ArticleBioMed research international2021
Analysis of Shared Genetic Regulatory Networks for Alzheimer's Disease and Epilepsy.
Article in BioMed research international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- Expanding the Phenotypic and Functional Evidence for KCNK3 as a Neurodevelopmental Disorder Gene: A New Chinese Case and Drosophila Validation.Clinical genetics · 2026Article
- Decoding epilepsy's molecular blueprint: Machine learning unravels transcriptomic subtypes and regulatory networks.Epilepsia · 2026Article
- Regulon Reconstruction Uncovers Novel Deregulated Factors in Alzheimer's Disease.Molecular neurobiology · 2026Article
- Identification of common core ion channel genes in epilepsy and Alzheimer's disease.Irish journal of medical science · 2024Review
- A review and analysis of key biomarkers in Alzheimer's disease.Frontiers in neuroscience · 2024Review
- The bidirectional relationship between Alzheimer's disease (AD) and epilepsy: A Mendelian randomization study.Brain and behavior · 2023Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
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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
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