健康对照组。未接受药物治疗的早期 PD 患者和与主要运动症状相对侧纹状体中 D2R 结合最高。PSP 和 MSA-P 患者的纹状体 D2R 结合低于 PD 患者（分别为 14.2%和 21.8%）。PD 患者纹状体 D2R 最初上调，平均在运动症状出现后 4 年下调，可能是由于激动剂诱导的作用。PD 纹状体中与主要运动症状相对侧的 D2R 持续上调表明受体变化是由神经退行性变和纹状体神经毡丧失驱动的。PSP 和 MSA 患者的纹状体 D2R 结合值均明显低于 PD 患者，这为鉴别诊断提供了机会。© 2021 作者。运动障碍由 Wiley 期刊公司代表国际帕金森病和运动障碍协会出版。
