Why the study?
To better understand the cellular mechanisms underlying KCNQ2-associated network dysfunction and their progression over time in Developmental and Epileptic Encephalopathy.
Population
Heterozygous knock-in mice carrying the p.T274M pathogenic variant and wild-type mice
Comparison
Heterozygous knock-in mice vs wild-type mice across neonatal, post-weaning, and juvenile stages
Design
In vivo and ex-vivo animal electrophysiological study
Authors
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Time-limited excitability changes in KCNQ2-DEE model; leaves open whether similar mechanisms drive age-related seizure remission in patients.
Key points are not available for this paper at this time.
Biba et al. (2020) studied this question.