Department of Radiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Parkinsonism Relat Disord. 2018 May;50:74-80. doi: 10.1016/j.parkreldis.2018.02.019. Epub 2018 Feb 9.
Depression is one of the most common non-motor symptoms in Parkinson's disease (PD), but its pathogenesis is still not very clear. Recently, degree centrality, a voxel-level whole-brain functional connectivity (FC) analysis of resting-state functional magnetic resonance imaging, has provided the most promising way to explore the neural network mechanisms underlying depressed PD.
Degree centrality, voxel-wise image and clinical symptoms correlation and secondary seed-based FC analyses were performed in twenty-seven drug-naïve, early stage depressed PD patients, 27 non-depressed PD patients and 27 healthy controls (HCs) to reveal voxel-level whole-brain FC changes in depressed PD.
Compared with the HCs, depressed PD and non-depressed PD patients shared similar brain degree centrality abnormalities mainly in the basal ganglia, insular cortex, motor cortices, default mode network, prefrontal gyrus and the cerebellum. However, compared with non-depressed PD, depressed PD showed degree centrality abnormalities in the right middle prefrontal gyrus, anterior cingulate cortices, supplementary motor cortices and cerebellum lobule VI. The right middle prefrontal gyrus degree centrality abnormalities were correlated with the clinical depression severity, and using it as a seed, a secondary seed-based FC analysis further revealed the FC changes in the anterior cingulate cortices and the cerebellum lobule VI.
Our findings revealed that dysfunction in extensive brain areas were involved in depressed PD, and among these regions, the right middle prefrontal gyrus, anterior cingulate cortices and the cerebellum may pose as pathogenesis hubs underlying depressed PD.
抑郁症是帕金森病（PD）最常见的非运动症状之一，但发病机制尚不清楚。最近，度中心度，一种基于静息态功能磁共振成像的全脑功能连接（FC）分析的体素水平，为探索抑郁 PD 的神经网络机制提供了最有希望的方法。
对 27 例未经药物治疗的早期抑郁 PD 患者、27 例非抑郁 PD 患者和 27 例健康对照者（HCs）进行度中心度、体素图像和临床症状相关性以及二次种子点 FC 分析，以揭示抑郁 PD 患者全脑 FC 的变化。
与 HCs 相比，抑郁 PD 和非抑郁 PD 患者的大脑度中心度异常主要在基底节、岛叶、运动皮质、默认模式网络、前额叶和小脑。然而，与非抑郁 PD 相比，抑郁 PD 患者的右侧额中回、前扣带回皮质、辅助运动皮质和小脑小叶 VI 度中心度异常。右侧额中回度中心度异常与临床抑郁严重程度相关，以其为种子点进行二次种子点 FC 分析进一步显示了前扣带回皮质和小脑小叶 VI 的 FC 变化。
我们的研究结果表明，广泛脑区的功能障碍参与了抑郁 PD，其中右侧额中回、前扣带回皮质和小脑可能是抑郁 PD 的发病机制枢纽。
