Introduction. Systemic inflammation with elevated oxidative stress causing neuroinflammation is considered a major factor in the pathogenesis of Parkinson’s disease (PD). The interface between systemic circulation and the brain parenchyma is the blood-brain barrier (BBB), which also plays a role in maintaining neurovascular homeostasis. Vascular cell adhesion molecule-1 (VCAM-1) and microRNAs (miRNAs) regulate brain vessel endothelial function, neoangiogenesis, and, in turn, neuronal homeostasis regulation, such that their dysregulation can result in neurodegeneration, such as gray matter atrophy, in PD. Objective. Our aim was to evaluate the associations among specific levels of gray matter atrophy, peripheral vascular adhesion molecules, miRNAs, and clinical disease severity in order to achieve a clearer understanding of PD pathogenesis. Methods. Blood samples were collected from 33 patients with PD and 27 healthy volunteers, and the levels of VCAM-1 and several miRNAs in those samples were measured. Voxel-based morphometry (VBM) analysis was performed using 3 T magnetic resonance imaging (MRI) and SPM (Statistical Parametric Mapping software program). The associations among the vascular parameter, miRNAs, gray matter volume, and clinical disease severity measurements were evaluated by partial correlation analysis. Results. The levels of VCAM-1, miRNA-22, and miRNA-29a expression were significantly elevated in the PD patients. The gray matter volume atrophy in the left parahippocampus, bilateral posterior cingulate gyrus, fusiform gyrus, left temporal gyrus, and cerebellum was significantly correlated with increased clinical disease severity, the upregulation of miRNA levels, and increased vascular inflammation. Conclusion. Patients with PD seem to have abnormal levels of vascular inflammatory markers and miRNAs in the peripheral circulation, and these levels are correlated with specific brain volume changes. This study reinforces the associations among peripheral inflammation, the BBB interface, and gray matter atrophy in PD and further demonstrates that BBB dysfunction with neurovascular impairment may play an important role in PD progression.

中文翻译：

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血管炎症是与帕金森病脑萎缩和疾病严重程度相关的危险因素：病例对照研究。

简介。全身性炎症伴随着升高的氧化应激导致神经炎症被认为是帕金森病 (PD) 发病机制的主要因素。体循环和脑实质之间的界面是血脑屏障（BBB），它在维持神经血管稳态方面也发挥着作用。血管细胞粘附分子-1 (VCAM-1) 和 microRNA (miRNA) 调节脑血管内皮功能、新血管生成，进而调节神经元稳态，因此它们的失调可导致 PD 中的神经退行性变，例如灰质萎缩. 客观的. 我们的目的是评估特定水平的灰质萎缩、外周血管粘附分子、miRNA 和临床疾病严重程度之间的关联，以便更清楚地了解 PD 发病机制。方法。采集了 33 名 PD 患者和 27 名健康志愿者的血液样本，并测量了这些样本中 VCAM-1 和几种 miRNA 的水平。使用 3 T 磁共振成像 (MRI) 和 SPM (统计参数映射软件程序) 进行基于体素的形态测量 (VBM) 分析。通过偏相关分析评估血管参数、miRNA、灰质体积和临床疾病严重程度测量之间的关联。结果. PD患者的VCAM-1、miRNA-22和miRNA-29a表达水平显着升高。左侧海马旁、双侧后扣带回、梭状回、左侧颞回和小脑的灰质体积萎缩与临床疾病严重程度增加、miRNA 水平上调和血管炎症增加显着相关。结论. PD 患者的外周循环中血管炎症标志物和 miRNA 的水平似乎异常，这些水平与特定的脑容量变化相关。本研究强化了 PD 中外周炎症、BBB 界面和灰质萎缩之间的关联，并进一步证明 BBB 功能障碍伴神经血管损伤可能在 PD 进展中起重要作用。