TY - JOUR
T1 - Association study of polymorphisms in the GluR7, KA1 and KA2 kainate receptor genes (GRIK3, GRIK4, GRIK5) with schizophrenia
AU - Shibata, Hiroki
AU - Aramaki, Toshihiro
AU - Sakai, Mayumi
AU - Ninomiya, Hideaki
AU - Tashiro, Nobutada
AU - Iwata, Nakao
AU - Ozaki, Norio
AU - Fukumaki, Yasuyuki
N1 - Funding Information:
The authors are grateful to all the medical staff who were involved in collecting specimens. They also thank Naoko S. Hashimoto for technical assistance on data analysis. This work was supported in part by Grant-in-Aid for Young Scientists (A), 14704056 and by Grant-in-Aid for Scientific Research on Priority Areas “Medical Genome Science”, 12204009 from the Ministry of Education, Science, Sports and Culture, Japan.
PY - 2006/1/30
Y1 - 2006/1/30
N2 - On the basis of the glutamatergic dysfunction hypothesis of schizophrenia, we have been conducting a systematic study of the association of glutamate receptor genes with schizophrenia. Here we report association studies of schizophrenia with polymorphisms in three kainate receptor genes: GRIK3, GRIK4 and GRIK5. We selected 16, 24 and 5 common single nucleotide polymorphisms (SNPs) distributed in the entire gene regions of GRIK3 (> 240 kb), GRIK4 (> 430 kb) and GRIK5 (> 90 kb), respectively. We tested associations of the polymorphisms with schizophrenia using 100 Japanese case-control pairs (the Kyushu set). We observed no significant "single marker" associations with the disease in any of the 45 SNPs tested except for one (rs3767092) in GRIK3 showing a nominal level of significance. The significant association, however, disappeared after the application of the Bonferroni correction. We also observed significant haplotype associations in seven SNP pairs in GRIK3 and in four SNP pairs in GRIK4. None, however, remained significant after Bonferroni correction. We also failed to replicate the nominally significant haplotype associations in a second sample set, the Aichi set (106 cases and 100 controls). We conclude that SNPs in the gene regions of GRIK3, GRIK4 or GRIK5 do not play a major role in schizophrenia pathogenesis in the Japanese population.
AB - On the basis of the glutamatergic dysfunction hypothesis of schizophrenia, we have been conducting a systematic study of the association of glutamate receptor genes with schizophrenia. Here we report association studies of schizophrenia with polymorphisms in three kainate receptor genes: GRIK3, GRIK4 and GRIK5. We selected 16, 24 and 5 common single nucleotide polymorphisms (SNPs) distributed in the entire gene regions of GRIK3 (> 240 kb), GRIK4 (> 430 kb) and GRIK5 (> 90 kb), respectively. We tested associations of the polymorphisms with schizophrenia using 100 Japanese case-control pairs (the Kyushu set). We observed no significant "single marker" associations with the disease in any of the 45 SNPs tested except for one (rs3767092) in GRIK3 showing a nominal level of significance. The significant association, however, disappeared after the application of the Bonferroni correction. We also observed significant haplotype associations in seven SNP pairs in GRIK3 and in four SNP pairs in GRIK4. None, however, remained significant after Bonferroni correction. We also failed to replicate the nominally significant haplotype associations in a second sample set, the Aichi set (106 cases and 100 controls). We conclude that SNPs in the gene regions of GRIK3, GRIK4 or GRIK5 do not play a major role in schizophrenia pathogenesis in the Japanese population.
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U2 - 10.1016/j.psychres.2005.07.015
DO - 10.1016/j.psychres.2005.07.015
M3 - Article
C2 - 16325263
AN - SCOPUS:29444438199
SN - 0165-1781
VL - 141
SP - 39
EP - 51
JO - Psychiatry Research
JF - Psychiatry Research
IS - 1
ER -
