ArticleFrontiers in cellular neuroscience2013
NMDA hypofunction as a convergence point for progression and symptoms of schizophrenia.
Article in Frontiers in cellular neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers, 1 of them a synthesis that pooled it.
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Who cites it
125 citing papers in PubMed, 1 synthesis or guideline pooled it, 237 citations in OpenAlex.
- A Systematic Review of the Effects of N-Methyl-D-Aspartate Receptor Antagonists on Pancreatic Islets.Neuroendocrinology · 2026Pooled it
- Effects of NMDA-receptor blockade by ketamine on mentalizing and its neural correlates in humans: a randomized control trial.Scientific reports · 2023Trial
- Effect of Damaging Rare Mutations in Synapse-Related Gene Sets on Response to Short-term Antipsychotic Medication in Chinese Patients With Schizophrenia: A Randomized Clinical Trial.JAMA psychiatry · 2018Trial
- Convergent multidimensional neural phenotypes in human patients and schizophrenia-relevant mouse models identify reduced recurrent excitation in cortical circuits.medRxiv : the preprint server for health sciences · 2026Article
- Restoring Synaptic Balance in Schizophrenia: Insights From a Thalamo-Cortical Conductance-Based Model.Schizophrenia bulletin · 2026Article
- The curious absence of psychosis in GRIN1-related neurodevelopmental disorder.European archives of psychiatry and clinical neuroscience · 2025Article
- Unraveling the mysteries of schizophrenia: Insights into prefrontal cortex dysfunction and therapeutic implications.World journal of psychiatry · 2025Review
- Mismatch Negativity in Subjects at Clinical High Risk for Psychosis: No Evidence of Progressive Decline.The European journal of neuroscience · 2025Article
- Targeting the Roots of Psychosis: The Role of Aberrant Salience.Pediatric reports · 2025Review
- Genetic Diversity in Schizophrenia: Developmental Implications of Ultra-Rare, Protein-Truncating Mutations.Genes · 2024Review
- A neural modeling approach to study mechanisms underlying the heterogeneity of visual spatial frequency sensitivity in schizophrenia.Schizophrenia (Heidelberg, Germany) · 2024Article
- Exploring the interplay of chronic toxoplasmosis and NMDAR dysfunction: Insights into schizophrenia-like behaviors and therapeutic potential.Open veterinary journal · 2024Article
- Focused Ultrasound Stimulates the Prefrontal Cortex and Prevents MK-801-Induced Psychiatric Symptoms of Schizophrenia in Rats.Schizophrenia bulletin · 2024Article
- Ketamine modulates disrupted in schizophrenia-1/glycogen synthase kinase-3β interaction.Frontiers in molecular neuroscience · 2024Article
- Activity of Protein Kinase A in the Frontal Cortex in Schizophrenia.Brain sciences · 2023Article
- A neural modeling approach to study mechanisms underlying the heterogeneity of visual spatial frequency sensitivity in schizophrenia.bioRxiv : the preprint server for biology · 2023Article
- Treatment resistance NMDA receptor pathway polygenic score is associated with brain glutamate in schizophrenia.Schizophrenia research · 2023Article
- Potential Roles for the GluN2D NMDA Receptor Subunit in Schizophrenia.International journal of molecular sciences · 2023Review
- Inhibition of Prolyl Oligopeptidase Restores Prohibitin 2 Levels in Psychosis Models: Relationship to Cognitive Deficits in Schizophrenia.International journal of molecular sciences · 2023Article
- In Silico and In Vitro Screening of Serine Racemase Agonist and In Vivo Efficacy on Alzheimer's DiseasePharmaceuticals (Basel, Switzerland) · 2023Article
65 more citing papers are in PubMed but not listed here.
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2 authors at 1 institution in 1 country.
Funding
Abstract
Schizophrenia is a disabling mental illness that is now recognized as a neurodevelopmental disorder. It is likely that genetic risk factors interact with environmental perturbations to affect normal brain development and that this altered trajectory results in a combination of positive, negative, and cognitive symptoms. Although the exact pathophysiology of schizophrenia is unknown, the N-methyl-D-aspartate receptor (NMDAR), a major glutamate receptor subtype, has received great attention. Proper expression and regulation of NMDARs in the brain is critical for learning and memory processes as well as cortical plasticity and maturation. Evidence from both animal models and human studies implicates a dysfunction of NMDARs both in disease progression and symptoms of schizophrenia. Furthermore, mutations in many of the known genetic risk factors for schizophrenia suggest that NMDAR hypofunction is a convergence point for schizophrenia. In this review, we discuss how disrupted NMDAR function leads to altered neurodevelopment that may contribute to the progression and development of symptoms for schizophrenia, particularly cognitive deficits. We review the shared signaling pathways among the schizophrenia susceptibility genes DISC1, neuregulin1, and dysbindin, focusing on the AKT/GSK3β pathway, and how their mutations and interactions can lead to NMDAR dysfunction during development. Additionally, we explore what open questions remain and suggest where schizophrenia research needs to move in order to provide mechanistic insight into the cause of NMDAR dysfunction, as well as generate possible new avenues for therapeutic intervention.
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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.