ArticleMolecular psychiatry2006
Cytogenetic and genetic evidence supports a role for the kainate-type glutamate receptor gene, GRIK4, in schizophrenia and bipolar disorder.
Article in Molecular psychiatry, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
51 citing papers in PubMed, 2 syntheses or guidelines pooled it, 113 citations in OpenAlex.
- GRIK4 polymorphism and its association with antidepressant response in depressed patients: a meta-analysis.Pharmacogenomics · 2014Pooled it
- Population-based linkage analysis of schizophrenia and bipolar case-control cohorts identifies a potential susceptibility locus on 19q13.Molecular psychiatry · 2010Pooled it
- The Molecular Machinery of Synaptic Plasticity and Its Potential Role in the Aetiology of Schizophrenia.Molecular neurobiology · 2026Review
- Effects of all-trans retinoic acid on glutamate receptor expression and dendritic spine density in the hypothalamus of rats.Frontiers in neuroscience · 2025Article
- GluK1 kainate receptors are necessary for functional maturation of parvalbumin interneurons regulating amygdala circuit function.Molecular psychiatry · 2024Article
- Ultrarare Loss-of-Function Mutations in the Genes Encoding the Ionotropic Glutamate Receptors of Kainate Subtypes Associated with Schizophrenia Disrupt the Interaction with PSD95.Journal of personalized medicine · 2022Article
- Structure, Function, and Regulation of the Kainate Receptor.Sub-cellular biochemistry · 2022Review
- Prediction of lithium response using genomic data.Scientific reports · 2021Article
- Canonical Correlation Analysis of Imaging Genetics Data Based on Statistical Independence and Structural Sparsity.IEEE journal of biomedical and health informatics · 2020Article
- Damaging coding variants within kainate receptor channel genes are enriched in individuals with schizophrenia, autism and intellectual disabilities.Scientific reports · 2019Article
- Assembly and Trafficking of Homomeric and Heteromeric Kainate Receptors with Impaired Ligand Binding Sites.Neurochemical research · 2019Article
- Exciting Times: New Advances Towards Understanding the Regulation and Roles of Kainate Receptors.Neurochemical research · 2019Review
- Neurobiological Mechanisms of Stress Resilience and Implications for the Aged Population.Current neuropharmacology · 2018Review
- Genetic Studies on the Tripartite Glutamate Synapse in the Pathophysiology and Therapeutics of Mood Disorders.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017Review
- Complete Disruption of the Kainate Receptor Gene Family Results in Corticostriatal Dysfunction in Mice.Cell reports · 2017Article
- A gain-of-function mutation in theNeurology. Genetics · 2017Article
- Emerging Synaptic Molecules as Candidates in the Etiology of Neurological Disorders.Neural plasticity · 2017Review
- de novo interstitial deletions at the 11q23.3-q24.2 region.Molecular cytogenetics · 2016Article
- Increased Dosage of High-Affinity Kainate Receptor Gene grik4 Alters Synaptic Transmission and Reproduces Autism Spectrum Disorders Features.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Characterization of a Novel Mutation in SLC1A1 Associated with Schizophrenia.Molecular neuropsychiatry · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.