Autism Spectrum Disorder (ASD) is a group of developmental disabilities that can cause debilitating social, communication and behavioural challenges. The diverse etiology of ASD presents difficulties in diagnosing and treating these developmental disorders. Yet, many syndromes share similar central intellectual impairments, indicating dysfunction of cognitive network operations within the brain. We currently do not have adequate objective biomarkers to diagnose and assess treatment strategies targeting cognitive impairments in neurodevelopmental disorders such as ASD. The overall goal of the proposed research is to evaluate the discoordination hypothesis as the basis of cognitive control impairments in ASD. The discoordination hypothesis states that neural discoordination, comprised of abnormally coordinated electrical activity within brain networks subserving cognition, is responsible for cognitive control impairments and abnormal social cognition. Cognitive control requires paying attention to relevant information in our environment while ignoring irrelevant information. Evidence demonstrates that this mental exercise involves the organized timing of electrical activity within and across networks of brain cells. We will utilize the Fragile X mutant mouse model of ASD to assess the discoordination hypothesis by directly recording and analyzing the neural activity of the brain networks responsible for cognitive control and social cognition. This model is homologous to human Fragile X Syndrome because it lacks the Fragile X Mental Retardation Protein and exhibits abnormal cognitive behavioural performance. The hypothesis predicts that cognitive control impairments in ASD, due to abnormally coordinated brain activity, is a common pathological phenotype of the disorder. Understanding abnormal neural coordination in ASD will provide objective biomarkers for diagnosis and developing individualized and targeted treatment strategies for neurodevelopmental disorders.