ArticleiScience2024
Multimodal single-cell profiling reveals neuronal vulnerability and pathological cell states in focal cortical dysplasia.
Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Molecular Signature in Focal Cortical Dysplasia: A Systematic Review of RNA and Protein Data.International journal of molecular sciences · 2025Pooled it
- Focal Cortical Dysplasia Type II: Somatic Mutations, Molecular Mechanisms, and Integrative Multi-Omics Framework.CNS neuroscience & therapeutics · 2026Review
- Single-nucleus transcriptomics-based drug screening platform for focal cortical dysplasia.Molecular psychiatry · 2026Article
- A multi-center cross-platform single-cell multimodal atlas of the mouse cerebral cortex.Scientific data · 2026Article
- Single cell protein profiling of focal cortical dysplasia in a patient requiring multiple resections.Acta neuropathologica communications · 2026Article
- From the brain cell atlas to precision neurology: a review of the application of AI-driven multi-omics in brain science.GigaScience · 2026Review
- Integrated Multi-Omics Profiling Identifies CD84-Associated Microglial Alterations in Focal Cortical Dysplasia Type II.Journal of inflammation research · 2026Article
- Seizure occurrence in FCD type II is predicted by lesion position and linked to cytoarchitectural alterations.Acta neuropathologica communications · 2025Article
- Article
- Beyond mTOR: Unraveling the Complex Pathophysiology and Signaling Pathways in Focal Cortical Dysplasia.Molecular neurobiology · 2025Review
- Cell type mapping of mild malformations of cortical development with oligodendroglial hyperplasia in epilepsy using single-nucleus multiomics.Epilepsia · 2025Article
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Focal cortical dysplasia (FCD) is a neurodevelopmental condition characterized by malformations of the cerebral cortex that often cause drug-resistant epilepsy. In this study, we performed multi-omics single-nuclei profiling to map the chromatin accessibility and transcriptome landscapes of FCD type II, generating a comprehensive multimodal single-nuclei dataset comprising 61,525 cells from 11 clinical samples of lesions and controls. Our findings revealed profound chromatin, transcriptomic, and cellular alterations affecting neuronal and glial cells in FCD lesions, including the selective loss of upper-layer excitatory neurons, significant expansion of oligodendrocytes and immature astrocytic populations, and a distinct neuronal subpopulation harboring dysmorphic neurons. Furthermore, we uncovered activated microglia subsets, particularly in FCD IIb cases. This comprehensive study unveils neuronal and glial cell states driving FCD development and epileptogenicity, enhancing our understanding of FCD and offering directions for targeted therapy development.
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Registered trials
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