No evidence of a role for cystatin B gene in juvenile myoclonic epilepsy

Epilepsia. 2015 Apr;56(4):e40-3. doi: 10.1111/epi.12944. Epub 2015 Mar 6.

Abstract

Genetic factors play a major role in the etiology of juvenile myoclonic epilepsy (JME), a common form of idiopathic generalized epilepsy, but so far, genes related to JME remain largely unknown. JME shares electroclinical features with Unverricht-Lundborg disease (progressive myoclonic epilepsy type 1; EPM1), a form of progressive myoclonus epilepsy characterized by myoclonus, epilepsy, and gradual neurologic deterioration. EPM1 is caused by mutations in the gene that codes for cystatin B (CSTB), an inhibitor of cysteine protease. In the present study, we wished to investigate the role of the CSTB gene in patients with JME. Fifty-seven unrelated patients (35 women; mean age ± standard deviation [SD], 24.1 ± 7.7; mean age ± SD at onset, 15.3 ± 2.4) with JME were enrolled. Twenty-three of 57 patients were the probands of families with JME. The molecular diagnosis was carried out to identify the common dodecamer repeat expansion mutation or other disease-causing mutations in the CSTB gene. The molecular analysis did not depict mutations in any of the 57 patients with JME. Our study did not support a role for the CSTB gene in patients with familial or sporadic JME.

Keywords: Cystatin B gene; EPM1; Genetics; Juvenile myoclonic epilepsy; Mutation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Cystatin B / genetics*
  • Female
  • Humans
  • Male
  • Mutation / genetics
  • Myoclonic Epilepsy, Juvenile / diagnosis*
  • Myoclonic Epilepsy, Juvenile / genetics*
  • Young Adult

Substances

  • CSTB protein, human
  • Cystatin B