Molecular basis for and chemogenetic modulation of comorbidities in GABRG2-deficient epilepsies.

Objective: γ-Aminobutyric acid type A (GABA ) receptor subunit gene mutations are significant causes of epilepsy, which are often accompanied by various neuropsychiatric comorbidities, but the underlying mechanisms are unclear. It has been suggested that the comorbidities are caused by seizures, as the comorbidities often present in severe epilepsy syndromes. However, findings from both humans and animal models argue against this conclusion.