No evidence for linkage of schizophrenia with the glutamate GluRS and GluR6 receptor genes in Taiwanese pedigrees

M. W. Lin*, P. C. Lee, C. H. Liu, H. G. Hwu

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract

Family, twin, and adoption studies have consistently shown that genetic factors play an important role in the etiology of schizophrenia. However, confirmed evidence of linkage between schizophrenia and any candidate genes is awaited. The role of glutamate involved in schizophrenia has attracted increasing awareness as phenocyclidine, a noncompetitive antagonist of the N-methyl-D-aspartate (NMDA), which produces a schizophreniform psychosis characterized by both positive and negative symptoms. The glutamate hypothesis proposes that dysfunction of glutamatergic neurotransmission and a disturbed balance between glutamatergic and dopaminergic systems in the brain may contribute to the pathogenesis of schizophrenia. We have carried out linkage studies between glutamate GluR5 and GluRG receptor genes and schizophrenia in a sample of 39 Taiwanese nuclear families with at least two affected siblings. The GluR5 receptor gene produced a slightly positive admixture lod score of 0.27 at 6 = 0 (α = 0.35); while GluR6 did not give any evidence of linkage with schizophrenia. Our results suggest that the polymorphisms of GluRS and GluR6 receptors are unlikely to provide a major contribution to the susceptibility to schizophrenia in our Taiwanese sample.

Original languageEnglish
Pages (from-to)529
Number of pages1
JournalAmerican Journal of Medical Genetics, Part B: Neuropsychiatric Genetics
Volume81
Issue number6
StatePublished - 6 Nov 1998

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