ArticleTranslational psychiatry2019
Synaptic deficits in iPSC-derived cortical interneurons in schizophrenia are mediated by NLGN2 and rescued by N-acetylcysteine.
Article in Translational psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.
- Integrating cell-type-specific gene expression and genome-wide associations identifies risk genes for schizophrenia.Molecular psychiatry · 2026Pooled it
- Alogliptin Reduces Oxidative Stress in Cardiomyocytes and Ameliorates Diabetic Cardiomyopathy via the AURKB/NLGN2 Signaling.The Kaohsiung journal of medical sciences · 2026Article
- Joint analysis ofNAR genomics and bioinformatics · 2025Article
- Molecular Signatures of Schizophrenia and Insights into Potential Biological Convergence.International journal of molecular sciences · 2025Review
- The antioxidant N-acetylcysteine prevents cortical neuropathological phenotypes caused by adolescent Δ-9-tetrahydrocannabinol exposure in male rats.Translational psychiatry · 2025Article
- Machine learning-enabled detection of electrophysiological signatures in iPSC-derived models of schizophrenia and bipolar disorder.APL bioengineering · 2025Article
- Effects of Complex I Inhibition on the Architecture of Neural Rosettes Differentiated from Human-Induced Pluripotent Stem Cells.Stem cells and development · 2025Article
- Model systems for emulating human tissue and physiology in psychiatric research.Frontiers in neuroscience · 2025Review
- Temporal Effects of Disease Signature Genes and Core Mechanisms in the Hyperacute Phase of Acute Ischemic Stroke: A Bioinformatics Analysis and Experimental Validation.Mediators of inflammation · 2025Article
- Human stem cell-based models to study synaptic dysfunction and cognition in schizophrenia: A narrative review.Schizophrenia research · 2024Review
- Probing the molecular and cellular pathological mechanisms of schizophrenia using human induced pluripotent stem cell models.Schizophrenia research · 2024Review
- Functional Neuroligin-2-MDGA1 interactions differentially regulate synaptic GABACommunications biology · 2024Article
- Induced pluripotent stem cells (iPSCs): molecular mechanisms of induction and applications.Signal transduction and targeted therapy · 2024Review
- The role of cell adhesion molecule IgSF9b at the inhibitory synapse and psychiatric disease.Neuroscience and biobehavioral reviews · 2024Review
- Advances and Applications of Brain Organoids.Neuroscience bulletin · 2023Review
- Brain microvascular endothelial cells and blood-brain barrier dysfunction in psychotic disorders.Molecular psychiatry · 2023Article
- Morphological and transcriptomic analyses of stem cell-derived cortical neurons reveal mechanisms underlying synaptic dysfunction in schizophrenia.Genome medicine · 2023Article
- The synaptic hypothesis of schizophrenia version III: a master mechanism.Molecular psychiatry · 2023Review
- Opioid induces increased DNA damage in prefrontal cortex and nucleus accumbens.Pharmacology, biochemistry, and behavior · 2023Article
- Disease-specific differences in gene expression, mitochondrial function and mitochondria-endoplasmic reticulum interactions in iPSC-derived cerebral organoids and cortical neurons in schizophrenia and bipolar disorder.Discover mental health · 2023Article
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Human postmortem studies suggest a major role for abnormalities in GABAergic interneurons in the prefrontal cortex in schizophrenia. Cortical interneurons differentiated from induced pluripotent stem cells (iPSCs) of schizophrenia subjects showed significantly lower levels of glutamate decarboxylase 67 (GAD67), replicating findings from multiple postmortem studies, as well as reduced levels of synaptic proteins gehpyrin and NLGN2. Co-cultures of the interneurons with excitatory cortical pyramidal neurons from schizophrenia iPSCs showed reduced synaptic puncta density and lower action potential frequency. NLGN2 overexpression in schizophrenia neurons rescued synaptic puncta deficits while NLGN2 knockdown in healthy neurons resulted in reduced synaptic puncta density. Schizophrenia interneurons also had significantly smaller nuclear area, suggesting an innate oxidative stressed state. The antioxidant N-acetylcysteine increased the nuclear area in schizophrenia interneurons, increased NLGN2 expression and rescued synaptic deficits. These results implicate specific deficiencies in the synaptic machinery in cortical interneurons as critical regulators of synaptic connections in schizophrenia and point to a nexus between oxidative stress and NLGN2 expression in mediating synaptic deficits in schizophrenia.
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