Network Analysis of Inflammatory Gene Expression in CNS Lesions of MS Patients (PP-20)

Background: Inflammation is a key biological pathway in the pathogenesis of Multiple Sclerosis (MS). The chronic inflammatory response within the central nervous system (CNS) leads to demyelination and neurodegeneration, resulting in various neurological deficits. Mapping the intricate network of inflammatory pathways in MS lesions is crucial for identifying therapeutic targets and could pave the way for more effective disease management. This study aims to map the inflammatory network by analyzing gene expression profiles in MS lesions.
Methods: To explore gene expression changes in CNS lesions of MS patients, we applied a customized RNA-seq analysis workflow on datasets from GSE179427 and GSE149326. The workflow included extensive quality control, precise read alignment, normalization, and differential expression analysis using DESeq2. Following this, a gene set enrichment analysis was conducted to pinpoint biological pathways overrepresented among the differentially expressed genes, shedding light on the molecular mechanisms underlying MS.
Results: Our analysis identified a subset of genes including TGFB3 and IRF7 with significantly altered expression in MS lesions. Both noted genes are considered to be involved in inflammatory response and related immune response pathways. Functional enrichment analysis revealed an overrepresentation of these genes in pathways associated with immunoregulation, inflammation, and neurotransmission. These findings highlight the involvement of specific inflammatory genes as potential biomarkers for MS progression and as novel therapeutic targets.
Conclusion: This bioinformatics study identified a subset of inflammatory genes with altered expression in CNS lesions of MS patients, suggesting their role in MS pathogenesis. The enrichment of these genes in pathways related to immune response, inflammation, and neuronal function underscores their potential as biomarkers and therapeutic targets. Further experimental validation is necessary to clarify the precise roles of these genes and to guide the development of inflammation-modulating therapies for MS.