| Literature DB >> 16716206 |
N Aoyama1, N Takahashi, S Saito, N Maeno, R Ishihara, X Ji, H Miura, M Ikeda, T Suzuki, T Kitajima, Y Yamanouchi, Y Kinoshita, K Yoshida, N Iwata, T Inada, N Ozaki.
Abstract
Several lines of evidence suggest that metabolic changes in the kynurenic acid (KYNA) pathway are related to the etiology of schizophrenia. The inhibitor of kynurenine 3-monooxygenase (KMO) is known to increase KYNA levels, and the KMO gene is located in the chromosome region associated with schizophrenia, 1q42-q44. Single-marker and haplotype analyses for 6-tag single nucleotide polymorphisms (SNPs) of KMO were performed (cases = 465, controls = 440). Significant association of rs2275163 with schizophrenia was observed by single-marker comparisons (P = 0.032) and haplotype analysis including this SNP (P = 0.0049). Significant association of rs2275163 and haplotype was not replicated using a second, independent set of samples (cases = 480, controls = 448) (P = 0.706 and P = 0.689, respectively). These results suggest that the KMO is unlikely to be related to the development of schizophrenia in Japanese.Entities:
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Year: 2006 PMID: 16716206 DOI: 10.1111/j.1601-183X.2006.00231.x
Source DB: PubMed Journal: Genes Brain Behav ISSN: 1601-183X Impact factor: 3.449