The present disclosure relates to an ASD genetically engineered model carrying a deletion of Shank2 gene and having reduced NMDA receptor function. According to the present disclosure, genetically engineered mice that show the clinical features of ASD due to the deletion of the Shank2 gene can be obtained, and the genetically engineered mice can be effectively used to screen candidate therapeutic agents.
Genetically engineered mouse model for autism spectrum disorder having deletion of Shank2 gene and use thereof