EXPLORING IMMUNE-RELATED HUB GENES IN PARKINSON’S DISEASE USING INTEGRATIVE BIOINFORMATICS APPROACH

Abstract

Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by motor dysfunction and the loss of dopaminergic neurons. Emerging evidence suggests that immune system dysregulation and neuroinflammation play key roles in PD pathogenesis. In this study, we aimed to explore immune-related hub genes and associated signaling pathways using bioinformatics analysis of the GSE20141 dataset. We identified 250 differentially expressed genes (DEGs) and constructed a protein-protein interaction (PPI) network to pinpoint key hub genes. Four hub genes, FGF17, MED26, LCK, and RPS12, were identified as central players in the network, and functional enrichment analysis revealed significant involvement of several immune-related pathways.Key pathways enriched in our analysis included the JAK-STAT signaling pathway, NF-kappa B signaling pathway, and T cell receptor signaling pathway, all of which are known to regulate immune responses and inflammation in neurodegenerative diseases. Interestingly, our study also identified pathways less commonly associated with PD, such as the adipocytokine signaling pathway and osteoclast differentiation, suggesting a potential link between metabolic dysregulation and neuroinflammation. Our findings highlight both established and novel immune mechanisms in PD, suggesting potential therapeutic targets aimed at modulating immune responses. This study provides valuable insights into the complex immune landscape of PD and emphasizes the importance of immune modulation in understanding and treating this debilitating disease. Further research is needed to validate the role of the identified hub genes and pathways and to explore their potential as targets for PD therapy.