ArticlePsychopharmacology2015
Pharmacogenetic associations of the type-3 metabotropic glutamate receptor (GRM3) gene with working memory and clinical symptom response to antipsychotics in first-episode schizophrenia.
Article in Psychopharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 3 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
27 citing papers in PubMed, 3 syntheses or guidelines pooled it, 53 citations in OpenAlex.
- Association Between the COMT Val158Met Polymorphism and Antipsychotic Efficacy in Schizophrenia: An Updated Meta-Analysis.Current neuropharmacology · 2021Pooled it
- Meta-analysis supports GWAS-implicated link between GRM3 and schizophrenia risk.Translational psychiatry · 2017Pooled it
- Catechol-O-Methyltransferase Val158Met Polymorphism and Clinical Response to Antipsychotic Treatment in Schizophrenia and Schizo-Affective Disorder Patients: a Meta-Analysis.The international journal of neuropsychopharmacology · 2016Pooled it
- Response to initial antipsychotic treatment in first episode psychosis is related to anterior cingulate glutamate levels: a multicentreMolecular psychiatry · 2018Trial
- Post-methamphetamine working memory decline predicts relapse vulnerability in rats and is rescued by mGlu3 receptor activation.Psychopharmacology · 2026Article
- Inhibition of brain glutamate carboxypeptidase II (GCPII) to enhance cognitive function.Advances in pharmacology (San Diego, Calif.) · 2025Review
- Resolving transitions between distinct phases of memory consolidation at high resolution iniScience · 2024Article
- Activation of Metabotropic Glutamate Receptor 3 Modulates Thalamo-accumbal Transmission and Rescues Schizophrenia-Like Physiological and Behavioral Deficits.Biological psychiatry · 2024Article
- Clinical Utility and Implementation of Pharmacogenomics for the Personalisation of Antipsychotic Treatments.Pharmaceutics · 2024Review
- Genetic variation in glutamatergic genes moderates the effects of childhood adversity on brain volume and IQ in treatment-resistant schizophrenia.Schizophrenia (Heidelberg, Germany) · 2023Article
- Gene Expressions Preferentially Influence Cortical Thickness of Human Connectome Project Atlas Parcellated Regions in First-Episode Antipsychotic-Naïve Psychoses.Schizophrenia bulletin open · 2023Article
- Metabotropic glutamate receptor 3 as a potential therapeutic target for psychiatric and neurological disorders.Pharmacology, biochemistry, and behavior · 2022Review
- Metabotropic Glutamate Receptors As Emerging Targets for the Treatment of Schizophrenia.Molecular pharmacology · 2022Review
- Peripheral biomarkers of treatment-resistant schizophrenia: Genetic, inflammation and stress perspectives.Frontiers in pharmacology · 2022Review
- Pharmacogenetics of Antipsychotic Treatment in Schizophrenia.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Pharmacogenetics of Antipsychotic Drug Treatment: Update and Clinical Implications.Molecular neuropsychiatry · 2020Review
- A longitudinal magnetic resonance spectroscopy study investigating effects of risperidone in the anterior cingulate cortex and hippocampus in schizophrenia.Schizophrenia research · 2019Article
- A role for N-acetylaspartylglutamate (NAAG) and mGluR3 in cognition.Neurobiology of learning and memory · 2019Review
- Treatment-Resistant Schizophrenia: Genetic and Neuroimaging Correlates.Frontiers in pharmacology · 2019Review
- The use of pharmacogenetic testing in patients with schizophrenia or bipolar disorder: A systematic review.The mental health clinician · 2018Article
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 7 institutions in 1 country.
Funding
Abstract
rationaleType-3 metabotropic glutamate receptor gene (GRM3) single nucleotide polymorphisms (SNPs) have been associated with cognitive performance and prefrontal cortex brain activity in chronically treated schizophrenia patients. Whether these SNPs are associated with cognitive and symptom response to antipsychotic therapy has not been extensively evaluated.
objectivesThe aim of the study was to examine pharmacogenetic relationships between GRM3 and selected variants in relevant dopamine genes with changes in spatial working memory and clinical symptoms after treatment.
methodsSixty-one untreated first-episode schizophrenia patients were assessed before and after 6 weeks of antipsychotic pharmacotherapy, primarily consisting of risperidone. Patients' level of cognitive performance on a spatial working memory task was assessed with a translational oculomotor paradigm. Changes after treatment in cognitive and clinical measures were examined in relationship to genetic polymorphisms in the GRM3, COMT, and DRD2/ANKK1 gene regions.
resultsSpatial working memory performance worsened after antipsychotic treatment. This worsening was associated with GRM3 rs1468412, with the genetic subgroup of patients known to have altered glutamate activity having greater adverse changes in working memory performance after antipsychotic treatment. Negative symptom improvement was associated with GRM3 rs6465084. There were no pharmacogenetic associations between DRD2/ANKK1 and COMT with working memory changes or symptom response to treatment.
conclusionsThese findings suggest important pharmacogenetic relationships between GRM3 variants and changes in cognition and symptom response with exposure to antipsychotics. This information may be useful in identifying patients susceptible to adverse cognitive outcomes associated with antipsychotic treatment and suggest that glutamatergic mechanisms contribute to such effects.
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.