Polymorphisms in immune/inflammatory cytokine genes are related to Parkinson's disease with cognitive impairment in the Han Chinese population

Abstract

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.