ArticleNeuron2025
Forebrain assembloids support the development of fast-spiking human PVALB+ cortical interneurons and uncover schizophrenia-associated defects.
Article in Neuron, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed.
- Modeling Epilepsies with Human Brain Organoids: Recent Advances and Ongoing Challenges.Epilepsy currents · 2026Review
- Article
- Establishing mouse forebrain organoids as models of intrinsic cortical network assembly.Stem cell reports · 2026Article
- Mechanistic Target of Rapamycin and Megalencephaly: Novel Research Strategies for Therapeutic Discovery.Epilepsy currents · 2026Article
- A distinct lineage pathway drives parvalbumin chandelier cell fate in human interneuron reprogramming.Science advances · 2026Article
- Focal cortical dysplasias: modeling pediatric drug-resistant epilepsy using human brain organoids.Frontiers in cellular neuroscience · 2026Review
- Towards learning and memory risk assessment with human brain organoids: barriers and opportunities.Frontiers in toxicology · 2026Review
- Recreating the human brain: Are assembloids merely descriptive models?Frontiers in cellular neuroscience · 2026Review
- Association Between Frontotemporal Atrophy and Cognitive Impairment in Patients with Schizophrenia Based on Computed Tomography Imaging.Neuropsychiatric disease and treatment · 2026Article
- Aberrant pace of cortical neuron development in brain organoids from patients with 22q11.2 deletion syndrome-associated schizophrenia.Nature communications · 2025Article
- Fate plasticity of interneuron specification.iScience · 2025Article
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Abstract
Disruption of parvalbumin positive (PVALB+) cortical interneurons is implicated in the pathogenesis of schizophrenia. However, how these defects emerge during development remains poorly understood. The protracted, postnatal maturation of PVALB+ cortical interneurons has complicated human pluripotent stem cell (hPSC)-based models for studying their role in neuropsychiatric disease. Here, we present a forebrain assembloid system yielding PVALB+ cortical interneurons that match the molecular identity and distinctive electrophysiology of primary PVALB+ interneurons. We further established a series of isogenic hPSC lines carrying structural variants associated with schizophrenia and identified variant-specific phenotypes affecting cortical interneuron migration, the molecular profile of PVALB+ cortical interneurons, and their ability to regulate cortical network activity, including γ-band oscillations. These findings offer plausible mechanisms for how the disruption of cortical interneuron development may impact schizophrenia risk and provide a human experimental platform to study PVALB+ cortical interneurons in health and disease.
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