Department of Neurology, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangdong Neuroscience Institute, 106 Zhongshan Er Road, Guangzhou 510080, China.
Neurosci Lett. 2013 Apr 29;541:111-5. doi: 10.1016/j.neulet.2013.02.024. Epub 2013 Feb 26.
Increasing evidence suggests that immune mediated inflammation contributes to the pathogenesis of Parkinson's disease (PD). However, whether genetic variants of genes coding for inflammatory cytokines influence the risk of cognitive impairment in PD is still unknown. In the present study, we examined whether interleukin-10 (IL-10, 1082G/A), interleukin-17A (IL-17A) rs8193036, rs2275913 and interferon-γ (IFN-γ) polymorphisms were associated with the risk of cognitive impairment in PD. The four gene polymorphisms were analyzed in 302 PD patients and results were compared to those obtained from 294 age- and gender-matched healthy controls (HC) enrolled from the Han Chinese population. PD patients were divided into two subgroups on the basis of mini mental state examination (MMSE) score: PD with cognitive impairment (MMSE scores<26) and PD without cognitive impairment (MMSE scores≥26). There was no significant difference in the distributions of genotype or allele between PD and control groups in the total population. However, the distribution of the rs8193036 (CC genotype, C allele) in PD individuals with an MMSE score<26 was significantly increased when compared to PD patients with an MMSE score≥26 (CC genotype: p=0.044; C allele: p=0.038). Also, there were significant differences in genotype and frequencies of the 1082G/A allele between PD cases with an MMSE score<26 and controls (genotype p=0.021; allele p=0.024). Logistic regression analysis showed that the 1082G/A (AA) genotype decreased (Odds ratio=0.440, p=0.042), while the rs8193036 (CC) genotype increased the risk of cognitive impairment in PD (OR=1.838, p=0.048). Based on our study, polymorphisms in immune/inflammatory-related genes such as IL-17A rs8193036 and IL-10 1082G/A might be correlated with the risk of PD with cognitive impairment in the Han Chinese population.
越来越多的证据表明,免疫介导的炎症导致帕金森病 (PD) 的发病机制。然而,编码炎症细胞因子的基因的遗传变异是否影响 PD 认知障碍的风险仍不清楚。在本研究中,我们研究了白细胞介素 10 (IL-10,1082G/A)、白细胞介素 17A (IL-17A) rs8193036、rs2275913 和干扰素-γ (IFN-γ) 多态性是否与 PD 认知障碍的风险相关。对 302 例 PD 患者和 294 名年龄和性别匹配的汉族健康对照者 (HC) 的四个基因多态性进行了分析。根据 mini mental state examination (MMSE) 评分,将 PD 患者分为两个亚组: MMSE 评分<26 的 PD 伴认知障碍和 MMSE 评分≥26 的 PD 无认知障碍。在总人群中,PD 组和对照组之间基因型或等位基因的分布无显著性差异。然而,与 MMSE 评分≥26 的 PD 患者相比,MMSE 评分<26 的 PD 患者 rs8193036 (CC 基因型,C 等位基因)的分布显著增加 (CC 基因型:p=0.044; C 等位基因:p=0.038)。此外,在 MMSE 评分<26 的 PD 病例与对照组之间,1082G/A 等位基因的基因型和频率存在显著差异 (基因型:p=0.021; 等位基因:p=0.024)。Logistic 回归分析显示,1082G/A (AA) 基因型降低 (比值比=0.440,p=0.042),而 rs8193036 (CC) 基因型增加 PD 认知障碍的风险 (OR=1.838,p=0.048)。基于我们的研究,免疫/炎症相关基因如 IL-17A rs8193036 和 IL-10 1082G/A 的多态性可能与汉族人群 PD 伴认知障碍的风险相关。