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Article

Scn8a Antisense Oligonucleotide Is Protective in Mouse Models of SCN8A Encephalopathy and Dravet Syndrome.

Annals of neurology - 1 Mar 2020

Lenk Guy M, Jafar-Nejad Paymaan, Hill Sophie F, Huffman Lucas D, Smolen Corrine E, Wagnon Jacy L, Petit Hayley, Yu Wenxi, Ziobro Julie, Bhatia Kritika, Parent Jack, Giger Roman J, Rigo Frank, Meisler Miriam H

Abstract excerpt

OBJECTIVE: SCN8A encephalopathy is a developmental and epileptic encephalopathy (DEE) caused by de novo gain-of-function mutations of sodium channel Nav 1.6 that result in neuronal hyperactivity. Affected individuals exhibit early onset drug-resistant seizures, developmental delay, and cognitive impairment. This study was carried out to determine whether reducing the abundance of the Scn8a transcript with an...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Dose-Response Relationship, Drug

Share to Epilepsies, Myoclonic

Share to NAV1.6 Voltage-Gated Sodium Channel

Share to Oligonucleotides, Antisense

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Source

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Identifiers

PMID: 31943325
DOI: 10.1002/ana.25676
PMCID: PMC7064908

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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