ArticleNature neuroscience2019
Dysregulated protocadherin-pathway activity as an intrinsic defect in induced pluripotent stem cell-derived cortical interneurons from subjects with schizophrenia.
Article in Nature neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
72 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Building on a Solid Foundation: Adding Relevance and Reproducibility to Neurological Modeling Using Human Pluripotent Stem Cells.Frontiers in cellular neuroscience · 2021Pooled it
- Advancements in differentiation of induced pluripotent stem cells into specialized neuronal subtypes.Neural regeneration research · 2026Article
- Gestational Hypoxia Disrupts Medial Ganglionic Eminence Progenitor Dynamics and Interneuron Development in Schizophrenia.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Convergence of schizophrenia risk genes on CALN1 disrupts human forebrain development and drives core psychotic behaviors including hallucination-like perception.BMC medicine · 2026Article
- Global transcriptional changes across multiple isogeniciScience · 2026Article
- Hyperdynamic microtubule-based structural changes in Monocyte-Derived-Neuronal-like cells from patients with schizophrenia.Schizophrenia (Heidelberg, Germany) · 2026Article
- DNA methylation signatures of treatment response in medication-overuse headache.The journal of headache and pain · 2026Observational
- Dysregulation of the BRD2-FGF17 Signal Pathway Induces Abnormal Forebrain Development Associated with Schizophrenia.Neuroscience bulletin · 2026Article
- Protocadherin γC4 regulates neuronal survival and dendritic self-avoidance.Communications biology · 2026Article
- A Pilot Epigenome-Wide Study of Posttraumatic Growth: Identifying Novel Candidates for Future Research.Epigenomes · 2025Article
- Molecular and developmental deficits in Smith-Magenis syndrome human stem cell-derived cortical neural models.American journal of human genetics · 2025Article
- Diversity of clustered protocadherin-α genes in neuronal identity and its role in short-term specific associative memory formation.Scientific reports · 2025Article
- Article
- Cell Adhesion Molecule Protocadherin-γC5 Ameliorates Aβ Plaque Pathogenesis by Modulating Astrocyte Function in Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Review
- Probing the molecular and cellular pathological mechanisms of schizophrenia using human induced pluripotent stem cell models.Schizophrenia research · 2024Review
- Human stem cell-based models to study synaptic dysfunction and cognition in schizophrenia: A narrative review.Schizophrenia research · 2024Review
- Modeling common and rare genetic risk factors of neuropsychiatric disorders in human induced pluripotent stem cells.Schizophrenia research · 2024Review
- Characterization of transcriptional profiles associated with stress-induced neuronal activation in Arc-GFP mice.Molecular psychiatry · 2024Article
- Induced pluripotent stem cells (iPSCs): molecular mechanisms of induction and applications.Signal transduction and targeted therapy · 2024Review
12 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
37 authors.
Funding
Abstract
We generated cortical interneurons (cINs) from induced pluripotent stem cells derived from 14 healthy controls and 14 subjects with schizophrenia. Both healthy control cINs and schizophrenia cINs were authentic, fired spontaneously, received functional excitatory inputs from host neurons, and induced GABA-mediated inhibition in host neurons in vivo. However, schizophrenia cINs had dysregulated expression of protocadherin genes, which lie within documented schizophrenia loci. Mice lacking protocadherin-α showed defective arborization and synaptic density of prefrontal cortex cINs and behavioral abnormalities. Schizophrenia cINs similarly showed defects in synaptic density and arborization that were reversed by inhibitors of protein kinase C, a downstream kinase in the protocadherin pathway. These findings reveal an intrinsic abnormality in schizophrenia cINs in the absence of any circuit-driven pathology. They also demonstrate the utility of homogenous and functional populations of a relevant neuronal subtype for probing pathogenesis mechanisms during development.
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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 Socratic graph.