ReviewSchizophrenia bulletin2012
Has an angel shown the way? Etiological and therapeutic implications of the PCP/NMDA model of schizophrenia.
Review in Schizophrenia bulletin, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 151 papers, 2 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
151 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Treatments for Social Interaction Impairment in Animal Models of Schizophrenia: A Critical Review and Meta-analysis.Schizophrenia bulletin · 2022Pooled it
- Cerebellar stimulation in schizophrenia: A systematic review of the evidence and an overview of the methods.Frontiers in psychiatry · 2022Pooled it
- Validation of ketamine as a pharmacological model of thalamic dysconnectivity across the illness course of schizophrenia.Molecular psychiatry · 2022Trial
- CDP-choline and galantamine, a personalized α7 nicotinic acetylcholine receptor targeted treatment for the modulation of speech MMN indexed deviance detection in healthy volunteers: a pilot study.Psychopharmacology · 2020Trial
- Effects of ketamine on brain function during smooth pursuit eye movements.Human brain mapping · 2016Trial
- 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
- Sex-specific association of IDO1 gene with schizophrenia and imbalanced levels of cytokines and neuroactive kynurenine metabolites in relapsed patients.European archives of psychiatry and clinical neuroscience · 2026Article
- Visual P300 and Risk for Psychosis Onset in Youth at Clinical High Risk.Biological psychiatry · 2026Article
- Targeting beta-2 adrenergic receptor attenuates schizophrenia-like behavioral effects induced by ketamine in mice: cAMP/PKA/BDNF-PEA-3 and RIM-1α signaling pathways involvement.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2026Article
- Theta Oscillations Assessed From a Passive Auditory Oddball Paradigm in Individuals at Clinical High-Risk for Psychosis and Healthy Control Individuals: Associations with Clinical Outcomes and Mismatch Negativity.Biological psychiatry global open science · 2026Article
- Association Between Caffeine Levels and Symptom Profile in Schizophrenia: Results from a Cohort Study in Central Greece.Brain sciences · 2026Article
- Schizophrenia Pathophysiology: Neurotransmitter Dysfunctions and Biomarker Frontiers.Current topics in medicinal chemistry · 2026Review
- Impaired effort allocation in schizophrenia.Schizophrenia research. Cognition · 2025Article
- Concerted elevations of cortical and striatal glutamate and GABA in antipsychotic-free individuals at clinical high-risk for psychosis.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025Article
- Impact of D-Amino Acids in Schizophrenia.Biomolecules · 2025Review
- N-Methyl-d-Aspartate Receptor Antibody and Sensory Gating Deficits in Non-smoking, Minimal Antipsychotic Medication Exposure, and First-Episode Patients With Schizophrenia.Schizophrenia bulletin · 2025Article
- Psychiatric manifestations of encephalitis.Annals of clinical and translational neurology · 2025Article
- A Computational Account of the Development and Evolution of Psychotic Symptoms.Biological psychiatry · 2025Review
- Nicotine's Effects on Schizophrenia-like Symptoms in a Mice Model: Time Matters.Brain sciences · 2024Article
- Article
91 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Over the last 20 years, glutamatergic models of schizophrenia have become increasingly accepted as etiopathological models of schizophrenia, based on the observation that phencyclidine (PCP) induces a schizophrenia-like psychosis by blocking neurotransmission at N-methyl-D-aspartate (NMDA)-type glutamate receptors. This article reviews developments in two key predictions of the model: first, that neurocognitive deficits in schizophrenia should follow the pattern of deficit predicted based on underlying NMDAR dysfunction and, second, that agents that stimulate NMDAR function should be therapeutically beneficial. As opposed to dopamine receptors, NMDAR are widely distributed throughout the brain, including subcortical as well as cortical brain regions, and sensory as well as association cortex. Studies over the past 20 years have documented severe sensory dysfunction in schizophrenia using behavioral, neurophysiological, and functional brain imaging approaches, including impaired generation of key sensory-related potentials such as mismatch negativity and visual P1 potentials. Similar deficits are observed in humans following administration of NMDAR antagonists such as ketamine in either humans or animal models. Sensory dysfunction, in turn, predicts impairments in higher order cognitive functions such as auditory or visual emotion recognition. Treatment studies have been performed with compounds acting directly at the NMDAR glycine site, such as glycine, D-serine, or D-cycloserine, and, more recently, with high-affinity glycine transport inhibitors such as RG1678 (Roche). More limited studies have been performed with compounds targeting the redox site. Overall, these compounds have been found to induce significant beneficial effects on persistent symptoms, suggesting novel approaches for treatment and prevention of schizophrenia.
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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.