ReviewCNS neuroscience & therapeutics2011
Possible role of glia in cognitive impairment in schizophrenia.
Review in CNS neuroscience & therapeutics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis 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
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- The Dual Role of Connexins in Stroke, Neurotrauma, Neurodegenerative and Psychiatric Disorders: A Global Systematic Review.Molecules (Basel, Switzerland) · 2026Pooled it
- Gut dysbiosis leads to cognitive decline through CNTF-mediated activation of microglia in mice.BMC biology · 2025Article
- A review on the relationship between the distal 1q21.1 microdeletion and schizophrenia.Frontiers in genetics · 2025Review
- The Neurobiology of Formal Thought Disorder.Current topics in medicinal chemistry · 2024Review
- Decreased Oligodendrocyte Number in Hippocampal Subfield CA4 in Schizophrenia: A Replication Study.Cells · 2022Article
- Disruption of the astrocyte-neuron interaction is responsible for the impairments in learning and memory in 5XFAD mice: an Alzheimer's disease animal model.Molecular brain · 2021Article
- Alterations of Astrocytes in the Context of Schizophrenic Dementia.Frontiers in pharmacology · 2019Review
- Decreased Oligodendrocyte and Neuron Number in Anterior Hippocampal Areas and the Entire Hippocampus in Schizophrenia: A Stereological Postmortem Study.Schizophrenia bulletin · 2016Article
- Oligodendrocyte and Interneuron Density in Hippocampal Subfields in Schizophrenia and Association of Oligodendrocyte Number with Cognitive Deficits.Frontiers in cellular neuroscience · 2016Article
- S100B is downregulated in the nuclear proteome of schizophrenia corpus callosum.European archives of psychiatry and clinical neuroscience · 2014Article
- Neuropathological changes in the substantia nigra in schizophrenia but not depression.European archives of psychiatry and clinical neuroscience · 2014Article
- Engram formation in psychiatric disorders.Frontiers in neuroscience · 2014Review
- The impact of environmental factors in severe psychiatric disorders.Frontiers in neuroscience · 2014Review
- Glia and mast cells as targets for palmitoylethanolamide, an anti-inflammatory and neuroprotective lipid mediator.Molecular neurobiology · 2013Review
- Intracellular ion channel CLIC1: involvement in microglia-mediated β-amyloid peptide(1-42) neurotoxicity.Neurochemical research · 2013Article
- Mast cell-glia axis in neuroinflammation and therapeutic potential of the anandamide congener palmitoylethanolamide.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cognitive impairment is a core disorder of the schizophrenia syndrome. Based on glial-neuronal interactions, a pathophysiological model is proposed that could be explanatory for cognitive impairment in schizophrenia. The model consists of three main hypotheses concerning the pathophysiology in tripartite synapses, oligodendrocyte-axonic interactions, and in the glial networks (astrocytic syncytium). In tripartite synapses nonfunctional astrocytic receptors may cause an unconstrained synaptic information flux, since they cannot be occupied by neurotransmitters (NTs). Therefore, a generalization of information processing may occur in the brain causing hallucinations, delusions, and thought disorder. If the oligodendrocyte-axonic system decomposes, the brain is unable to process information in qualitative domains or categories. This may lead to severe incoherence phenomena such as thought disorder. Supposing that in the astrocytic syncytium gap junctions (g.js) normally form plaques functioning as memory devices, loss of function of g.j. may also cause cognitive impairment, since the syncytium decomposes and g.j. plaques cannot be generated. These hypotheses are experimentally testable. Finally, the problem of treatment of patients with schizophrenia is discussed, in case the presented model of schizophrenia might be verified.
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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.