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• W4386047520 abstract "Abstract Introduction: Previous studies have indicated epilepsy as a risk factor for PD, and a growing body of evidence links neurodegenerative disease markers to increased neuronal excitability before seizures. Understanding the underlying mechanisms of this correlation could provide valuable insights into the complex relationship between PD and epilepsy. Method: Microarray data were gathered and processed from PD and epilepsy patients. Using the weighted coexpression network analysis (WGCNA) method, gene modules correlated with both PD and epilepsy were identified, revealing genetic links between the disorders. Functional enrichment analysis explored the roles of selected genes in crucial biological processes. Employing LASSO analysis, key hub genes significantly involved in both PD and epilepsy were identified. Result: Analyses revealed specific gene modules correlated with PD and epilepsy, suggesting shared genetic components. Functional enrichment indicated the involvement of selected genes in neurodegenerative pathways and essential synaptic processes, further supporting the PD-epilepsy connection. LASSO analysis identified 19 hub genes strongly associated with both diseases, including GSK3β and SRA1. Gene expression analysis showed significant downregulation of GSK3β, SRA1, LINC00889, SLC35F1, AGK, and SPG11, and upregulation of ADCY8, KLHL32, KAT2B, and CIAPIN1. Conclusion: This study highlights potential mechanisms linking PD and epilepsy, such as dendritic spines and synaptic vesicle recycling. Common hub genes and cellular pathways offer promising targets for future therapies. Further investigations are needed to fully understand the molecular mechanisms and develop effective treatments for these complex neurological disorders." @default.
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• W4386047520 date "2023-08-22" @default.
• W4386047520 modified "2023-09-25" @default.
• W4386047520 title "Parkinson’s Disease and Epilepsy: A bioinformatics analysis" @default.
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• W4386047520 doi "https://doi.org/10.21203/rs.3.rs-3257860/v1" @default.
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