Evidence map›Paper›PMID 16389274›Full record

ArticleMolecular psychiatry2006

A neuronal nitric oxide synthase (NOS-I) haplotype associated with schizophrenia modifies prefrontal cortex function.

A Reif, S Herterich, A Strobel, A-C Ehlis, D Saur, C P Jacob, T Wienker, T Töpner, S Fritzen, U Walter and 3 more

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Molecular psychiatry, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 1 pooled it
7.2field-weighted citation impact, top 2% 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

80 citing papers in PubMed, 1 synthesis or guideline pooled it, 210 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Biological psychiatry global open science · 2023
    Article
  6. Article
  7. Article
  8. The rs2682826 Polymorphism of theLife (Basel, Switzerland) · 2023
    Article
  9. Article
  10. Review
  11. Clinical practice and epidemiology in mental health : CP & EMH · 2022
    Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Genetic Factors of Nitric Oxide's System in Psychoneurologic Disorders.International journal of molecular sciences · 2020
    Review
  20. Article

20 more citing papers are in PubMed but not listed here.

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

13 authors at 4 institutions in 1 country.

A ReifDepartment of Psychiatry and Psychotherapy (Section for Clinical and Molecular Psychobiology and Laboratory for Psychophysiology and Functional Imaging), Julius-Maximilians-University Würzburg, Würzburg, Germany. a.reif@gmx.net
S Herterich
A Strobel
A-C Ehlis
D Saur
C P Jacob
T Wienker
T Töpner
S Fritzen
U Walter
A Schmitt
A J Fallgatter
K-P Lesch
University of Würzburg · DETechnical University of Munich · DETU Dresden · DEUniversity of Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nitric oxide (NO) is a gaseous neurotransmitter thought to play important roles in several behavioral domains. On a neurobiological level, NO acts as the second messenger of the N-methyl-D-aspartate receptor and interacts with both the dopaminergic as well as the serotonergic system. Thus, NO is a promising candidate molecule in the pathogenesis of endogenous psychoses and a potential target in their treatment. Furthermore, the chromosomal locus of the gene for the NO-producing enzyme NOS-I, 12q24.2, represents a major linkage hot spot for schizophrenic and bipolar disorder. To investigate whether the gene encoding NOS-I (NOS1) conveys to the genetic risk for those diseases, five NOS1 polymorphisms as well as a NOS1 mini-haplotype, consisting of two functional polymorphisms located in the transcriptional control region of NOS1, were examined in 195 chronic schizophrenic, 72 bipolar-I patients and 286 controls. Single-marker association analysis showed that the exon 1c promoter polymorphism was linked to schizophrenia (SCZ), whereas synonymous coding region polymorphisms were not associated with disease. Long promoter alleles of the repeat polymorphism were associated with less severe psychopathology. Analysis of the mini-haplotype also revealed a significant association with SCZ. Mutational screening did not detect novel exonic polymorphisms in patients, suggesting that regulatory rather than coding variants convey the genetic risk on psychosis. Finally, promoter polymorphisms impacted on prefrontal functioning as assessed by neuropsychological testing and electrophysiological parameters elicited by a Go-Nogo paradigm in 48 patients (continuous performance test). Collectively these findings suggest that regulatory polymorphisms of NOS1 contribute to the genetic risk for SCZ, and modulate prefrontal brain functioning.

Indexed as

Polymorphism, GeneticAdultBipolar DisorderChromosome MappingDNA Mutational AnalysisFemaleGene Expression Regulation, EnzymologicGenetic LinkageHumansMaleMiddle AgedMinisatellite RepeatsNitric Oxide Synthase Type IPolymorphism, Single NucleotidePrefrontal CortexPromoter Regions, GeneticNitric Oxide Synthase Type I

Identifiers

PMID16389274
OpenAlexW2133760600

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.