Maternal transmission disequilibrium of the glutamate receptor GRIK2 in schizophrenia

被引：28

作者：

Bah, J

Quach, H

Ebstein, RP

Segman, RH

Melke, J

Jamain, S

Rietschel, M

Modai, I

Kanas, K

Karni, O

Lerer, B

Gourion, D

Krebs, MO

Etain, B

Schürhoff, F

Szöke, A

Leboyer, M

Bourgeron, T

机构：

[1] Univ Paris 07, Inst Pasteur, F-75724 Paris 15, France

[2] Herzog Hosp, Jerusalem, Israel

[3] Hadassah Hebrew Univ Med Ctr, Jerusalem, Israel

[4] Univ Bonn, D-5300 Bonn, Germany

[5] Shaar Menashe Mental Hlth Ctr, Hefer, Israel

[6] Hop St Anne, INSERM E 0117 Paris 5, F-75674 Paris, France

[7] Hop Albert Chenevier & Henri Mondor, Creteil, France

[8] Lab INSERM U513, Creteil, France

来源：

NEUROREPORT | 2004年 / 15卷 / 12期

关键词：

chromosome; 6q; glutamate; imprinting; kainate; polymorphism; schizophrenia;

D O I：

10.1097/00001756-200408260-00031

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Schizophrenia is characterized by thought disorders, hallucinations and delusions. Genetic studies have shown a high linkage at chromosome 6q16-21. Among the genes located in this region is the glutamate receptor ionotropic kainate 2 gene (GRIK2 or GLUR6), a functional candidate for susceptibility to schizophrenia. In this study, transmission of GRIK2 was evaluated in 356 schizophrenic patients from three different clinical centers. Whereas paternal transmission shows equilibrium, we observed maternal transmission disequilibrium of GRIK2 in the largest population (p=0.03), which was still significant when all populations were added (p=0.05). These results are similar to the maternal GRIK2 transmission disequilibrium previously reported for autism, and support the presence of a susceptibility gene for schizophrenia at 6q16.

引用

页码：1987 / 1991

页数：5

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