SynthesisSchizophrenia bulletin2015
Glutamate Networks Implicate Cognitive Impairments in Schizophrenia: Genome-Wide Association Studies of 52 Cognitive Phenotypes.
Synthesis in Schizophrenia bulletin, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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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
43 citing papers in PubMed, 81 citations in OpenAlex.
- Effects of Augmenting N-Methyl-D-Aspartate Receptor Signaling on Working Memory and Experience-Dependent Plasticity in Schizophrenia: An Exploratory Study Using Acute d-cycloserine.Schizophrenia bulletin · 2017Trial
- Synaptic dysfunction and adaptation after NMDA receptor ablation in the mouse medial prefrontal cortex.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Modulation of glycine transporters as a novel therapeutic strategy in neuropsychiatry.Psychopharmacology · 2026Review
- SNP-based prediction of schizophrenia using machine learning.Bioinformatics advances · 2026Article
- Topoisomerase 3b facilitates piRNA biogenesis to promote transposon silencing and germ cell development.Cell reports · 2025Article
- Therapeutic potential of D-amino acid oxidase inhibitors for cognitive impairment associated with schizophrenia: learnings from luvadaxistat.The international journal of neuropsychopharmacology · 2024Review
- Association of neurotransmitter pathway polygenic risk with specific symptom profiles in psychosis.Molecular psychiatry · 2024Article
- Tdrd3-null mice show post-transcriptional and behavioral impairments associated with neurogenesis and synaptic plasticity.Progress in neurobiology · 2024Article
- Pharmacological Treatment of Cognitive Impairment Associated With Schizophrenia: State of the Art and Future Perspectives.Schizophrenia bulletin open · 2024Article
- Association of neurotransmitter pathway polygenic risk with specific symptom profiles in psychosis.medRxiv : the preprint server for health sciences · 2023Article
- Tdrd3-null mice show post-transcriptional and behavioral impairments associated with neurogenesis and synaptic plasticity.Research square · 2023Article
- A role for endothelial NMDA receptors in the pathophysiology of schizophrenia.Schizophrenia research · 2022Review
- Beyond NMDA Receptors: Homeostasis at the Glutamate Tripartite Synapse and Its Contributions to Cognitive Dysfunction in Schizophrenia.International journal of molecular sciences · 2022Review
- Machine Learning algorithm unveils glutamatergic alterations in the post-mortem schizophrenia brain.Schizophrenia (Heidelberg, Germany) · 2022Article
- Encore: Behavioural animal models of stress, depression and mood disorders.Frontiers in behavioral neuroscience · 2022Review
- Neuroimaging studies within Cognitive Genetics Collaborative Research Organization aiming to replicate and extend works of ENIGMA.Human brain mapping · 2022Review
- Cognitive impairment in psychiatric diseases: Biomarkers of diagnosis, treatment, and prevention.Frontiers in cellular neuroscience · 2022Review
- Eye movement characteristics in male patients with deficit and non-deficit schizophrenia and their relationships with psychiatric symptoms and cognitive function.BMC neuroscience · 2021Article
- Control of protein synthesis and memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly.eLife · 2021Article
- Polygenic Risk Scores Differentiating Schizophrenia From Bipolar Disorder Are Associated With Premorbid Intelligence in Schizophrenia Patients and Healthy Subjects.The international journal of neuropsychopharmacology · 2021Article
Corrections and comments
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Authors and funding
15 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cognitive impairments are a core feature in patients with schizophrenia. These deficits could serve as effective tools for understanding the genetic architecture of schizophrenia. This study investigated whether genetic variants associated with cognitive impairments aggregate in functional gene networks related to the pathogenesis of schizophrenia. Here, genome-wide association studies (GWAS) of a range of cognitive phenotypes relevant to schizophrenia were performed in 411 healthy subjects. We attempted to replicate the GWAS data using 257 patients with schizophrenia and performed a meta-analysis of the GWAS findings and the replicated results. Because gene networks, rather than a single gene or genetic variant, may be strongly associated with the susceptibility to schizophrenia and cognitive impairments, gene-network analysis for genes in close proximity to the replicated variants was performed. We observed nominal associations between 3054 variants and cognitive phenotypes at a threshold of P < 1.0 × 10(-) (4). Of the 3054 variants, the associations of 191 variants were replicated in the replication samples (P < .05). However, no variants achieved genome-wide significance in a meta-analysis (P > 5.0 × 10(-) (8)). Additionally, 115 of 191 replicated single nucleotide polymorphisms (SNPs) have genes located within 10 kb of the SNPs (60.2%). These variants were moderately associated with cognitive phenotypes that ranged from P = 2.50 × 10(-) (5) to P = 9.40 × 10(-) (8). The genes located within 10 kb from the replicated SNPs were significantly grouped in terms of glutamate receptor activity (false discovery rate (FDR) q = 4.49 × 10(-) (17)) and the immune system related to major histocompatibility complex class I (FDR q = 8.76 × 10(-) (11)) networks. Our findings demonstrate that genetic variants related to cognitive trait impairment in schizophrenia are involved in the N-methyl-d-aspartate glutamate network.
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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.