Background: Epilepsy and Alzheimer's disease are common neuropathies with a complex
pathogenesis. Both of them have some correlations in etiology, pathogenesis, pathological changes,
clinical manifestations and treatment.
Objective: This study investigated the key genes and molecular genetic mechanism in epilepsy and
Alzheimer’s disease by bioinformatics analysis.
Method: Two gene expression profiles were used to screen differentially expressed genes by GEO2R
tool. The Gene Ontology (GO) and Kyoto Encyclopedia of Gene and Genome (KEGG) pathway enrichment
analysis was performed using the Database for Annotation, Visualization and Integrated Discovery
(DAVID). Then the protein-protein interaction (PPI) network was constructed by Search Tool
for the Retrieval of Interacting Genes (STRING) and Cytoscape software which can be used to analyze
modules with MCODE.
Results: A total of 199 differentially expressed genes (DEGs) in the two groups. According to GO_BP
analysis and KEGG pathway enrichment by DAVID, we found DEGs referring to several pathways
significantly down-regulated in endocytosis, such as endocytosis, synaptic vesicle cycle, lysosome,
cAMP signaling pathway, circadian entrainment, LTP, glutamatergic synapse and GABAergic synapse
pathway. The regulator genes of the upstream pathway of circadian rhythms were obviously downgraded.
Conclusion: Our research demonstrated that the regulatory genes of the upstream pathway of circadian
rhythms were obviously downgraded. These biological pathways and DEGs or hub genes may contribute
to revealing the molecular relationship between Alzheimer's disease and epilepsy.