Evidence map›Paper›PMID 11526472›Full record

ArticleMolecular psychiatry2001

Variability of 5-HT2C receptor cys23ser polymorphism among European populations and vulnerability to affective disorder.

B Lerer, F Macciardi, R H Segman, R Adolfsson, D Blackwood, S Blairy, J Del Favero, D G Dikeos, R Kaneva, R Lilli and 13 more

Abstract readComparative StudyMulticenter Study
PubMed Publisher
In one paragraph

Article in Molecular psychiatry, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 4 pooled it
4.8field-weighted citation impact, top 5% 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, 4 syntheses or guidelines pooled it, 160 citations in OpenAlex.

  1. Meta-analysis of genetic association studies on bipolar disorder.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2012
    Pooled it
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  5. Article
  6. Review
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  8. Serotonin and beyond-a tribute to Manfred Göthert (1939-2019).Naunyn-Schmiedeberg's archives of pharmacology · 2021
    Review
  9. Article
  10. Article
  11. Serotonin 5-HTScientific reports · 2019
    Article
  12. Article
  13. Association of SerotoninFrontiers in psychiatry · 2019
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  14. Review
  15. Article
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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

23 authors at 11 institutions in 10 countries.

B LererBiological Psychiatry Laboratory, Hadassah Medical Organization, Jerusalem, Israel. lerer@cc.huji.ac.il
F Macciardi
R H Segman
R Adolfsson
D Blackwood
S Blairy
J Del Favero
D G Dikeos
R Kaneva
R Lilli
I Massat
V Milanova
W Muir
M Noethen
L Oruc
T Petrova
G N Papadimitriou
M Rietschel
A Serretti
D Souery
S Van Gestel
C Van Broeckhoven
J Mendlewicz
Erasmus Hospital · BEMedical University of Sofia · BGUniversity of Antwerp · BEHadassah Medical Center · ILInstitute of Genetics and Cancer · GBUniversity Mental Health Research Institute · GRUniversity of Bonn · DEUniversity of Milan · ITToronto Centre for Phenogenomics · CAUmeå University · SEUniversity Hospital Centre Zagreb · HR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Substantial evidence supports a role for dysfunction of brain serotonergic (5-HT) systems in the pathogenesis of major affective disorder, both unipolar (recurrent major depression) and bipolar.(1) Modification of serotonergic neurotransmission is pivotally implicated in the mechanism of action of antidepressant drugs(2) and also in the action of mood stabilizing agents, particularly lithium carbonate.(3) Accordingly, genes that code for the multiple subtypes of serotonin receptors that have been cloned and are expressed in brain,(4) are strong candidates for a role in the genetic etiology of affective illness. We examined a structural variant of the serotonin 2C (5-HT2C) receptor gene (HTR2C) that gives rise to a cysteine to serine substitution in the N terminal extracellular domain of the receptor protein (cys23ser),(5) in 513 patients with recurrent major depression (MDD-R), 649 patients with bipolar (BP) affective disorder and 901 normal controls. The subjects were drawn from nine European countries participating in the European Collaborative Project on Affective Disorders. There was significant variation in the frequency of the HT2CR ser23 allele among the 10 population groups included in the sample (from 24.6% in Greek control subjects to 9.2% in Scots, chi(2) = 20.9, df 9, P = 0.01). Logistic regression analysis demonstrated that over and above this inter-population variability, there was a significant excess of HT2CR ser23 allele carriers in patients compared to normal controls that was demonstrable for both the MDD (chi(2) = 7.34, df 1, P = 0.006) and BP (chi(2) = 5.45, df 1, P = 0.02) patients. These findings support a possible role for genetically based structural variation in 5-HT2C receptors in the pathogenesis of major affective disorder.

Indexed as

Genetic Predisposition to DiseaseGenetic VariationPolymorphism, GeneticAmino Acid SubstitutionBipolar DisorderCysteineDepressive DisorderEthnicityEuropeFemaleGene FrequencyGenetic LinkageHumansIsraelLeast-Squares AnalysisLikelihood FunctionsCysteineReceptor, Serotonin, 5-HT2CReceptors, SerotoninSerine

Identifiers

PMID11526472
OpenAlexW1995930538

What OpenQuestion holds

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Registered trials

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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.