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Depressed glutamate transporter 1 expression in a mouse model of Dravet syndrome.

Mustafa Q HameedBenjamin HuiRui LinPaul C MacMullinAndres Pascual-LeoneSheryl Anne D VermudezAlexander Rotenberg
Published in: Annals of clinical and translational neurology (2023)
Dravet syndrome (DS) is a monogenic, often refractory, epilepsy resultant from SCN1A haploinsufficiency in humans. A novel therapeutic target in DS that can be engaged in isolation or as adjunctive therapy is highly desirable. Here, we demonstrate reduced expression of the rodent glutamate transporter type 1 (GLT-1) in a DS mouse model, and in wild type mouse strains where Scn1a haploinsufficiency is most likely to cause epilepsy, indicating that GLT-1 depression may play a role in DS seizures. As GLT-1 can be upregulated by common and safe FDA-approved medications, this strategy may be an attractive, viable, and novel avenue for DS treatment.
Keyphrases
  • mouse model
  • poor prognosis
  • wild type
  • escherichia coli
  • depressive symptoms
  • binding protein
  • physical activity
  • mesenchymal stem cells
  • long non coding rna
  • temporal lobe epilepsy
  • cell therapy
  • replacement therapy