Evidence map›Paper›PMID 26096691›Full record

Trial reportGenes, brain, and behavior2015

COMT polymorphism modulates the resting-state EEG alpha oscillatory response to acute nicotine in male non-smokers.

H Bowers, D Smith, S de la Salle, J Choueiry, D Impey, T Philippe, H Dort, A Millar, M Daigle, P R Albert and 2 more

Open access · bronzeAbstract readRandomized Controlled Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in Genes, brain, and behavior, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 25% 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

5 citing papers in PubMed, 14 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. Review
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

12 authors at 4 institutions in 1 country.

H BowersDepartment of Psychology, University of Guelph, Guelph, ON, Canada.
D SmithDepartment of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, Canada.
S de la SalleSchool of Psychology, University of Ottawa, Ottawa, ON, Canada.
J ChoueiryDepartment of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, Canada.
D ImpeySchool of Psychology, University of Ottawa, Ottawa, ON, Canada.
T PhilippeUniversity of Ottawa Institute of Mental Health Research, Royal Ottawa Mental Health Care Centre, Ottawa, ON, Canada.
H DortUniversity of Ottawa Institute of Mental Health Research, Royal Ottawa Mental Health Care Centre, Ottawa, ON, Canada.
A MillarDepartment of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, Canada.
M DaigleOttawa Hospital Research Institute, University of Ottawa, Ottawa, ON, Canada.
P R AlbertDepartment of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, Canada.
A BeaudoinUniversity of Ottawa Institute of Mental Health Research, Royal Ottawa Mental Health Care Centre, Ottawa, ON, Canada.
V KnottDepartment of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, Canada.
University of Ottawa · CARoyal Ottawa Mental Health Centre · CAOttawa Hospital · CAUniversity of Guelph · CA

Funding

CIHR 115098-1
6 · The paper itself

Abstract

Performance improvements in cognitive tasks requiring executive functions are evident with nicotinic acetylcholine receptor (nAChR) agonists, and activation of the underlying neural circuitry supporting these cognitive effects is thought to involve dopamine neurotransmission. As individual difference in response to nicotine may be related to a functional polymorphism in the gene encoding catechol-O-methyltransferase (COMT), an enzyme that strongly influences cortical dopamine metabolism, this study examined the modulatory effects of the COMT Val158Met polymorphism on the neural response to acute nicotine as measured with resting-state electroencephalographic (EEG) oscillations. In a sample of 62 healthy non-smoking adult males, a single dose (6 mg) of nicotine gum administered in a randomized, double-blind, placebo-controlled design was shown to affect α oscillatory activity, increasing power of upper α oscillations in frontocentral regions of Met/Met homozygotes and in parietal/occipital regions of Val/Met heterozygotes. Peak α frequency was also found to be faster with nicotine (vs. placebo) treatment in Val/Met heterozygotes, who exhibited a slower α frequency compared to Val/Val homozygotes. The data tentatively suggest that interindividual differences in brain α oscillations and their response to nicotinic agonist treatment are influenced by genetic mechanisms involving COMT.

Indexed as

AdultBrainCatechol O-MethyltransferaseCognitionDopamineDouble-Blind MethodElectroencephalographyExecutive FunctionGenotypeHumansMaleNicotinePlacebosPolymorphism, Single NucleotideReceptors, NicotinicYoung AdultCatechol O-MethyltransferaseCOMT protein, humanDopamineNicotinePlacebosReceptors, NicotinicAlphacatechol-O-methyltransferasecognitiondopamineelectroencephalographygenotypenicotineoscillationspolymorphismresting state

Identifiers

PMID26096691
PMCPMC4514526
OpenAlexW1541723963

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.