THALAMOCORTICAL DYSRHYTHMIA AS A UNIFYING MODEL OF NEUROPSYCHIATRIC AND NEUROSENSORY DYSFUNCTION IN FRAGILE X SYNDROME

Abstract

The silencing of the Fmr1 gene in fragile X syndrome (FXS) leads to varying levels of intellectual disability, sensory hyperarousal, and neuropsychiatric symptoms. EEG studies in FXS have demonstrated marked changes in low-frequency (theta, alpha) and high-frequency (gamma) activity which, if better understood, may provide insight into mechanisms for precision targeting of therapies. Here, in a large sample of males and females with FXS (including ascertainment of mosaic status), we use source/network modeling to investigate evidence of thalamocortical dysfunction in FXS.