ArticleCommunications biology2023
Regulation of synaptic connectivity in schizophrenia spectrum by mutual neuron-microglia interaction.
Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Multi-Trait Genetic Insights Into Schizophrenia Across Ancestries: Genome-Wide Association Meta-Analyses, Machine Learning, and Drug Repurposing Study.Brain and behavior · 2026Pooled it
- Microglia and neuroinflammation: An in-depth analysis from functional diversity to disease mechanisms.Clinical and translational medicine · 2026Review
- The NLRP3 inflammasome: pathophysiology and therapeutic implications for schizophrenia and neuropsychiatric disorders.Molecular psychiatry · 2026Review
- A co-culture model of dopaminergic and glutamatergic neurons derived from patients with idiopathic schizophrenia reveals a hypodopaminergic phenotype.Molecular psychiatry · 2026Article
- The NLRP3 Inflammasome in Neuropsychiatric Disorders: Molecular Mechanisms and Emerging Therapeutic Strategies.International journal of molecular sciences · 2026Review
- Defining functional states and roles of microglia in neuropsychiatric disorders.Frontiers in cellular neuroscience · 2026Review
- Blood‑brain barrier dysfunction in schizophrenia: Mechanisms and implications (Review).International journal of molecular medicine · 2025Review
- Role of Glial Trace Amine Associated Receptor 1 (TAAR1) and Microbiota in Schizophrenia.Neurochemical research · 2025Review
- Key regions aberrantly connected within cerebello-thalamo-cortical circuit and their genetic mechanism in schizophrenia: an fMRI meta-analysis and transcriptome study.Schizophrenia (Heidelberg, Germany) · 2025Review
- Proteomic insights into the biology of dopaminergic neurons.Frontiers in molecular neuroscience · 2025Review
- The Role of Neuroglia in the Development and Progression of Schizophrenia.Biomolecules · 2024Review
- Harnessing stem cell-based approaches for clinically meaningful discoveries in schizophrenia.Schizophrenia research · 2024Article
- Patient iPSC-derived neural progenitor cells display aberrant cell cycle control, p53, and DNA damage response protein expression in schizophrenia.BMC psychiatry · 2024Article
- Genetic contribution to microglial activation in schizophrenia.Molecular psychiatry · 2024Article
- Unlocking the Therapeutic Potential of Exosomes Derived From Nasal Olfactory Mucosal Mesenchymal Stem Cells: Restoring Synaptic Plasticity, Neurogenesis, and Neuroinflammation in Schizophrenia.Schizophrenia bulletin · 2024Article
- Regulation of Zbp1 by miR-99b-5p in microglia controls the development of schizophrenia-like symptoms in mice.The EMBO journal · 2024Article
- Increased NLRP1 mRNA and Protein Expression Suggests Inflammasome Activation in the Dorsolateral Prefrontal and Medial Orbitofrontal Cortex in Schizophrenia.Biomolecules · 2024Article
- Glial modulation of synapse development and plasticity: oligodendrocyte precursor cells as a new player in the synaptic quintet.Frontiers in cell and developmental biology · 2024Review
- Microglia-neuron interactions in schizophrenia.Frontiers in cellular neuroscience · 2024Review
- Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The examination of post-mortem brain tissue suggests synaptic loss as a central pathological hallmark of schizophrenia spectrum (SCZ), which is potentially related to activated microglia and increased inflammation. Induced pluripotent stem cells serve as a source for neurons and microglia-like cells to address neuron-microglia interactions. Here, we present a co-culture model of neurons and microglia, both of human origin, to show increased susceptibility of neurons to microglia-like cells derived from SCZ patients. Analysis of IBA-1 expression, NFκB signaling, transcription of inflammasome-related genes, and caspase-1 activation shows that enhanced, intrinsic inflammasome activation in patient-derived microglia exacerbates neuronal deficits such as synaptic loss in SCZ. Anti-inflammatory pretreatment of microglia with minocycline specifically rescued aberrant synapse loss in SCZ and reduced microglial activation. These findings open up possibilities for further research in larger cohorts, focused clinical work and longitudinal studies that could facilitate earlier therapeutic intervention.
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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.