Research “Altered mGluR5-Homer scaffolds and corticostriatal connectivity in a Shank3 complete knockout model of autism”

Studies have suggested that behavioral deficiencies in autism spectrum disorder (ASD) can be attributed to abnormal neural connectivity. However, the molecular and neural mechanisms underlying ASD are still unknown. In this study by researchers at Duke University, researchers eliminated exons 4-22 in order to generate Shank3 complete knockout mice. After removing exons 4-22 and establishing knockout mice, differing striatal synapse function, aberrant brain structure, abnormal structural connectivity and behavior similar to that found in ASD were observed. Findings suggest that a lack of Shank3 can impair mGluR5 scaffolding, which can lead to cortico-striatal circuit abnormalities. These abnormalities underlie learning deficiencies and ASD-like behaviors, suggesting causal links between genetic, molecular and circuit systems related to the pathophysiology of ASD. Further research should aim to establish precise links between the molecular changes, behavioral impairments and neurological dysfunction aforementioned.

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