Associated Papers
GRIN2A null variants confer a high risk for early-onset schizophrenia and other mental disorders and potentially enable precision therapy.
Lemke JR et al.
Molecular Psychiatry, 2026
41087560 (PubMed )
Supplement: 41380_2025_3279_MOESM2_ESM.xlsx › final
Loss of Grin2a causes a transient delay in the electrophysiological maturation of hippocampal parvalbumin interneurons.
Camp CR et al.
Communications Biology, 2023
37723282 (PubMed )
Supplement: 42003_2023_5298_MOESM1_ESM.pdf
Idiopathic encephalopathy related to status epilepticus during slow sleep (ESES) as a "pure" model of epileptic encephalopathy. An electroclinical, genetic, and follow-up study.
Pavlidis E et al.
Epilepsy & Behavior : E&b, 2019
GRIN2A-related disorders: genotype and functional consequence predict phenotype.
Strehlow V et al.
Brain : a Journal of Neurology, 2019
30544257 (PubMed )
Supplement: awy304_supp.zip › awy304-suppl_data › brain-2018-01122-File012.xlsx › Tabelle1
Genetic etiologies of the electrical status epilepticus during slow wave sleep: systematic review.
Kessi M et al.
Bmc Genetics, 2018
New genes for focal epilepsies with speech and language disorders.
Turner SJ et al.
Current Neurology and Neuroscience Reports, 2015
NMDA receptor subunit mutations in neurodevelopmental disorders.
Burnashev N et al.
Current Opinion in Pharmacology, 2015
Mutations in GRIN2A cause idiopathic focal epilepsy with rolandic spikes.
Lemke JR et al.
Nature Genetics, 2013
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