Literature DB >> 8500430

Progressive myoclonus epilepsies: clinical and genetic aspects.

S F Berkovic1, J Cochius, E Andermann, F Andermann.   

Abstract

The progressive myoclonus epilepsies (PMEs) are a group of rare genetic disorders previously shrouded in nosological confusion. Recent advances have clarified the features of these disorders and provided a rational approach to diagnosis. The major causes of PME are now known to be Unverricht-Lundborg disease, myoclonus epilepsy ragged-red fiber (MERRF) syndrome, Lafora disease, neuronal ceroid lipofuscinoses, and sialidoses. Over the past 3 years, a series of molecular genetic findings have further refined the understanding of the PMEs. The specific mutation responsible for many cases of MERRF has been identified, and the genes for Unverricht-Lundborg disease and for juvenile neuronal ceroid lipofuscinosis have been linked to chromosomes 21 and 16, respectively. Although the PMEs are among the rarest of the inherited epilepsies, because of molecular genetic discoveries they may soon be the best understood at the neurobiologic level.

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Year:  1993        PMID: 8500430     DOI: 10.1111/j.1528-1167.1993.tb06256.x

Source DB:  PubMed          Journal:  Epilepsia        ISSN: 0013-9580            Impact factor:   5.864


  7 in total

Review 1.  Progressive myoclonic epilepsies: review of clinical, molecular and therapeutic aspects.

Authors:  Luis Felipe Mendonça de Siqueira
Journal:  J Neurol       Date:  2010-07-01       Impact factor: 4.849

Review 2.  Definition and classification of hyperkinetic movements in childhood.

Authors:  Terence D Sanger; Daofen Chen; Darcy L Fehlings; Mark Hallett; Anthony E Lang; Jonathan W Mink; Harvey S Singer; Katharine Alter; Hilla Ben-Pazi; Erin E Butler; Robert Chen; Abigail Collins; Sudarshan Dayanidhi; Hans Forssberg; Eileen Fowler; Donald L Gilbert; Sharon L Gorman; Mark E Gormley; H A Jinnah; Barbara Kornblau; Kristin J Krosschell; Rebecca K Lehman; Colum MacKinnon; C J Malanga; Ronit Mesterman; Margaret Barry Michaels; Toni S Pearson; Jessica Rose; Barry S Russman; Dagmar Sternad; Kathy J Swoboda; Francisco Valero-Cuevas
Journal:  Mov Disord       Date:  2010-08-15       Impact factor: 10.338

3.  Insights into Lafora disease: malin is an E3 ubiquitin ligase that ubiquitinates and promotes the degradation of laforin.

Authors:  Matthew S Gentry; Carolyn A Worby; Jack E Dixon
Journal:  Proc Natl Acad Sci U S A       Date:  2005-06-01       Impact factor: 11.205

Review 4.  Myoclonus and epilepsies.

Authors:  N Fejerman
Journal:  Indian J Pediatr       Date:  1997 Sep-Oct       Impact factor: 1.967

Review 5.  Epilepsy and inborn errors of metabolism in adults: a diagnostic approach.

Authors:  F Sedel; I Gourfinkel-An; O Lyon-Caen; M Baulac; J-M Saudubray; V Navarro
Journal:  J Inherit Metab Dis       Date:  2007-10-22       Impact factor: 4.982

Review 6.  Mitochondrial Neurodegeneration.

Authors:  Massimo Zeviani; Carlo Viscomi
Journal:  Cells       Date:  2022-02-11       Impact factor: 6.600

7.  Conservation of the glucan phosphatase laforin is linked to rates of molecular evolution and the glucan metabolism of the organism.

Authors:  Matthew S Gentry; Rachel M Pace
Journal:  BMC Evol Biol       Date:  2009-06-22       Impact factor: 3.260

  7 in total

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