| Literature DB >> 26220384 |
Dennis Lal1, Sandra Steinbrücker2, Julian Schubert3, Thomas Sander4, Felicitas Becker5, Yvonne Weber6, Holger Lerche7, Holger Thiele8, Roland Krause9, Anna-Elina Lehesjoki10, Peter Nürnberg11, Aarno Palotie12, Bernd A Neubauer13, Hiltrud Muhle14, Ulrich Stephani15, Ingo Helbig16, Albert J Becker17, Susanne Schoch18, Jörg Hansen19, Thomas Dorn20, Christin Hohl21, Nicole Lüscher22, Sarah von Spiczak23, Johannes R Lemke24.
Abstract
Recently, mutations and deletions in the GRIN2A gene have been identified to predispose to benign and severe idiopathic focal epilepsies (IFE), revealing a higher incidence of GRIN2A alterations among the more severe phenotypes. This study aimed to explore the phenotypic boundaries of GRIN2A mutations by investigating patients with the two most common epilepsy syndromes: (i) idiopathic generalized epilepsy (IGE) and (ii) temporal lobe epilepsy (TLE). Whole exome sequencing data of 238 patients with IGE as well as Sanger sequencing of 84 patients with TLE were evaluated for GRIN2A sequence alterations. Two additional independent cohorts comprising 1469 IGE and 330 TLE patients were screened for structural deletions (>40kb) involving GRIN2A. Apart from a presumably benign, non-segregating variant in a patient with juvenile absence epilepsy, neither mutations nor deletions were detected in either cohort. These findings suggest that mutations in GRIN2A preferentially are involved in genetic variance of pediatric IFE and do not contribute significantly to either adult focal epilepsies as TLE or generalized epilepsies.Entities:
Keywords: Copy number variation; GRIN2A; Idiopathic generalized epilepsy; Mutation; Temporal lobe epilepsy
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Year: 2015 PMID: 26220384 DOI: 10.1016/j.eplepsyres.2015.05.010
Source DB: PubMed Journal: Epilepsy Res ISSN: 0920-1211 Impact factor: 3.045