The Knockout of <i>Cntn4</i>, <i>Sapap3</i> and <i>Shank3</i> Causes Autistic-like Mouse Model with synaptic dysfunction

In this study, Data-independent acquisition (DIA)-based SWATH (Sequential window acquisition of all theoretical spectra)-MS quantitative proteomics was applied to identify and compare the proteomes of the cerebral cortex and cerebral cortex synaptosomes of three ASD-like mouse models (<i>Cntn4</i>KO, <i>Sapap3</i>KO and <i>Shank3</i>KO). The experimental mouse models have all demonstrated face validity of autism through behavioral tests, exhibiting ASD signature behavioral correlates such as deficits in social interactions and the emergence of repetitive, stereotyped behaviors. Understanding and predicting the convergent synaptic changes underlying ASD through bioinformatics analysis plays a crucial role in determining the pathogenic mechanisms. Analysis of changes in nerve function and protein regulatory pathways following <i>CNTN4</i>, <i>SAPAP3</i> and <i>SHANK3</i> gene deletion using these animal models is important for exploring the disease mechanisms associated with ASD.