ArticleClinical and translational medicine2026
Excitatory neurons and astrocytes-specific dysregulation and aberrant interactions are vulnerable to FCDI as suggested by single-cell spatial transcriptomics.
Article in Clinical and translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundFocal cortical dysplasia (FCD) is a common neurodevelopmental disorder characterised by cortical malformations and is a major cause of drug-resistant epilepsy. FCD type I (FCDI) presents with architectural abnormalities of the neocortex but without cytological abnormalities. Currently, FCDI remains a significant clinical challenge.
methodsEpileptogenic cortical tissues from three FCDI patients and three relatively normal neocortical tissues as controls were analysed using single-nucleus RNA sequencing and spatial transcriptomic for multi-omics integration.
resultsThis study constructed a single-cell spatial transcriptomic atlas of the epileptogenic cortex from FCDI patients. Excitatory neurons (ENs) and astrocytes (Ast) exhibited the most prominent alterations in FCDI. Hub genes associated with FCDI were identified in ENs, and a transcription factor (TF)‒hub gene regulatory network was constructed. Notably, CBLN2
conclusionsThis study highlights the specific dysregulation of ENs and Ast, along with aberrant cellular communication, which may play a critical role in the pathogenesis of FCDI. These findings provide novel insights into the molecular mechanisms underlying FCDI and offer potential therapeutic targets for precision treatment and drug development.
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