Key result
Scn8a mutations in mice produce a broad spectrum of neurological diseases, ranging from lethal paralysis to ataxia and dystonia, providing insight into human sodium channel diseases.
Mouse models of Scn8a mutations demonstrate a broad spectrum of neurological diseases and provide insight into the pathophysiology of human sodium channel diseases.
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Animal models of Scn8a mutations should not alter patient care; leaves open mechanistic insights for future human channelopathy research.
Meisler et al. (2001) conducted a review in Neurological disease associated with Scn8a mutations. Scn8a mutations was evaluated. Scn8a mutations in mice produce a broad spectrum of neurological diseases, ranging from lethal paralysis to ataxia and dystonia, providing insight into human sodium channel diseases.
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