ArticleMolecular psychiatry2022
Pathological oligodendrocyte precursor cells revealed in human schizophrenic brains and trigger schizophrenia-like behaviors and synaptic defects in genetic animal model.
Article in Molecular psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 60 citations in OpenAlex.
- Review
- Article
- CRP Deficiency Rescues Periodontitis-Induced Hippocampal Neurogenesis Impairment by Suppressing OPC-Derived BMP4 Signaling in Rats.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Serum Levels of Wnt/β-catenin Pathway Regulators Dkk-1, PORCN, Notum, and Tiki-1 in Children with Autism Spectrum Disorder.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2026Article
- Glutamate Delta 1 Receptor in Synapses, Circuits, and Disease.The European journal of neuroscience · 2026Review
- Dual phosphorylation of DISC1 at Ser58 and Ser713 regulates polarization of cortical neurons via GSK3β.Science China. Life sciences · 2026Article
- Effects of troxerutin on schizophrenia-like behaviors and oxidative damage in mice.Current research in physiology · 2026Article
- From synapse to sheath: how OPCs couple neural activity to adaptive myelination and behavioral plasticity.Frontiers in cell and developmental biology · 2026Review
- Chromatin remodeling factor BAF155 coordinates oligodendroglial-neuronal communications linked to regional myelination and autism-like behavioral deficits in mice.Nature communications · 2025Article
- Impaired macroautophagy in oligodendrocyte precursor cells suppresses neuronal plasticity via a senescence-associated signaling.Science advances · 2025Article
- iPSC-modelling reveals genetic associations and morphological alterations of oligodendrocytes in schizophrenia.Translational psychiatry · 2025Article
- Aberrant Modular Dynamics of Functional Networks in Schizophrenia and Their Relationship With Neurotransmitter and Gene Expression Profiles.Human brain mapping · 2025Article
- Myelin dysfunction in aging and brain disorders: mechanisms and therapeutic opportunities.Molecular neurodegeneration · 2025Review
- An Efficient Electroporation Protocol Supporting In Vitro Studies of Oligodendrocyte Biology.Methods and protocols · 2025Article
- Psychiatric Implications of Genetic Variations in Oligodendrocytes: Insights from hiPSC Models.Life (Basel, Switzerland) · 2025Review
- Quantitative magnetization transfer and g-ratio imaging of white matter myelin in early psychotic spectrum disorders.Molecular psychiatry · 2025Article
- Canonical and non-canonical roles of oligodendrocyte precursor cells in mental disorders.Npj mental health research · 2025Review
- Glial cell deficits are a key feature of schizophrenia: implications for neuronal circuit maintenance and histological differentiation from classical neurodegeneration.Molecular psychiatry · 2025Review
- Role of Glial Cells and Receptors in Schizophrenia Pathogenesis.Neurochemical research · 2025Review
- Oligodendroglia and Myelin: Supporting the Connectome.Advances in neurobiology · 2025Review
Corrections and comments
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Authors and funding
18 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although the link of white matter to pathophysiology of schizophrenia is documented, loss of myelin is not detected in patients at the early stages of the disease, suggesting that pathological evolution of schizophrenia may occur before significant myelin loss. Disrupted-in-schizophrenia-1 (DISC1) protein is highly expressed in oligodendrocyte precursor cells (OPCs) and regulates their maturation. Recently, DISC1-Δ3, a major DISC1 variant that lacks exon 3, has been identified in schizophrenia patients, although its pathological significance remains unknown. In this study, we detected in schizophrenia patients a previously unidentified pathological phenotype of OPCs exhibiting excessive branching. We replicated this phenotype by generating a mouse strain expressing DISC1-Δ3 gene in OPCs. We further demonstrated that pathological OPCs, rather than myelin defects, drive the onset of schizophrenic phenotype by hyperactivating OPCs' Wnt/β-catenin pathway, which consequently upregulates Wnt Inhibitory Factor 1 (Wif1), leading to the aberrant synaptic formation and neuronal activity. Suppressing Wif1 in OPCs rescues synaptic loss and behavioral disorders in DISC1-Δ3 mice. Our findings reveal the pathogenetic role of OPC-specific DISC1-Δ3 variant in the onset of schizophrenia and highlight the therapeutic potential of Wif1 as an alternative target for the treatment of this disease.
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