An exploratory analysis on gene-environment interactions for Parkinson disease.

Jianjun Gao, Michael A. Nalls, Min Shi, Bonnie R. Joubert, Dena G. Hernandez, Xuemei Huang, Albert Hollenbeck, Andrew B. Singleton, Honglei Chen

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
JournalNeurobiology of Aging
Volume33
Issue number10
StatePublished - Oct 1 2012

Fingerprint

Gene-Environment Interaction
Parkinson Disease
Caffeine
Single Nucleotide Polymorphism
Smoking
Environmental Exposure
Odds Ratio
Genome-Wide Association Study
Alleles
Confidence Intervals

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Aging
  • Clinical Neurology
  • Developmental Biology
  • Geriatrics and Gerontology

Cite this

Gao, J., Nalls, M. A., Shi, M., Joubert, B. R., Hernandez, D. G., Huang, X., ... Chen, H. (2012). An exploratory analysis on gene-environment interactions for Parkinson disease. Neurobiology of Aging, 33(10).
Gao, Jianjun ; Nalls, Michael A. ; Shi, Min ; Joubert, Bonnie R. ; Hernandez, Dena G. ; Huang, Xuemei ; Hollenbeck, Albert ; Singleton, Andrew B. ; Chen, Honglei. / An exploratory analysis on gene-environment interactions for Parkinson disease. In: Neurobiology of Aging. 2012 ; Vol. 33, No. 10.
@article{9c124e5fa5ba4402b20cd08973a6589a,
title = "An exploratory analysis on gene-environment interactions for Parkinson disease.",
abstract = "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.",
author = "Jianjun Gao and Nalls, {Michael A.} and Min Shi and Joubert, {Bonnie R.} and Hernandez, {Dena G.} and Xuemei Huang and Albert Hollenbeck and Singleton, {Andrew B.} and Honglei Chen",
year = "2012",
month = "10",
day = "1",
language = "English (US)",
volume = "33",
journal = "Neurobiology of Aging",
issn = "0197-4580",
publisher = "Elsevier Inc.",
number = "10",

}

Gao, J, Nalls, MA, Shi, M, Joubert, BR, Hernandez, DG, Huang, X, Hollenbeck, A, Singleton, AB & Chen, H 2012, 'An exploratory analysis on gene-environment interactions for Parkinson disease.', Neurobiology of Aging, vol. 33, no. 10.

An exploratory analysis on gene-environment interactions for Parkinson disease. / Gao, Jianjun; Nalls, Michael A.; Shi, Min; Joubert, Bonnie R.; Hernandez, Dena G.; Huang, Xuemei; Hollenbeck, Albert; Singleton, Andrew B.; Chen, Honglei.

In: Neurobiology of Aging, Vol. 33, No. 10, 01.10.2012.

Research output: Contribution to journalArticle

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

PY - 2012/10/1

Y1 - 2012/10/1

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.

UR - http://www.scopus.com/inward/record.url?scp=84872680273&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84872680273&partnerID=8YFLogxK

M3 - Article

C2 - 22763023

VL - 33

JO - Neurobiology of Aging

JF - Neurobiology of Aging

SN - 0197-4580

IS - 10

ER -

Gao J, Nalls MA, Shi M, Joubert BR, Hernandez DG, Huang X et al. An exploratory analysis on gene-environment interactions for Parkinson disease. Neurobiology of Aging. 2012 Oct 1;33(10).