TY - JOUR
T1 - An exploratory analysis on gene-environment interactions for Parkinson disease
AU - Gao, Jianjun
AU - Nalls, Michael A.
AU - Shi, Min
AU - Joubert, Bonnie R.
AU - Hernandez, Dena G.
AU - Huang, Xuemei
AU - Hollenbeck, Albert
AU - Singleton, Andrew B.
AU - Chen, Honglei
N1 - Funding Information:
The authors are grateful to the continuous contribution of the NIH-AARP Diet and Health Study participants. This study was supported by the intramural research program of the National Institute of Environmental Health Sciences, National Cancer Institute, National Institute on Aging, National Institute of Neurological Disorders and Stroke, the National Human Genome Research Institute of the National Institutes of Health ( Z01–ES–101986 , Z01 CP010196–02 , Z01–AG000949–02 , NIA human subjects protocol 2003–077). This work was also supported by the US Department of Defense (award no. W81XWH–09–2–0128); National Institutes of Health (grants NS057105 and RR024992 ) and a NIH extramural grant ( R01-NS060722 ) to Dr. Huang.
PY - 2012/10
Y1 - 2012/10
N2 - Little is known about gene-environment interactions in Parkinson disease (PD). We examined potential interactions of smoking and caffeine intake with 10 genome-wide association studies single nucleotide polymorphisms (SNPs) at or near the SNCA, MAPT, LRRK2, and HLA loci among 584 PD patients and 1571 controls. The main effects of these SNPs and environmental exposures were consistent with previous reports. Family history of PD was associated with PD risk (odds ratio = 2.71, 95% confidence interval, 1.97-3.74), which was little affected by further adjustment for these SNPs and environmental exposures. Overall, we did not find significant interactions of either smoking or caffeine intake with these SNPs. However, with a combined smoking and caffeine intake exposure, we found a significant interaction with rs2896905 at SLC2A13, near LRRK2 (p uncorrected = 0.0008). Each A allele was associated with a 35% higher PD risk among never smokers with low caffeine intake, but with a 32% lower risk among smokers with high caffeine intake. This study provides preliminary evidence of a potential gene-environment interaction for PD, which should be investigated in future studies. Published by Elsevier Inc.
AB - Little is known about gene-environment interactions in Parkinson disease (PD). We examined potential interactions of smoking and caffeine intake with 10 genome-wide association studies single nucleotide polymorphisms (SNPs) at or near the SNCA, MAPT, LRRK2, and HLA loci among 584 PD patients and 1571 controls. The main effects of these SNPs and environmental exposures were consistent with previous reports. Family history of PD was associated with PD risk (odds ratio = 2.71, 95% confidence interval, 1.97-3.74), which was little affected by further adjustment for these SNPs and environmental exposures. Overall, we did not find significant interactions of either smoking or caffeine intake with these SNPs. However, with a combined smoking and caffeine intake exposure, we found a significant interaction with rs2896905 at SLC2A13, near LRRK2 (p uncorrected = 0.0008). Each A allele was associated with a 35% higher PD risk among never smokers with low caffeine intake, but with a 32% lower risk among smokers with high caffeine intake. This study provides preliminary evidence of a potential gene-environment interaction for PD, which should be investigated in future studies. Published by Elsevier Inc.
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U2 - 10.1016/j.neurobiolaging.2012.06.007
DO - 10.1016/j.neurobiolaging.2012.06.007
M3 - Article
C2 - 22763023
AN - SCOPUS:84864386591
SN - 0197-4580
VL - 33
SP - 2528.e1-2528.e6
JO - Neurobiology of Aging
JF - Neurobiology of Aging
IS - 10
ER -