Evidence map›Paper›PMID 21968931›Full record

ReviewMolecular psychiatry2012

The CHRNA5-A3-B4 gene cluster in nicotine addiction.

W H Berrettini, G A Doyle

Abstract readReview
PubMed Publisher
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 3 pooled it
2.7field-weighted citation impact, top 10% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

54 citing papers in PubMed, 3 syntheses or guidelines pooled it, 99 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
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  7. Article
  8. 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 · 2025
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. 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 · 2023
    Article
  14. Article
  15. Article
  16. Article
  17. Article
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  19. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

W H BerrettiniDepartment of Psychiatry, Center for Neurobiology and Behavior, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA. wadeb@mail.med.upenn.edu
G A Doyle
University of Pennsylvania · US

Funding

TREATMENT STRATEGIES FOR METHODONE NONRESPONDERSP60DA005186 · NIDA · UNIVERSITY OF PENNSYLVANIA · PI O'BRIEN, CHARLES P · 1997 to 2012
$28.1M
Mu Opioid Receptor in AddictionP20DA025995 · NIDA · UNIVERSITY OF PENNSYLVANIA · PI BERRETTINI, WADE H · 2008 to 2011
$3.4M
Genetics of Nicotine DependenceR01DA025201 · NIDA · UNIVERSITY OF PENNSYLVANIA · PI BERRETTINI, WADE H · 2009 to 2013
$1.7M
NIDA NIH HHS P20 DA 025995NIDA NIH HHS P60 DA 05186NIDA NIH HHS R01 DA 025201
6 · The paper itself

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

AlcoholismAnimalsDisease Models, AnimalGenetic Association StudiesGenetic LinkageGenetic Predisposition to DiseaseHumansMultigene FamilyMutation, MissenseNerve Tissue ProteinsPolymorphism, Single NucleotidePsychiatric Status Rating ScalesReceptors, NicotinicSmoking CessationTobacco Use DisorderWhite PeopleCHRNA5 protein, humanCHRNB4 protein, humanNerve Tissue ProteinsReceptors, Nicotinic

Identifiers

PMID21968931
OpenAlexW2015935450

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.