An exploratory study on the CHRNA3-CHRNA5-CHRNB4 cluster, smoking, and Parkinson's disease

Jianjun Gao, Hong Xu, Clarice Weinberg, Xuemei Huang, Yikyung Park, Albert Hollenbeck, Aaron Blair, Arthur Schatzkin, Lauranell Burch, Honglei Chen

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Background: Smokers have a lower risk of Parkinson's disease (PD). Recent genome-wide association studies (GWAS) have consistently linked several single nucleotide polymorphisms (SNPs) in the CHRNA3-CHRNA5-CHRNB4 cluster on chromosome 15.q25 to smoking behaviors and nicotine dependence. Investigations into these SNPs may help explain the nature and mechanisms of the smoking-PD relationship. Objective: To examine whether the genetic variations that were consistently associated with smoking or nicotine dependence in recent GWAS also predict the risk of PD. Methods: This is a population-based case-control study of 788 physician-diagnosed PD patients and 911 controls, all non-Hispanic Whites. Seven SNPs were selected based on findings from recent GWAS on smoking and nicotine dependence, all from the nicotinic acetylcholine receptor subunits (CHRN) A3-A5-B4. Odds ratios (ORs) and 95% confidence intervals were derived from logistic regression models under the assumption of logit-additive allelic effects. Results: Four SNPs in linkage disequilibrium from the CHRNA3-CHRNA5-CHRNB4 cluster were associated with smoking duration (OR >1.3, p < 0.05). However, none of the SNPs from this cluster was associated with PD risk in the overall analysis or after stratifying on smoking status. Conclusion: This preliminary analysis does not support a relationship between these smoking-related GWAS SNPs and PD.

Original languageEnglish (US)
Pages (from-to)296-299
Number of pages4
JournalNeurodegenerative Diseases
Volume8
Issue number5
DOIs
StatePublished - Jun 1 2011

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Parkinson Disease
Single Nucleotide Polymorphism
Smoking
Genome-Wide Association Study
Tobacco Use Disorder
Logistic Models
Odds Ratio
Chromosomes, Human, Pair 15
Linkage Disequilibrium
Nicotinic Receptors
Case-Control Studies
Confidence Intervals
Physicians
Population

All Science Journal Classification (ASJC) codes

  • Neurology
  • Clinical Neurology

Cite this

Gao, Jianjun ; Xu, Hong ; Weinberg, Clarice ; Huang, Xuemei ; Park, Yikyung ; Hollenbeck, Albert ; Blair, Aaron ; Schatzkin, Arthur ; Burch, Lauranell ; Chen, Honglei. / An exploratory study on the CHRNA3-CHRNA5-CHRNB4 cluster, smoking, and Parkinson's disease. In: Neurodegenerative Diseases. 2011 ; Vol. 8, No. 5. pp. 296-299.
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Gao, J, Xu, H, Weinberg, C, Huang, X, Park, Y, Hollenbeck, A, Blair, A, Schatzkin, A, Burch, L & Chen, H 2011, 'An exploratory study on the CHRNA3-CHRNA5-CHRNB4 cluster, smoking, and Parkinson's disease', Neurodegenerative Diseases, vol. 8, no. 5, pp. 296-299. https://doi.org/10.1159/000323190

An exploratory study on the CHRNA3-CHRNA5-CHRNB4 cluster, smoking, and Parkinson's disease. / Gao, Jianjun; Xu, Hong; Weinberg, Clarice; Huang, Xuemei; Park, Yikyung; Hollenbeck, Albert; Blair, Aaron; Schatzkin, Arthur; Burch, Lauranell; Chen, Honglei.

In: Neurodegenerative Diseases, Vol. 8, No. 5, 01.06.2011, p. 296-299.

Research output: Contribution to journalArticle

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AU - Gao, Jianjun

AU - Xu, Hong

AU - Weinberg, Clarice

AU - Huang, Xuemei

AU - Park, Yikyung

AU - Hollenbeck, Albert

AU - Blair, Aaron

AU - Schatzkin, Arthur

AU - Burch, Lauranell

AU - Chen, Honglei

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N2 - Background: Smokers have a lower risk of Parkinson's disease (PD). Recent genome-wide association studies (GWAS) have consistently linked several single nucleotide polymorphisms (SNPs) in the CHRNA3-CHRNA5-CHRNB4 cluster on chromosome 15.q25 to smoking behaviors and nicotine dependence. Investigations into these SNPs may help explain the nature and mechanisms of the smoking-PD relationship. Objective: To examine whether the genetic variations that were consistently associated with smoking or nicotine dependence in recent GWAS also predict the risk of PD. Methods: This is a population-based case-control study of 788 physician-diagnosed PD patients and 911 controls, all non-Hispanic Whites. Seven SNPs were selected based on findings from recent GWAS on smoking and nicotine dependence, all from the nicotinic acetylcholine receptor subunits (CHRN) A3-A5-B4. Odds ratios (ORs) and 95% confidence intervals were derived from logistic regression models under the assumption of logit-additive allelic effects. Results: Four SNPs in linkage disequilibrium from the CHRNA3-CHRNA5-CHRNB4 cluster were associated with smoking duration (OR >1.3, p < 0.05). However, none of the SNPs from this cluster was associated with PD risk in the overall analysis or after stratifying on smoking status. Conclusion: This preliminary analysis does not support a relationship between these smoking-related GWAS SNPs and PD.

AB - Background: Smokers have a lower risk of Parkinson's disease (PD). Recent genome-wide association studies (GWAS) have consistently linked several single nucleotide polymorphisms (SNPs) in the CHRNA3-CHRNA5-CHRNB4 cluster on chromosome 15.q25 to smoking behaviors and nicotine dependence. Investigations into these SNPs may help explain the nature and mechanisms of the smoking-PD relationship. Objective: To examine whether the genetic variations that were consistently associated with smoking or nicotine dependence in recent GWAS also predict the risk of PD. Methods: This is a population-based case-control study of 788 physician-diagnosed PD patients and 911 controls, all non-Hispanic Whites. Seven SNPs were selected based on findings from recent GWAS on smoking and nicotine dependence, all from the nicotinic acetylcholine receptor subunits (CHRN) A3-A5-B4. Odds ratios (ORs) and 95% confidence intervals were derived from logistic regression models under the assumption of logit-additive allelic effects. Results: Four SNPs in linkage disequilibrium from the CHRNA3-CHRNA5-CHRNB4 cluster were associated with smoking duration (OR >1.3, p < 0.05). However, none of the SNPs from this cluster was associated with PD risk in the overall analysis or after stratifying on smoking status. Conclusion: This preliminary analysis does not support a relationship between these smoking-related GWAS SNPs and PD.

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