| Abstract |
Background: It is believed that the genetic cause of complex diseases, such as Eating Disorder (ED), is linked to a large genetic network. In recent years, there has been an increased number of studies reporting dozens of genes associated with ED, posing an increased need of a systematically evaluation of the genetic markers underlying the disease. Methods: ED-Gene relation data were extracted from the ResNet Mammalian database, containing 69 ED candidate genes. Pathway Enrichment Analysis, Sub-Network Enrichment Analysis, Network Connectivity Analysis and Network Metrics Analysis were conducted to study network attributes and select the top genes for ED. Additionally, ED-Drug and Drug-Gene relation data were employed to study the ED-Gene relation at the small molecule level. Results: 66 out of 69 genes enriched 104 ED candidate pathways (p-values< 1e-5), demonstrating strong gene-gene interactions. Metrics analysis suggest 6 genes worthy of further study for ED, including CHR, DRD2, AVP, OPRM1, IL6, and ESR2. Additionally, the majority of the ED candidate genes (64/69) demonstrated strong interaction with 46/55 ED effective drugs, providing support for the ED-gene relationships identified. Conclusion: Our results suggested that the genetic causes of ED were linked to a genetic network composed of a large group of genes. The gene network, together with the literature and enrichment metrics provided in this study, laid the groundwork for further biological/genetic studies in the field.
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