ReviewMolecular psychiatry2023
GRIN2A (NR2A): a gene contributing to glutamatergic involvement in schizophrenia.
Review in Molecular psychiatry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
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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.
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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.
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Who cites it
44 citing papers in PubMed, 57 citations in OpenAlex.
- Sex-stratified insights into the genetics of brain volumes in late adulthood.Biology of sex differences · 2026Article
- Lead (Pb) and the NMDA Receptor Hypofunction Hypothesis: A Comparative Review of Non-Essential Metal Exposures in Schizophrenia.Current environmental health reports · 2026Review
- Genetic architecture of white matter microstructure captured by unsupervised deep representation learning of fractional anisotropy maps.Nature communications · 2026Article
- A Framework for Advancing Mechanistic Neurobehavioral Biomarkers in Psychiatry.Biological psychiatry · 2026Review
- Why Is Clozapine Uniquely Effective in Treatment-Resistant Schizophrenia? A Review and Proposal.Biological psychiatry · 2026Review
- A co-culture model of dopaminergic and glutamatergic neurons derived from patients with idiopathic schizophrenia reveals a hypodopaminergic phenotype.Molecular psychiatry · 2026Article
- Genetic Variants from Large Cohorts and Familial Studies Implicate Common Mechanisms in Schizophrenia.Biology · 2026Review
- Phosphatase Signaling as a Therapeutic Strategy in Schizophrenia.International journal of molecular sciences · 2026Review
- Exploring the roots of schizophrenia: Current research and future directions (Review).Experimental and therapeutic medicine · 2026Review
- GluN2A-mediated currents and calcium signal in human iPSC-derived neurons.Scientific reports · 2026Article
- scRiskDB: a single-cell epigenomic resource linking complex traits to regulatory mechanisms across human tissues.Database : the journal of biological databases and curation · 2026Article
- Genetic control of non-coding RNAs in the human brain and their implications for complex traits.American journal of human genetics · 2026Article
- GluN2A-NMDA receptor inhibition disinhibits the prefrontal cortex, reduces forced swim immobility, and impairs sensorimotor gating.Acta pharmacologica Sinica · 2026Article
- Spatially resolved translational dysregulation inbioRxiv : the preprint server for biology · 2025Article
- Glutamate, Contextual Insensitivity, and Disorganized Speech in First-Episode Schizophrenia: A 7T Magnetic Resonance Spectroscopy Study.Biological psychiatry global open science · 2025Article
- Linking spatial omics to patient phenotypes at the population scale by BSNMani: Bayesian scalar-on-network regression with manifold learning.medRxiv : the preprint server for health sciences · 2025Article
- Unveiling genetic architecture of white matter microstructure through unsupervised deep representation learning of fractional anisotropy maps.Research square · 2025Article
- Trisomy 21 Disrupts Thyroid Hormones Signaling During Human iPSC-Derived Neural Differentiation In Vitro.Cells · 2025Article
- An ace in the hole? Opportunities and limits of using mice to understand schizophrenia neurobiology.Molecular psychiatry · 2025Review
- Use of Proteomics to Explore Biomarkers of Amyotrophic Lateral Sclerosis (ALS): Proof of Principle from Humanized SOD1 Mouse to Human ALS.ACS pharmacology & translational science · 2025Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Involvement of the glutamate system, particularly N-methyl-D-aspartate (NMDA) receptor hypofunction, has long been postulated to be part of the pathophysiology of schizophrenia. An important development is provided by recent data that strongly implicate GRIN2A, the gene encoding the NR2A (GluN2A) NMDA receptor subunit, in the aetiology of the disorder. Rare variants and common variants are both robustly associated with genetic risk for schizophrenia. Some of the rare variants are point mutations likely affecting channel function, but most are predicted to cause protein truncation and thence result, like the common variants, in reduced gene expression. We review the genomic evidence, and the findings from Grin2a mutant mice and other models which give clues as to the likely phenotypic impacts of GRIN2A genetic variation. We suggest that one consequence of NR2A dysfunction is impairment in a form of hippocampal synaptic plasticity, producing deficits in short-term habituation and thence elevated and dysregulated levels of attention, a phenotype of relevance to schizophrenia and its cognitive aspects.
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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.