Kynurenine 3-monooxygenase polymorphisms: relevance for kynurenic acid synthesis in patients with schizophrenia and healthy controls
Author(s) -
M. 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
Publication year - 2011
Publication title -
journal of psychiatry and neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.767
H-Index - 99
eISSN - 1488-2434
pISSN - 1180-4882
DOI - 10.1503/jpn.100175
Subject(s) - kynurenic acid , kynurenine , kynurenine pathway , single nucleotide polymorphism , haloperidol , schizophrenia (object oriented programming) , medicine , metabolite , snp , pharmacology , endocrinology , nmda receptor , chemistry , psychology , biochemistry , receptor , dopamine , amino acid , psychiatry , tryptophan , gene , genotype
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.
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