Am J Psychiatry 1996; 153:1634-1636
Copyright © 1996 by American Psychiatric Association
Lack of evidence for close linkage of the glutamate GluR6 receptor gene with schizophrenia
AC Chen, G Kalsi, J Brynjolfsson, T Sigmundsson, D Curtis, R Butler, T Read, P Murphy, H Petursson, EA Barnard and HM Gurling
Department of Psychiatry, University College London Medical School, U.K.
OBJECTIVE: Previous research has consistently implicated genetic factors in
the pathogenesis of schizophrenia. It has been hypothesized that an
abnormality in glutamatergic function is of etiologic importance in
schizophrenia, and therefore the glutamate receptor family of genes are
potential susceptibility loci for schizophrenia. To test this hypothesis
the authors sought to detect linkage between the GluR6 glutamate receptor
gene and schizophrenia. METHOD: Twenty-three English and Icelandic families
containing multiple cases of schizophrenia were genotyped with a
microsatellite trinucleotide repeat polymorphism localized at the GluR6
glutamate receptor locus. Lod scores, model-free linkage analysis, and
extended relative pair analysis were used to test for linkage. RESULTS: No
statistically significant evidence of linkage between GluR6 and
schizophrenia was found. CONCLUSIONS: The results do not support the
hypothesis that GluR6 allelic variants provide a major gene contribution to
the etiology of schizophrenia in a large proportion of these pedigrees.
