A key requirement for the effective development of novel therapies for Intellectual Disabilities is the ability to directly compare findings from basic neuroscience in rodent models with human studies. Functional magnetic resonance imaging offers a platform to overcome this translational barrier. Here, we use a parallel resting state fMRI approach in individuals with Fragile X Syndrome (FXS) and in a rat model of FXS using a 3T and 7T scanner respectively, and show that the loss of Fragile X mental retardation protein leads to a shared decrease in DMN connectivity in humans with FXS and rats that model this disorder.
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