Cytogenetic and genetic evidence supports a role for the kainate-type glutamate receptor gene, GRIK4, in schizophrenia and bipolar disorder
In the search for the biological causes of schizophrenia and bipolar disorder, glutamate neurotransmission has emerged as one of a number of candidate processes and pathways where underlying gene deficits may be present. The analysis of chromosomal rearrangements in individuals diagnosed with neurop...
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Published in | Molecular psychiatry Vol. 11; no. 9; pp. 847 - 857 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
London
Nature Publishing Group UK
01.09.2006
Nature Publishing Group |
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Abstract | In the search for the biological causes of schizophrenia and bipolar disorder, glutamate neurotransmission has emerged as one of a number of candidate processes and pathways where underlying gene deficits may be present. The analysis of chromosomal rearrangements in individuals diagnosed with neuropsychiatric disorders is an established route to candidate gene identification in both Mendelian and complex disorders. Here we describe a set of genes disrupted by, or proximal to, chromosomal breakpoints (2p12, 2q31.3, 2q21.2, 11q23.3 and 11q24.2) in a patient where chronic schizophrenia coexists with mild learning disability (US: mental retardation). Of these disrupted genes, the most promising candidate is a member of the kainate-type ionotropic glutamate receptor family,
GRIK4
(
KA1
). A subsequent systematic case–control association study on
GRIK4
assessed its contribution to psychiatric illness in the karyotypically normal population. This identified two discrete regions of disease risk within the
GRIK4
locus: three single single nucleotide polymorphism (SNP) markers with a corresponding underlying haplotype associated with susceptibility to schizophrenia (
P
=0.0005, odds ratio (OR) of 1.453, 95% CI 1.182–1.787) and two single SNP markers and a haplotype associated with a protective effect against bipolar disorder (
P
=0.0002, OR of 0.624, 95% CI 0.485–0.802). After permutation analysis to correct for multiple testing, schizophrenia and bipolar disorder haplotypes remained significant (
P
=0.0430, s.e. 0.0064 and
P
=0.0190, s.e. 0.0043, respectively). We propose that these convergent cytogenetic and genetic findings provide molecular evidence for common aetiologies for different psychiatric conditions and further support the ‘glutamate hypothesis’ of psychotic illness. |
---|---|
AbstractList | In the search for the biological causes of schizophrenia and bipolar disorder, glutamate neurotransmission has emerged as one of a number of candidate processes and pathways where underlying gene deficits may be present. The analysis of chromosomal rearrangements in individuals diagnosed with neuropsychiatric disorders is an established route to candidate gene identification in both Mendelian and complex disorders. Here we describe a set of genes disrupted by, or proximal to, chromosomal breakpoints (2p12, 2q31.3, 2q21.2, 11q23.3 and 11q24.2) in a patient where chronic schizophrenia coexists with mild learning disability (US: mental retardation). Of these disrupted genes, the most promising candidate is a member of the kainate-type ionotropic glutamate receptor family, GRIK4 (KA1). A subsequent systematic case-control association study on GRIK4 assessed its contribution to psychiatric illness in the karyotypically normal population. This identified two discrete regions of disease risk within the GRIK4 locus: three single single nucleotide polymorphism (SNP) markers with a corresponding underlying haplotype associated with susceptibility to schizophrenia (P=0.0005, odds ratio (OR) of 1.453, 95% CI 1.182-1.787) and two single SNP markers and a haplotype associated with a protective effect against bipolar disorder (P=0.0002, OR of 0.624, 95% CI 0.485-0.802). After permutation analysis to correct for multiple testing, schizophrenia and bipolar disorder haplotypes remained significant (P=0.0430, s.e. 0.0064 and P=0.0190, s.e. 0.0043, respectively). We propose that these convergent cytogenetic and genetic findings provide molecular evidence for common aetiologies for different psychiatric conditions and further support the 'glutamate hypothesis' of psychotic illness. In the search for the biological causes of schizophrenia and bipolar disorder, glutamate neurotransmission has emerged as one of a number of candidate processes and pathways where underlying gene deficits may be present. The analysis of chromosomal rearrangements in individuals diagnosed with neuropsychiatric disorders is an established route to candidate gene identification in both Mendelian and complex disorders. Here we describe a set of genes disrupted by, or proximal to, chromosomal breakpoints (2p12, 2q31.3, 2q21.2, 11q23.3 and 11q24.2) in a patient where chronic schizophrenia coexists with mild learning disability (US: mental retardation). Of these disrupted genes, the most promising candidate is a member of the kainate-type ionotropic glutamate receptor family, GRIK4 (KA1). A subsequent systematic case-control association study on GRIK4 assessed its contribution to psychiatric illness in the karyotypically normal population. This identified two discrete regions of disease risk within the GRIK4 locus: three single single nucleotide polymorphism (SNP) markers with a corresponding underlying haplotype associated with susceptibility to schizophrenia (P=0.0005, odds ratio (OR) of 1.453, 95% CI 1.182-1.787) and two single SNP markers and a haplotype associated with a protective effect against bipolar disorder (P=0.0002, OR of 0.624, 95% CI 0.485-0.802). After permutation analysis to correct for multiple testing, schizophrenia and bipolar disorder haplotypes remained significant (P=0.0430, s.e. 0.0064 and P=0.0190, s.e. 0.0043, respectively). We propose that these convergent cytogenetic and genetic findings provide molecular evidence for common aetiologies for different psychiatric conditions and further support the 'glutamate hypothesis' of psychotic illness.Molecular Psychiatry (2006) 11, 847-857. doi:10.1038/sj.mp.4001867; published online 4 July 2006 In the search for the biological causes of schizophrenia and bipolar disorder, glutamate neurotransmission has emerged as one of a number of candidate processes and pathways where underlying gene deficits may be present. The analysis of chromosomal rearrangements in individuals diagnosed with neuropsychiatric disorders is an established route to candidate gene identification in both Mendelian and complex disorders. Here we describe a set of genes disrupted by, or proximal to, chromosomal breakpoints (2p12, 2q31.3, 2q21.2, 11q23.3 and 11q24.2) in a patient where chronic schizophrenia coexists with mild learning disability (US: mental retardation). Of these disrupted genes, the most promising candidate is a member of the kainate-type ionotropic glutamate receptor family, GRIK4 ( KA1 ). A subsequent systematic case–control association study on GRIK4 assessed its contribution to psychiatric illness in the karyotypically normal population. This identified two discrete regions of disease risk within the GRIK4 locus: three single single nucleotide polymorphism (SNP) markers with a corresponding underlying haplotype associated with susceptibility to schizophrenia ( P =0.0005, odds ratio (OR) of 1.453, 95% CI 1.182–1.787) and two single SNP markers and a haplotype associated with a protective effect against bipolar disorder ( P =0.0002, OR of 0.624, 95% CI 0.485–0.802). After permutation analysis to correct for multiple testing, schizophrenia and bipolar disorder haplotypes remained significant ( P =0.0430, s.e. 0.0064 and P =0.0190, s.e. 0.0043, respectively). We propose that these convergent cytogenetic and genetic findings provide molecular evidence for common aetiologies for different psychiatric conditions and further support the ‘glutamate hypothesis’ of psychotic illness. |
Audience | Academic |
Author | Evans, K L Christoforou, A Morris, S W Thomson, P A Pickard, B S Porteous, D J Blackwood, D H R Muir, W J Malloy, M P Hampson, M |
Author_xml | – sequence: 1 givenname: B S surname: Pickard fullname: Pickard, B S email: ben.pickard@ed.ac.uk organization: Medical Genetics Section, School of Clinical and Molecular Medicine, Molecular Medicine Centre, University of Edinburgh – sequence: 2 givenname: M P surname: Malloy fullname: Malloy, M P organization: Medical Genetics Section, School of Clinical and Molecular Medicine, Molecular Medicine Centre, University of Edinburgh – sequence: 3 givenname: A surname: Christoforou fullname: Christoforou, A organization: Medical Genetics Section, School of Clinical and Molecular Medicine, Molecular Medicine Centre, University of Edinburgh – sequence: 4 givenname: P A surname: Thomson fullname: Thomson, P A organization: Medical Genetics Section, School of Clinical and Molecular Medicine, Molecular Medicine Centre, University of Edinburgh – sequence: 5 givenname: K L surname: Evans fullname: Evans, K L organization: Medical Genetics Section, School of Clinical and Molecular Medicine, Molecular Medicine Centre, University of Edinburgh – sequence: 6 givenname: S W surname: Morris fullname: Morris, S W organization: Medical Genetics Section, School of Clinical and Molecular Medicine, Molecular Medicine Centre, University of Edinburgh – sequence: 7 givenname: M surname: Hampson fullname: Hampson, M organization: Medical Genetics Section, School of Clinical and Molecular Medicine, Molecular Medicine Centre, University of Edinburgh, Department of Advanced Biotechnologies, Janssen Pharmaceutica NV – sequence: 8 givenname: D J surname: Porteous fullname: Porteous, D J organization: Medical Genetics Section, School of Clinical and Molecular Medicine, Molecular Medicine Centre, University of Edinburgh – sequence: 9 givenname: D H R surname: Blackwood fullname: Blackwood, D H R organization: Psychiatry, Kennedy Tower, Royal Edinburgh Hospital, University of Edinburgh – sequence: 10 givenname: W J surname: Muir fullname: Muir, W J organization: Psychiatry, Kennedy Tower, Royal Edinburgh Hospital, University of Edinburgh |
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Keywords | chromosome abnormality haplotype psychiatry glutamate receptor association study Mood disorder Schizophrenia Bipolar disorder Glutamate receptor Genetic determinism Kainate receptor Psychosis Gene Cytogenetics Genetics Haplotype Psychiatry |
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SubjectTerms | Adult and adolescent clinical studies Behavioral Sciences Biological and medical sciences Biological Psychology Bipolar disorder Bipolar Disorder - genetics Bipolar disorders Breakpoints Cells, Cultured Chromosome rearrangements Chromosomes Chromosomes, Human, Pair 2 - genetics Cytogenetics DNA Primers Exons Female Gene polymorphism Gene Rearrangement Genes Glutamic acid receptors (ionotropic) Haplotypes Humans Hypotheses Illnesses In Situ Hybridization, Fluorescence Intellectual disabilities Intellectual Disability - genetics Karyotyping Learning disabilities Medical sciences Medicine Medicine & Public Health Mental disorders Mood disorders Neurosciences Neurotransmission original-article Patients Pharmacotherapy Polymerase Chain Reaction Polymorphism Psychiatry Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Psychoses Psychosis Receptors, Kainic Acid - genetics Schizophrenia Schizophrenia - genetics Single-nucleotide polymorphism Translocation, Genetic |
Title | Cytogenetic and genetic evidence supports a role for the kainate-type glutamate receptor gene, GRIK4, in schizophrenia and bipolar disorder |
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