Highlights
- •The study population had high lifetime ultraviolet radiation (UVR) exposure.
- •Increasing UVR exposure was not inversely associated with Parkinson's disease risk.
- •Homozygotes for rs731236 (TaqI) TT (major allele) genotype had 31% lower PD risk.
- •rs7975232 (ApaI) GG (minor allele) genotype was associated with 27% lower PD risk.
- •Vitamin D receptor gene polymorphisms may modulate risk under high UVR conditions.
Abstract
Introduction
A high prevalence of vitamin D deficiency has been reported in Parkinson's disease
(PD). Epidemiologic studies examining variability in genes involved in vitamin D metabolism
have not taken into account level of exposure to ultraviolet radiation (UVR). We examined
whether exposure to UVR (as a surrogate for vitamin D levels) and variations in the
vitamin D receptor gene (VDR) are associated with PD.
Methods
Within a geographical information system (GIS) we linked participants' geocoded residential
address data to ground level UV data to estimate historical exposure to UVR. Six SNPs
in VDR were genotyped in non-Hispanic Caucasian subjects.
Results
Average lifetime UVR exposure levels were >5000 Wh/m2, which was higher than levels for populations in previous studies, and UVR exposure
did not differ between cases and controls. Homozygotes for the rs731236 TT (major
allele) genotype had a 31% lower risk of PD risk (OR = 0.69; 95% CI = 0.49, 0.98; p = 0.04 for TT vs. TC + CC). The rs7975232 GG (minor allele) genotype was also associated with decreased risk
of PD (OR = 0.63; 95% CI = 0.42, 0.93; p = 0.02 for GG vs. TG + TT). The association between PD risk and a third locus, rs1544410 (BsmI), was not
statistically significant after adjustment for covariates, although there was a trend
for lower risk with the GG genotype.
Conclusions
This study provides initial evidence that VDR polymorphisms may modulate risk of PD in a population highly exposed to UVR throughout
lifetime.
Keywords
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Article info
Publication history
Published online: April 06, 2015
Accepted:
March 25,
2015
Received in revised form:
March 21,
2015
Received:
October 14,
2014
Identification
Copyright
© 2015 Published by Elsevier Inc.