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      An intriguing "silent" mutation and a founder effect in antiquitin (ALDH7A1).

      Annals of Neurology
      Adult, Aldehyde Dehydrogenase, genetics, Epilepsy, Female, Founder Effect, Genetic Predisposition to Disease, Heterozygote, Humans, Male, Mutation

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          Abstract

          Recently, alpha-aminoadipic semialdehyde (alpha-AASA) dehydrogenase deficiency was shown to cause pyridoxine-dependent epilepsy in a considerable number of patients. alpha-AASA dehydrogenase deficiency is an autosomal recessive disorder characterized by a neonatal-onset epileptic encephalopathy in which seizures are resistant to antiepileptic drugs but respond immediately to the administration of pyridoxine (OMIM 266100). Increased plasma and urinary levels of alpha-AASA are associated with pathogenic mutations in the alpha-AASA dehydrogenase (ALDH7A1/antiquitin) gene. Here, we report an intriguing "silent" mutation in ALDH7A1, a novel missense mutation and a founder mutation in a Dutch cohort (10 patients) with alpha-AASA dehydrogenase deficiency.

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          Author and article information

          Journal
          17721876
          10.1002/ana.21206
          03645134

          Chemistry
          Adult,Aldehyde Dehydrogenase,genetics,Epilepsy,Female,Founder Effect,Genetic Predisposition to Disease,Heterozygote,Humans,Male,Mutation

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