Evidence map›Paper›PMID 17521439›Full record

ArticleBMC psychiatry2007

Association between 5-HT2A, TPH1 and GNB3 genotypes and response to typical neuroleptics: a serotonergic approach.

Sami Anttila, Olli Kampman, Ari Illi, Riikka Rontu, Terho Lehtimäki, Esa Leinonen

Abstract read
In one paragraph

Article in BMC psychiatry, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

14 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Review
  6. Pharmacogenetics of Antipsychotic Treatment in Schizophrenia.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  7. Article
  8. Article
  9. Pharmacogenetics of antipsychotics.Canadian journal of psychiatry. Revue canadienne de psychiatrie · 2014
    Review
  10. Article
  11. Genome-wide pharmacogenomic study of neurocognition as an indicator of antipsychotic treatment response in schizophrenia.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2011
    Article
  12. Pharmacogenetics of antidepressants.Frontiers in pharmacology · 2011
    Article
  13. The promise and reality of pharmacogenetics in psychiatry.The Psychiatric clinics of North America · 2010
    Review
  14. Article
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

6 authors.

Sami AnttilaUniversity of Tampere, Medical School, University of Tampere, Finland. samia@koti.soon.fi <samia@koti.soon.fi>
Olli Kampman
Ari Illi
Riikka Rontu
Terho Lehtimäki
Esa Leinonen

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSchizophrenia is a common psychiatric disease affecting about 1% of population. One major problem in the treatment is finding the right the drug for the right patients. However, pharmacogenetic results in psychiatry can seldom be replicated.

methodsWe selected three candidate genes associated with serotonergic neurotransmission for the study: serotonin 2A (5-HT2A) receptor gene, tryptophan hydroxylase 1 (TPH1) gene, and G-protein beta-3 subunit (GNB3) gene. We recruited 94 schizophrenia patients representing extremes in treatment response to typical neuroleptics: 43 were good responders and 51 were poor responders. The control group consisted of 392 healthy blood donors.

resultsWe do, in part, replicate the association between 5-HT2A T102C polymorphism and response to typical neuroleptics. In female patients, C/C genotype was significantly more common in non-responders than in responders [OR = 6.04 (95% Cl 1.67-21.93), p = 0.005] or in the control population [OR = 4.16 (95% CI 1.46-11.84), p = 0.005]. TPH1 A779C C/A genotype was inversely associated with good treatment response when compared with non-responders [OR = 0.59 (95% Cl 0.36-0.98), p = 0.030] or with the controls [OR = 0.44 (95% CI 0.23-0.86, p = 0.016], and GNB3 C825T C/T genotype showed a trend-like positive association among the male patients with a good response compared with non-responders [OR = 3.48 (95% Cl 0.92-13.25), p = 0.061], and a clearer association when compared with the controls [OR = 4.95 (95% CI 1.56-15.70), p = 0.004].

conclusionMore findings on the consequences of functional polymorphisms for the role of serotonin in the development of brain and serotonergic neurotransmission are needed before more detailed hypotheses regarding susceptibility and outcome in schizophrenia can be formulated. The present results may highlight some of the biological mechanisms in different courses of schizophrenia between men and women.

Indexed as

AdultAntipsychotic AgentsCase-Control StudiesDrug ResistanceFemaleGenotypeHeterotrimeric GTP-Binding ProteinsHumansMaleMiddle AgedOdds RatioPolymorphism, GeneticReceptors, SerotoninSchizophreniaSerotoninSex FactorsAntipsychotic AgentsG-protein beta3 subunitHeterotrimeric GTP-Binding ProteinsReceptors, SerotoninSerotoninserotonin 5 receptorTPH1 protein, humanTryptophan Hydroxylase

Identifiers

PMID17521439
PMCPMC1888684

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.