ReviewMolecular psychiatry2012
The CHRNA5-A3-B4 gene cluster in nicotine addiction.
Review in Molecular psychiatry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 3 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
54 citing papers in PubMed, 3 syntheses or guidelines pooled it, 99 citations in OpenAlex.
- The role of nicotinic receptors in alcohol consumption.Pharmacological research · 2023Pooled it
- A systematic review of genetic variation within nicotinic acetylcholine receptor genes and cigarette smoking cessation.Drug and alcohol dependence · 2022Pooled it
- Genome-wide association study of smoking trajectory and meta-analysis of smoking status in 842,000 individuals.Nature communications · 2020Pooled it
- Association of CHRNA5-A3-B4 SNP rs2036527 with smoking cessation therapy response in African-American smokers.Clinical pharmacology and therapeutics · 2014Trial
- Rare coding variants in CHRNB3 associate with reduced daily cigarette smoking across ancestries.Nature communications · 2026Article
- The influence of CHRNA5 and D398N missense variation on social and emotional behaviors in rodents and humans.Translational psychiatry · 2025Article
- Multiomic Mendelian randomization analysis of metabolic gene methylation expression and protein levels in lung adenocarcinoma.Discover oncology · 2025Article
- CHRNA5-A3-B4, CYP2A6, and DBH Genetic Associations With Smoking Cessation Throughout Adulthood Within Two Longitudinal Studies of Women.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2025Article
- The association of genetic polymorphisms within the dopaminergic system with nicotine dependence: A narrative review.Heliyon · 2024Review
- An in-depth association analysis of genetic variants within nicotine-related loci: Meeting in middle of GWAS and genetic fine-mapping.Molecular and cellular neurosciences · 2023Article
- Biochemical and genetic biomarkers associated with nicotine dependence in Mexican smokers.Pharmacology research & perspectives · 2023Article
- Rare coding variants in CHRNB2 reduce the likelihood of smoking.Nature genetics · 2023Article
- CHRNA5-A3-B4 and DRD2 Genes and Smoking Cessation Throughout Adulthood: A Longitudinal Study of Women.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2023Article
- Genetic Associations with Smoking Relapse and Proportion of Follow-up in Smoking Relapse throughout Adulthood in Pre- and Postmenopausal Women.Cancer prevention research (Philadelphia, Pa.) · 2023Article
- Evaluating the causal effect of tobacco smoking on white matter brain aging: a two-sample Mendelian randomization analysis in UK Biobank.Addiction (Abingdon, England) · 2023Article
- FOXN3 and GDNF Polymorphisms as Common Genetic Factors of Substance Use and Addictive Behaviors.Journal of personalized medicine · 2022Article
- The Intergenerational Transmission of Developmental Nicotine Exposure-Induced Neurodevelopmental Disorder-Like Phenotypes is Modulated by the Chrna5 D397N Polymorphism in Adolescent Mice.Behavior genetics · 2021Article
- Epigenome-wide association study of whole blood gene expression in Framingham Heart Study participants provides molecular insight into the potential role of CHRNA5 in cigarette smoking-related lung diseases.Clinical epigenetics · 2021Article
- The α5 Nicotinic Acetylcholine Receptor Subunit Differentially Modulates α4β2Frontiers in synaptic neuroscience · 2020Review
- Differences in mechanisms underlying reinstatement of cigarette smoke extract- and nicotine-seeking behavior in rats.Neuropharmacology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Nicotine addiction (NA) is a common and devastating disease, such that the annual number of deaths (world-wide) from tobacco-related diseases will double from 5 million in the year 2000 to 10 million in 2020. Nicotine is the only substance in tobacco which animals and humans will self-administer. NA, as a lifetime diagnosis, has been assessed in various approaches, including the concept of cigarettes per day (CPD). Other assessments of NA are somewhat more comprehensive, such as the Fagerstrom Test for Nicotine Dependence or the American Psychiatric Association's Diagnostic and Statistical Manual (fourth edition) diagnosis of nicotine dependence. These different measures have moderate agreement with one another. Twin, family and adoption studies have shown that these different assessments of NA have substantial heritability (that fraction of risk attributable to genetic factors). The heritability of NA has been estimated at 50-75%, depending on the definition and the population under study. DNA-based studies of NA have been somewhat successful in identifying a common haplotype, which increases risk for NA among European-origin populations. This haplotype explains a small amount of variance, accounting for ∼1 CPD, and it includes the α5 and the α3 nicotinic receptor subunit genes (CHRNA5 and CHRNA3). The review will focus on this implicated region. In this risk region, there is a common (among European-origin people) mis-sense single-nucleotide polymorphism in the CHRNA5 gene (D398N), which changes a conserved amino acid from aspartic acid to asparagine. The risk allele (398N) confers decreased calcium permeability and more extensive desensitization, according to in vitro cellular studies, raising the possibility that a positive allosteric modulator of the (α4β2)(2)α5 type of nicotinic receptor might have therapeutic potential in NA. There are other genetic influences on NA in this region, apart from the mis-sense variant, and additional biological experiments must be done to understand them.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.