期刊
JOURNAL OF PSYCHIATRY & NEUROSCIENCE
卷 37, 期 1, 页码 53-57出版社
CMA-CANADIAN MEDICAL ASSOC
DOI: 10.1503/jpn.100175
关键词
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资金
- Uppsala University, Uppsala University Hospital
- Knut and Alice Wallenberg Foundation
- Hallstens Forskningsstiftelse
- Swedish Brain Foundation
- Svenska Lakaresallskapet
- Karolinska Institutet
- Torsten och Ragnar Soderbergs stiftelse
- Swedish Medical Research Council
- Soderstrom-Konigska stiftelsen
- Stockholm County Council
- Copenhagen Hospital Corporation
- Danish National Psychiatric Research Foundation
- Danish Agency for Science, Technology and Innovation (Centre for Pharmacogenetics)
- Research Council of Norway [147787, 167153]
- Eastern Norway Health Authority [RHF 123/2004]
- Ulleval University Hospital
- University of Oslo
- Swedish Research Council [2009-4046, 2009-7053, K2009-62X-07484-24-3, K2007-62X-15077-04-1, K2007-62X-15078-04-3, K2008-62P-20597-01-3, 10909]
- HUBIN
Background: 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. Methods: 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. Results: 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. Limitations: Given the limited sample size, the results are tentative until replication. Conclusion: Our results suggest that the nonsynonymous KMO SNP rs1053230 influences CSF concentrations of KYNA.
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