Evidence map›Paper›PMID 15505638›Full record

Trial reportMolecular psychiatry2005

Separate and interacting effects within the catechol-O-methyltransferase (COMT) are associated with schizophrenia.

H Y Handoko, D R Nyholt, N K Hayward, D A Nertney, D E Hannah, L C Windus, C M McCormack, H J Smith, C Filippich, M R James and 1 more

Abstract readClinical TrialControlled Clinical Trial
PubMed Publisher
In one paragraph

Trial report in Molecular psychiatry, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.

  1. Pooled it
  2. Association study of single nucleotide polymorphism rs165599 ofMolecular biology research communications · 2015
    Article
  3. Article
  4. Review
  5. Article
  6. Association of catechol-O-methyltransferase gene polymorphisms with schizophrenia and negative symptoms in a Chinese population.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2012
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Prediction of psychosis onset in Alzheimer disease: the role of depression symptom severity and the HTR2A T102C polymorphism.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2007
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

11 authors at 4 institutions in 1 country.

H Y HandokoQueensland Centre for Mental Health Research, The Park, Centre for Mental Health, Wacol, QLD, Australia.
D R Nyholt
N K Hayward
D A Nertney
D E Hannah
L C Windus
C M McCormack
H J Smith
C Filippich
M R James
B J Mowry
Park Centre for Mental Health · AUQIMR Berghofer Medical Research Institute · AUQueensland Centre for Mental Health Research · AUUniversity of Queensland · AU

Funding

MOLECULAR GENETICS OF SCHIZOPHRENIAR01MH059588 · NIMH · UNIVERSITY OF QUEENSLAND · PI MOWRY, BRYAN JOHN · 1999 to 2006
$1.4M
NIMH NIH HHS R01 MH 59588
6 · The paper itself

Abstract

Several lines of evidence have implicated the catechol-O-methyltransferase (COMT) gene as a candidate for schizophrenia (SZ) susceptibility, not only because it encodes a key dopamine catabolic enzyme but also because it maps to the velocardiofacial syndrome region of chromosome 22q11 which has long been associated with SZ predisposition. The interest in COMT as a candidate SZ risk factor has led to numerous case-control and family-based studies, with the majority placing emphasis on examining a functional Val/Met polymorphism within this enzyme. Unfortunately, these studies have continually produced conflicting results. To assess the genetic contribution of other COMT variants to SZ susceptibility, we investigated three single-nucleotide polymorphisms (SNPs) (rs737865, rs4633, rs165599) in addition to the Val/Met variant (rs4680) in a highly selected sample of Australian Caucasian families containing 107 patients with SZ. The Val/Met and rs4633 variants showed nominally significant associations with SZ (P<0.05), although neither of the individual SNPs remained significant after adjusting for multiple testing (most significant P=0.1174). However, haplotype analyses showed strong evidence of an association; the most significant being the three-marker haplotype rs737865-rs4680-rs165599 (global P=0.0022), which spans more than 26 kb. Importantly, conditional analyses indicated the presence of two separate and interacting effects within this haplotype, irrespective of gender. In addition, our results indicate the Val/Met polymorphism is not disease-causing and is simply in strong linkage disequilibrium with a causative effect, which interacts with another as yet unidentified variant approximately 20 kb away. These results may help explain the inconsistent results reported on the Val/Met polymorphism and have important implications for future investigations into the role of COMT in SZ susceptibility.

Indexed as

Amino Acid SubstitutionAustraliaCatechol O-MethyltransferaseChromosomes, Human, Pair 22FamilyFemaleGenetic Predisposition to DiseaseHumansLinkage DisequilibriumMalePedigreePolymorphism, Single NucleotideRisk FactorsSchizophreniaWhite PeopleCatechol O-Methyltransferase

Identifiers

PMID15505638
OpenAlexW2050074375

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.