Purpose. To identify gene signatures that are shared by autism spectrum disorder (ASD) and epilepsy (EP) and explore the potential molecular mechanism of the two diseases using WGCNA analysis. Additionally, to verify the effects of the shared molecular mechanism on ADHD, which is another neurological comorbidity. Methods. We screened the crosstalk genes between ASD and EP based on WGCNA and differential expression analysis from GEO and DisGeNET database and analyzed the function of the genes’ enrichment by GO and KEGG analyses. Then, with combination of multiple datasets and multiple bioinformatic analysis methods, the shared gene signatures were identified. Moreover, we explored whether the shared gene signature had influence on the other neurological disorder like ADHD by analyzing the difference of the relative genes’ expression based on bioinformatic analysis and molecular experiment. Results. By comprehensive bioinformatic analysis for multiple datasets, we found that abnormal immune response and abnormal lipid metabolic pathway played important roles in coincidence of ASD and EP. Base on the results of WGCNA, we got the hub genes in ASD and EP. In attention deficit and hyperactivity disorder (ADHD) animal model, we also found a significant difference of gene expression related to sulfatide metabolism, indicating that the abnormal sphingolipid metabolism was common in multiple neurological disorders. Conclusion. This study reveals shared gene signatures between ASD and EP and identifies abnormal sphingolipid metabolism as an important participant in the development of ASD, EP, and ADHD.

Objective To investigate the interaction between the Nf1 (Neurofibromin 1)and the BDNF (brain derived neurotrophic factor) in the mechanism of attention deficit hyperactivity disorder (ADHD).Methods Spontaneously hypertensive rats were chosen as the experimental group and WKY servesd as control.RT-PCR,Western-blot were used to detect the mRNA and protein expression levels of Nf1 and BDNF.To explore their relationship,BDNF expression levels were detected after Nf1 expression plasmid transferred and transfection in PC12H and CBRH-7919 cells.Results were quantified by Image-pro plus software.Results In the PFC of ADHD model rats SHR,Nf1 expression was abnormally degressive(P =0.000),in common with the expression of BDNF(P =0.000).Ectopic expression of Nf1 further encouraged the expression of BDNF (PC12H:P =0.000,7919:P ＜0.05).Conclusion Nf1 expression was significantly lower in PFC of SHR than control,and positively correlated with the levels of BDNF.These findings show that in the prefrontal cortex,Nf1-BDNF dysregulation may be involved in the pathomechanism of ADHD.