Abstract
BackgroundEpidemiological studies showed that higher plasma urate was associated with lower risk for Parkinson’s disease (PD) and slower disease progression. Recent genome-wide association studies (GWAS) consistently showed that several single nucleotide polymorphisms (SNPs) in the solute carrier family 2 member 9 gene (SLC2A9 ) were associated with plasma urate concentration and the risk of gout.MethodsWe conducted a case–control study to examine twelve tag SNPs of the SLC2A9 gene in relation to PD among 788 cases and 911 controls of European ancestry. Odds ratios (OR) and 95% confidence intervals (CI) were derived from logistic regression models, adjusting for age, sex, smoking and caffeine consumption.ResultsThese SNPs were all in linkage disequilibrium (R2 > 0.7). None of them were associated with PD risk. Among women, however, there was a suggestion that the presence of the minor allele of one SNP (rs7442295) was related to a small increase in PD risk [OR (95% CI) = 1.48 (1.01-2.16)].ConclusionThis study provides little support for genetic variations of SLC2A9 and PD risk.
Highlights
Epidemiological studies showed that higher plasma urate was associated with lower risk for Parkinson’s disease (PD) and slower disease progression
The nature of this association is debatable as one may argue that the association is due to reverse causation that lower plasma urate is secondary to the underlying PD pathogenesis
By examining the association of urate related genetic alleles with PD, we may have an unbiased assessment of urate in relation to PD risk to the extent that these genetic alleles affect plasma urate, a concept called “Mendelian randomization” [4]
Summary
We conducted a case–control study to examine twelve tag SNPs of the SLC2A9 gene in relation to PD among 788 cases and 911 controls of European ancestry. We first identified self-reported PD cases from a large population-based cohort – the NIH-AARP Diet and Health Study. Controls were randomly selected from participants of the same cohort who did not report a PD diagnosis and they were frequency matched to cases by sex, ethnicity, and year of birth. Both cases and controls were from the same base population and no additional exclusion criteria were applied. The current analysis was limited to 788 cases and 911 controls who self-reported as non-Hispanic Whites
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