Abstract
Alzheimer's disease (AD) and epilepsy are neurological disorders that affect a large cohort of people worldwide. Although both of the two diseases could be influenced by genetic factors, the shared genetic mechanism underlying the pathogenesis of them is still unclear. In this study, we aimed to identify the shared genetic networks and corresponding hub genes for AD and epilepsy. Firstly, the gene coexpression modules (GCMs) were constructed by weighted gene coexpression network analysis (WGCNA), and 16 GCMs were identified. Through further integration of GCMs, genome-wide association studies (GWASs), and expression quantitative trait loci (eQTLs), 4 shared GCMs of AD and epilepsy were identified. Functional enrichment analysis was performed to analyze the shared biological processes of these GCMs and explore the functional overlaps between these two diseases. The results showed that the genes in shared GCMs were significantly enriched in nervous system-related pathways, such as Alzheimer's disease and neuroactive ligand-receptor interaction pathways. Furthermore, the hub genes of AD- and epilepsy-associated GCMs were captured by weighted key driver analysis (wKDA), including TRPC1, C2ORF40, NR3C1, KIAA0368, MMT00043109, STEAP1, MSX1, KL, and CLIC6. The shared GCMs and hub genes might provide novel therapeutic targets for AD and epilepsy.
Highlights
Alzheimer’s disease (AD) is a neurodegenerative disease characterized by memory difficulty, daily activity dysfunction, and cognitive decline, with neuropathological lesion and neuron loss in the brain [1,2,3]
The hub genes of AD- and epilepsy-associated gene coexpression modules (GCMs) were captured by weighted key driver analysis
A Total of 16 GCMs Were Identified for AD and Epilepsy Samples
Summary
Alzheimer’s disease (AD) is a neurodegenerative disease characterized by memory difficulty, daily activity dysfunction, and cognitive decline, with neuropathological lesion and neuron loss in the brain [1,2,3] This disease affects approximately 36 million people worldwide, and the number of AD patients is estimated to triple by 2050, along with the prolonged life expectancy of global population [4, 5]. The therapies of AD mainly focus on counterbalancing the neurotransmitter disturbance, and there have not been effective pharmacotherapeutic options for the prevention and treatment of AD yet [6, 7] Another neurological disorder, epilepsy, is a common brain condition with an unprovoked seizure of high recurrence rate, which is defined epilepsy based on at least one of the following conditions: (1). The etiologies of AD and epilepsy are still unclear [12, 13]
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