Functional connectivity aberrancies as measured with resting-state fMRI (rsfMRI) have been consistently observed in the brains of autism spectrum disorders (ASD) patients. However, genetic and neurobiological underpinnings of these findings remain unclear. Here we used rsfMRI to show that homozygous mice lacking the strongly ASD-associated gene CNTNAP2 exhibit default-mode network connectivity alterations associated with reduced social investigation, a core “autism trait” in mice. These findings reveal a causal link between an ASD-associated mutation and functional connectivity aberrancies and suggest that homozygous loss-of-function mutations in CNTNAP2 may predispose to ASD through a selective dysregulation of functional coupling between integrative cortical areas.
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