Variants in Nicotinic Receptors and Risk for Nicotine Dependence
Open accessAbstract
OBJECTIVE: A recent study provisionally identified numerous genetic variants as risk factors for the transition from smoking to the development of nicotine dependence, including an amino acid change in the alpha5 nicotinic cholinergic receptor (CHRNA5). The purpose of this study was to replicate these findings in an independent data set and more thoroughly investigate the role of genetic variation in the cluster of physically linked nicotinic receptors, CHRNA5-CHRNA3-CHRNB4, and the risk of smoking. METHOD: Individuals from 219 European American families (N=2,284) were genotyped across this gene cluster to test the genetic association with smoking. The frequency of the amino acid variant (rs16969968) was studied in 995 individuals from diverse ethnic populations. In vitro studies were performed to directly test whether the amino acid variant in the CHRNA5 influences receptor function. RESULTS: A genetic variant marking an amino acid change showed association with the smoking phenotype (p=0.007). This variant is within a highly conserved region across nonhuman species, but its frequency varied across human populations (0% in African populations to 37% in European populations). Furthermore, functional studies demonstrated that the risk allele decreased response to a nicotine agonist. A second independent finding was seen at rs578776 (p=0.003), and the functional significance of this association remains unknown. CONCLUSIONS: This study confirms that at least two independent variants in this nicotinic receptor gene cluster contribute to the development of habitual smoking in some populations, and it underscores the importance of multiple genetic variants contributing to the development of common diseases in various populations.
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The CHRNA5 SNP rs16969968 increases risk of tobacco dependence by about 30% in individuals carrying one copy and more than doubles risk in those carrying two risk alleles.
“For example, a singlenucleotide polymorphism (SNP) in CHRNA5 (rs16969968), which is very common in those of European descent (minor allele frequency = 0.42), increases the risk of tobacco dependence by ∼30% in individuals carrying a single copy of the variant, and more than doubles the risk in those carrying two risk alleles (Bierut et al. 2008;Wang et al. 2009); this finding has been consistently”
From Mechanisms of Nicotine Addiction (2021) · cites this paper as Bierut et al. 2008
The Results (page unavailable) associate CHRNA5 rs16969968 with habitual versus light smoking, and the Discussion says the variant increases susceptibility to nicotine dependence. Our copy does not give the claimed risk increases of about 30% for one copy or more than twofold for two copies; a search for genotype-specific risk estimates did not find them. (LLM, conf=0.86)
Experimental — accuracy not yet measuredThe rs16969968 risk variant is associated with heavy smoking, early onset of smoking behavior, and a pleasurable buzz from tobacco.
“The rs16969968 risk variant is associated with heavy smoking (Berrettini et al. 2008;Bierut et al. 2008;Grucza et al. 2008;Stevens et al. 2008), early onset of smoking behavior (Weiss et al. 2008), and with a”
From Mechanisms of Nicotine Addiction (2021) · cites this paper as Bierut et al. 2008
The association with rs16969968 has been replicated either directly or using highly correlated SNPs by several groups.
“This association has been replicated either directly or using highly correlated SNPs by several groups (92–97).”
From Nicotine is a selective pharmacological chaperone of acetylcholine receptor number and stoichiometry. Implications for drug discovery (2009) · cites this paper as [93]
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- Authors
- Bierut, L. J., Stitzel, J. A., Wang, J. C., Hinrichs, A. L., Grucza, R. A., Xuei, X., Saccone, N. L., Saccone, S. F., Bertelsen, S., Fox, L., Horton, W. J., Breslau, N., Budde, J., Cloninger, C. R., Dick, D. M., Foroud, T., Hatsukami, D., Hesselbrock, V., Johnson, E. O., Kramer, J., Kuperman, S., Madden, P. A. F., Mayo, K., Nurnberger, J., Pomerleau, O., Porjesz, B., Reyes, O., Schuckit, M., Swan, G., Tischfield, J. A., Edenberg, H. J., Rice, J. P., & Goate, A. M.
- Affiliations
- Washington University in St. Louis (US)
- ORCID
- Bierut, Laura Jean
- Stitzel, Jerry A.
- Wang, Jen C.
- Grucza, Richard A.
- Xuei, Xiaoling
- Saccone, Nancy L.
- Bertelsen, Sarah
- Fox, Louis
- Horton, William J.
- Budde, John
- Cloninger, C. Robert
- Dick, Danielle M.
- Foroud, Tatiana
- Hatsukami, Dorothy
- Hesselbrock, Victor
- Johnson, Eric O.
- Kramer, John
- Madden, Pamela A.F.
- Pomerleau, Ovide
- Reyes, Oliver
- Schuckit, Marc
- Swan, Gary
- Tischfield, Jay A.
- Edenberg, Howard J.
- Rice, John P.
- Goate, Alison M.
- Venue
- American Journal of Psychiatry
- Published
- 2008-09
- Volume
- 165
- Issue
- 9
- Pages
- 1163-1171
- ISSN
- 0002-953X (ISSN-L)
- 1535-7228
- PMC
- PMC2574742
- OpenAlex
- W2128306943
- Cited by
- 648
- References
- 45
- Citations by year
- 2026: 8 · 2025: 7 · 2024: 19 · 2023: 20 · 2022: 21 · 2021: 22 · 2020: 33 · 2019: 32 · 2018: 35 · 2017: 37 · 2016: 41 · 2015: 54 · 2014: 49 · 2013: 52 · 2012: 52
- FWCI
- 37.02
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- IUScholarWorks (Indiana University) (submittedVersion)
- SUNY Digital Repository Support (State University of New York System) (submittedVersion, cc-by-nc-nd)
- Funders
- State University of New York
- Washington University in St. Louis
- University of Connecticut
- National Institutes of Health
- SUNY Downstate Medical Center
- National Institute on Alcohol Abuse and Alcoholism (K01AA015572, U10AA008401)
- National Institute on Drug Abuse (K01 DA021237, R01DA002854, R01DA014369, K01DA015129, K02DA021237, K01DA016618, R01DA012854, R01 DA16618, R01 DA02854)
- National Cancer Institute (P01CA089392, P01 CA89392)
- Topics
- Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- nicotine dependence, nicotinic acetylcholine receptors, CHRNA5, CHRNA3, CHRNB4, rs16969968, smoking, genetic association, gene clusters, European American families
- MeSH terms
- Cell Line, Genotype, Humans, Nerve Tissue Proteins, Phenotype, Receptors, Nicotinic, Risk Factors, Species Specificity, Tobacco Use Disorder, Linkage Disequilibrium, Polymerase Chain Reaction, DNA Primers, Polymorphism, Single Nucleotide
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