ArticleMetabolic brain disease2024
Identification and verification of key molecules in the epileptogenic process of focal cortical dysplasia.
Article in Metabolic brain disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Identification of Novel Biomarkers of Bacterial Lipopolysaccharides in Diabetic Nephropathy via Transcriptomics and Mendelian Randomization.Current gene therapy · 2026Article
- Integrated Multi-Omics Profiling Identifies CD84-Associated Microglial Alterations in Focal Cortical Dysplasia Type II.Journal of inflammation research · 2026Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Focal cortical dysplasia (FCD) represents a common developmental malformation associated with drug-resistant epilepsy (DRE) among children. However, the exact molecular mechanisms behind this condition are still unclear. In our study, FCD-associated microarray data from the Gene Expression Omnibus (GEO) database were analyzed. A comprehensive series of bioinformatics analyses were conducted, including screening for differentially expressed genes (DEGs), functional enrichment analysis, weighted gene co-expression network analysis (WGCNA), and protein-protein interaction (PPI) analysis. Subsequently, a freezing lesion (FL) rat model was developed to validate expression levels of hub genes along with the molecular pathways behind FCD epileptogenicity. 320 DEGs were identified, and functional enrichment analysis revealed significant enrichment of these DEGs in "Neuroinflammatory response", "Cytokine production involved in immune response", and "Macrophage activation". Ultimately, 5 potential hub genes (CYBB, ITGAM, FCG3A, LY86, and CD86) were pinpointed. Notably, 4 hub genes (CYBB, ITGAM, FCG3A, and CD86) were validated in in vivo experiments, suggesting possible associations with neuroinflammation triggered by microglia. This underscores the tight relationship between microglia-induced neuroinflammation and the pathological progression of epileptic seizures in FCD. ITGAM, FCG3A, CD86, CYBB, and LY86 may emerge as promising candidate biomarkers, influencing diagnostic and therapeutic strategies.
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39612062What Socratic holds
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.