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Inflammation has been demonstrated to be involved in Parkinson's disease (PD) pathogenesis. There were evidences that the disturbance of the protective function of IL-10 gene contributed to PD. In our study, haplotype analyses were conducted of IL-10 rs1800871 and rs1800872 on 371 PD patients. Because the two SNPs exposed significant linkage disequilibrium demonstrated by Haploview software, we included 177 carriers of both rs1800871 and rs1800872 and 190 noncarriers in clinical phenotype analyses. As to nonmotor symptoms, the score of the gastrointestinal dysfunction domain in Nonmotor Symptom Scale (NMSS) was lower in the carrier group of both SNPs than in the noncarrier group in PD patients (SC: −0.198, p:0.023). Other nonmotor symptoms reflected by relevant rating scales showed negative results. As to comorbidity, no significant statistical significance was observed between the two SNPs and Charlson Comorbidity Index (CCI). In conclusion, we found less severe gastrointestinal dysfunctions of both IL-10 rs1800871 and rs1800872 carriers than noncarriers in PD. [ABSTRACT FROM AUTHOR]

SNCA-rs11931074 had been demonstrated to be strongly correlated with PD risk. However, there was lack of comprehensive analysis of SNCA-rs11931074-related clinical features which may help explain clinical heterogeneity of PD. In our study, we performed association analyses on the relationship between SNCA-rs11931074 and motor symptoms, nonmotor symptoms, and comorbidities in PD. 611 rs11931074 carriers and 113 rs11931074 noncarriers were enrolled. In the clinical phenotype analyses, the Unified Parkinson's Disease Rating Scale part II (UPDRS II) and part III (UPDRS III) scores of rs11931074 carriers were lower than those of noncarriers (SC: −0.083, p=0.035; SC: −0.140, p≤0.001). The Charlson Comorbidity Index (CCI) score of carriers was lower than that of noncarriers (SC: −0.097, p=0.009). No significant statistical differences were found between the variant and other clinical features such as motor complications and nonmotor symptoms. The SNCA-rs11931074 carriers may present with more benign clinical profiles than noncarriers with less severe motor symptoms and comorbidity burden. [ABSTRACT FROM AUTHOR]

Background. GBA gene had been proved to be a crucial gene to the risk of PD. Numerous studies had discussed about the unique clinical characteristics of PD patients with GBA carriers (GBA + PD). However, there was lack of updated comprehensive analysis on the topic. In order to clarify the association between GBA variants and the clinical phenotypes of PD, we conducted this comprehensive meta-analysis. Method. Medline, Embase, and Cochrane were used to perform the searching. Strict selection criteria were followed in screening for new published articles or data. Revman 5.3 software was applied to perform the total statistical analysis, and funnel plots in the software were used to assess the publication biases. Results. A total of 26 articles including 931 GBA + PD and 14861 GBA noncarriers of PD (GBA − PD) were involved in the final meta-analysis, and 14 of them were either newly added publications or related data newly analyzed compared with the version published in 2015. Then, a series of symptoms containing depression, orthostatic hypotension, motor fluctuation, wearing-off, and freezing were newly analyzed due to more articles eligible. Besides, clinical features like family history, AAO, UPDRS-III, H-Y, and dementia previously analyzed were updated with new data added. Significant statistical differences were found in wearing-off, family history, AAO, UPDRS-III, and dementia (OR: 1.14, 1.65; MD: −3.61, 2.17; OR: 2.44; p: 0.03, <0.00001, <0.00001, 0.003, and <0.00001). Depression was slightly associated with GBA + PD (OR: 1.47; p: 0.04). Clinical symptoms such as H-Y, orthostatic hypotension, motor fluctuation, and freezing did not feature GBA + PD. Conclusion. Our results demonstrated that there were unique clinical features in GBA + PD which can help the management of the whole duration of PD patients. [ABSTRACT FROM AUTHOR]