Petersburg Nuclear Physics Institute named by B.P. Konstantinov of National Research Centre, «Kurchatov Institute», Gatchina, Russia; Pavlov First Saint Petersburg State Medical University, Saint-Petersburg, Russia.
Petersburg Nuclear Physics Institute named by B.P. Konstantinov of National Research Centre, «Kurchatov Institute», Gatchina, Russia; Pavlov First Saint Petersburg State Medical University, Saint-Petersburg, Russia.
J Clin Neurosci. 2020 Aug;78:323-326. doi: 10.1016/j.jocn.2020.04.058. Epub 2020 Apr 23.
Immune response may play a pivotal role in the pathogenesis of the common synucleinopathy as Parkinson's disease (PD) and could be mediated with the accumulation of neurotoxic alpha-synuclein. There is limited evidence for immune response in another synucleinopathy as dementia with Lewy bodies (DLB). Recent data suggest that immune response may contribute to cognitive impairment. We aimed to estimate plasma cytokine profile in patients with synucleinopathies with dementia (PD dementia (PDD), DLB). Plasma cytokine levels (interferon-gamma (IFN-gamma), interleukin (IL)-4 (IL-4), IL-6, IL-10, tumor necrosis factor alpha (TNF-alpha), monocyte chemoattractant protein-1 (MCP-1)). were estimated in 16 patients with DLB, 19 patients with PDD, 28 patients with PD without dementia (PD) and 19 individuals without neurological disorders (controls) using Luminex array system. Cognitive status was assessed with the Mini-Mental State Examination (MMSE). TNF-alpha and IL-6 plasma levels were elevated in patients with synucleinopathies with dementia (DLB, PDD) compared to controls and IL-10 plasma level was increased in PDD compared to controls (p < 0.05). IFN-gamma levels were decreased in PD and PDD patients compared to controls (p < 0.001, p = 0.026, respectively) and in PD patients than in DLB patients (p = 0.032). Patients with PD, PDD, and DLB were characterized by increased plasma levels of MCP-1 compared to controls (p < 0.001). At the same time, no differences in TNF-alpha, IL-10, IL-6 plasma levels in PD patients compared to controls were found. Our study demonstrated more pronounced immune response in synucleinopathies associated with dementia compared to PD without demetia.
免疫反应可能在常见的突触核蛋白病(如帕金森病 (PD))的发病机制中起关键作用,并可能通过神经毒性α-突触核蛋白的积累来介导。在另一种突触核蛋白病——路易体痴呆 (DLB) 中,免疫反应的证据有限。最近的数据表明,免疫反应可能导致认知障碍。我们旨在评估伴有痴呆的突触核蛋白病(帕金森病伴痴呆 (PDD)、DLB)患者的血浆细胞因子谱。使用 Luminex 阵列系统,我们在 16 名 DLB 患者、19 名 PDD 患者、28 名无痴呆的 PD 患者(PD)和 19 名无神经障碍的个体(对照组)中评估了血浆细胞因子水平(干扰素-γ (IFN-γ)、白细胞介素 (IL)-4 (IL-4)、IL-6、IL-10、肿瘤坏死因子-α (TNF-α)、单核细胞趋化蛋白-1 (MCP-1))。认知状态采用简易精神状态检查 (MMSE) 进行评估。与对照组相比,伴有痴呆的突触核蛋白病(DLB、PDD)患者的 TNF-α 和 IL-6 血浆水平升高,而与对照组相比,PDD 患者的 IL-10 血浆水平升高(p < 0.05)。与对照组相比,PD 和 PDD 患者的 IFN-γ 水平降低(p < 0.001,p = 0.026),PD 患者比 DLB 患者降低(p = 0.032)。与对照组相比,PD、PDD 和 DLB 患者的 MCP-1 血浆水平升高(p < 0.001)。与此同时,我们未发现 PD 患者与对照组相比,TNF-α、IL-10、IL-6 血浆水平存在差异。我们的研究表明,与无痴呆的 PD 相比,与痴呆相关的突触核蛋白病中存在更为明显的免疫反应。