Kynurenine 3-monooxygenase polymorphisms: relevance for kynurenic acid synthesis in patients with schizophrenia and healthy controls.

Maria Holtze, Peter Saetre, Göran Engberg, Lilly Schwieler, Thomas Werge, Ole A Andreassen, Håkan Hall, Lars Terenius, Ingrid Agartz, Erik G Jönsson, Martin Schalling, Sophie Erhardt

Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.

Journal Article: Journal of psychiatry & neuroscience: JPN (impact factor: 3.58). 07/2011; 37(1):53-7. DOI: 10.1503/jpn.100175

Abstract

Patients with schizophrenia show increased brain and cerebrospinal fluid (CSF) concentrations of the endogenous N-methyl-D-aspartate receptor antagonist kynurenic acid (KYNA). This compound is an end-metabolite of the kynurenine pathway, and its formation indirectly depends on the activity of kynurenine 3-monooxygenase (KMO), the enzyme converting kynurenine to 3-hydroxykynurenine.
We analyzed the association between KMO gene polymorphisms and CSF concentrations of KYNA in patients with schizophrenia and healthy controls. Fifteen single nucleotide polymorphisms (SNPs) were selected covering KMO and were analyzed in UNPHASED.
We included 17 patients with schizophrenia and 33 controls in our study. We found an association between a KMO SNP (rs1053230), encoding an amino acid change of potential importance for substrate interaction, and CSF concentrations of KYNA.
Given the limited sample size, the results are tentative until replication.
Our results suggest that the nonsynonymous KMO SNP rs1053230 influences CSF concentrations of KYNA.

Source: PubMed

Comments on this publication

ResearchGate members can add comments. Sign up now and post your comment!

Similar publications

Science & Research Jobs

Keywords

17 patients
 
33 controls
 
amino acid change
 
cerebrospinal fluid
 
endogenous N-methyl-D-aspartate receptor antagonist kynurenic acid
 
healthy controls
 
KMO
 
KMO gene polymorphisms
 
KMO SNP
 
KYNA
 
kynurenine pathway
 
limited sample size
 
nonsynonymous KMO SNP rs1053230 influences CSF concentrations
 
patients
 
potential importance
 
replication
 
schizophrenia
 
single nucleotide polymorphisms
 
SNPs
 
substrate interaction