Early-onset absence epilepsy caused by mutations in the glucose transporter GLUT1.

Article Details

Citation

Suls A, Mullen SA, Weber YG, Verhaert K, Ceulemans B, Guerrini R, Wuttke TV, Salvo-Vargas A, Deprez L, Claes LR, Jordanova A, Berkovic SF, Lerche H, De Jonghe P, Scheffer IE

Early-onset absence epilepsy caused by mutations in the glucose transporter GLUT1.

Ann Neurol. 2009 Sep;66(3):415-9. doi: 10.1002/ana.21724.

PubMed ID
19798636 [ View in PubMed
]
Abstract

Absence epilepsies of childhood are heterogeneous with most cases following complex inheritance. Those cases with onset before 4 years of age represent a poorly studied subset. We screened 34 patients with early-onset absence epilepsy for mutations in SLC2A1, the gene encoding the GLUT1 glucose transporter. Mutations leading to reduced protein function were found in 12% (4/34) of patients. Two mutations arose de novo, and two were familial. These findings suggest GLUT1 deficiency underlies a significant proportion of early-onset absence epilepsy, which has both genetic counseling and treatment implications because the ketogenic diet is effective in GLUT1 deficiency.

DrugBank Data that Cites this Article

Polypeptides
NameUniProt ID
Solute carrier family 2, facilitated glucose transporter member 1P11166Details