Autism is a complicated neurodevelopmental disorder, and most studies on autism focus on social contact, communication, and cognitive difficulties related to the condition. Early comprehensive and specific behavioral interventions can enhance social communication, attenuating anxiety and attacks. Therefore, this study, based on a modular comprehensive analysis method, explored the mechanism of neurotransmitter conduction on the pathogenesis of autism. We downloaded autism-related data from the GEO database, performed a differential analysis, a WGCNA analysis, and a GO function, as well as a KEGG pathway enrichment analysis. Finally, non-coding RNAs (ncRNAs) and transcription factors regulating the module were predicted on the basis of hypergeometric testing. In summary, we obtained five co-expression modules, in which the MTA3, PHB2, TNXB, and DCTN2 and RBM23 genes have positive regulatory effects on the dysfunction modules. The enrichment results indicated that the module gene significantly participates in the biological processes involving ion channel activity, the active regulation of cellular amide metabolism, and small molecule catabolism. It also significantly regulates the mRNA monitoring pathways, the calcium signaling pathways, and other signaling pathways such as the neuroactive ligand-receptor interactions and the ECM-receptor interactions. In addition, we found that the ncRNApivot (including CRNDE, miR-103a-3p, miR106b-5p, etc.) and the TF pivot (including MYC) significantly regulate the dysfunction modules. In general, we decoded a comprehensive network of key gene regulation involving autism. These analyses reveal core dysfunctional modules, the underlying regulatory factors, and the driving genes for autism, helping us to further understand the mechanisms of autism neuronal conduction disorders.
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