ReviewSchizophrenia research2020
NMDA receptor hypofunction for schizophrenia revisited: Perspectives from epigenetic mechanisms.
Review in Schizophrenia research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 2 of them syntheses that pooled it.
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.
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
36 citing papers in PubMed, 2 syntheses or guidelines pooled it, 88 citations in OpenAlex.
- Resting-state gamma power in schizophrenia: a systematic review and meta-analysis.Frontiers in psychiatry · 2025Pooled it
- Identifying the differentially expressed peripheral blood microRNAs in psychiatric disorders: a systematic review and meta-analysis.Frontiers in psychiatry · 2024Pooled it
- NMDA receptor ablation in medial prefrontal cortex disrupts value updating and reward history integration.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Aberrant Fear: Biological Underpinnings Relevant to Psychosis, Antipsychotic Drugs, and Psychotherapeutic Treatments, a Translational Approach.International journal of molecular sciences · 2026Review
- 16p11.2 duplication and NMDA receptor antagonism have distinct impacts on reward learning and decision making.Psychopharmacology · 2026Article
- Elucidating the Complex Etiology of Schizophrenia: Comprehensive Insights into the Therapeutic Roles of Natural Compounds and Pharmacological Interventions.Current pharmaceutical design · 2026Review
- Epigenetic and Genotoxic Mechanisms of PFAS-Induced Neurotoxicity: A Molecular and Transgenerational Perspective.Toxics · 2025Review
- 16p11.2 duplication shows early male-biased impacts on reward learning, but NMDA receptor antagonism reduces optimal choice selection in both wildtypes and 16p11.2 duplication.bioRxiv : the preprint server for biology · 2025Article
- Glutamate-Based Therapeutic Strategies for Schizophrenia: Emerging Approaches Beyond Dopamine.International journal of molecular sciences · 2025Review
- Epigenetic Control in Schizophrenia.Sub-cellular biochemistry · 2025Review
- Advances in the Treatment of Cognitive Impairment in Schizophrenia: Targeting NMDA Receptor Pathways.International journal of molecular sciences · 2024Review
- The Underlying Neurobiological Mechanisms of Psychosis: Focus on Neurotransmission Dysregulation, Neuroinflammation, Oxidative Stress, and Mitochondrial Dysfunction.Antioxidants (Basel, Switzerland) · 2024Review
- DNA methylation and the opposing NMDAR dysfunction in schizophrenia and major depression disorders: a converging model for the therapeutic effects of psychedelic compounds in the treatment of psychiatric illness.Molecular psychiatry · 2023Review
- Influence of inter-stimulus interval on 40-Hz auditory steady-state response in patients with schizophrenia.Schizophrenia (Heidelberg, Germany) · 2023Article
- Membrane Lipids in Ultra-High-Risk Patients: Potential Predictive Biomarkers of Conversion to Psychosis.Nutrients · 2023Article
- Herniarin, Dimethylfraxetin and Extracts fromPlants (Basel, Switzerland) · 2022Article
- DRUG-seq Provides Unbiased Biological Activity Readouts for Neuroscience Drug Discovery.ACS chemical biology · 2022Article
- Neurobiological Highlights of Cognitive Impairment in Psychiatric Disorders.International journal of molecular sciences · 2022Review
- Derivatives of (Journal of medicinal chemistry · 2022Article
- Aberrant maturation and connectivity of prefrontal cortex in schizophrenia-contribution of NMDA receptor development and hypofunction.Molecular psychiatry · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Schizophrenia (SZ) is a neurodevelopmental disorder with cognitive deficits manifesting during early stages of the disease. Evidence suggests that genetic factors in combination with environmental insults lead to complex changes to glutamatergic, GABAergic, and dopaminergic systems. In particular, the N-methyl-d-aspartate receptor (NMDAR), a major glutamate receptor subtype, is implicated in both the disease progression and symptoms of SZ. NMDARs are critical for synaptic plasticity and cortical maturation, as well as learning and memory processes. In fact, any deviation from normal NMDAR expression and function can have devastating consequences. Surprisingly, there is little evidence from human patients that direct mutations of NMDAR genes contribute to SZ. One intriguing hypothesis is that epigenetic changes, which could result from early insults, alter protein expression and contribute to the NMDAR hypofunction found in SZ. Epigenetics is referred to as modifications that alter gene transcription without changing the DNA sequence itself. In this review, we first discuss how epigenetic changes to NMDAR genes could contribute to NMDAR hypofunction. We then explore how NMDAR hypofunction may contribute to epigenetic changes in other proteins or genes that lead to synaptic dysfunction and symptoms in SZ. We argue that NMDAR hypofunction occurs in early stage of the disease, and it may consequentially initiate GABA and dopamine deficits. Therefore, targeting NMDAR dysfunction during the early stages would be a promising avenue for prevention and therapeutic intervention of cognitive and social deficits that remain untreatable. Finally, we discuss potential questions regarding the epigenetic of SZ and future directions for research.
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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.