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Cree leukoencephalopathy and CACH/VWM disease are allelic at the EIF2B5 locus

Anne Fogli1, Kondi Wong, Eleonore Eymard-Pierre

  • 1Institut National de la Santé et de la Recherche Médicale UMR 384, Facultéde Médecine, Clermont-Ferrand, France.

Annals of Neurology
|September 27, 2002
PubMed

Insights

Cree leukoencephalopathy, a fatal infantile disorder, is linked to mutations in the eukaryotic translation initiation factor 2B (eIF2B) gene. Researchers identified a specific homozygous missense mutation in epsilon-eIF2B in affected individuals.

Area of Science:

  • Neurogenetics
  • Molecular Biology
  • Pediatric Neurology

Background:

  • Cree leukoencephalopathy is a rare, fatal, autosomal recessive leukodystrophy affecting infants in North American indigenous populations.
  • The condition is characterized by white matter abnormalities and is clinically similar to central hypomyelination syndrome/vanishing white matter disease.
  • Vanishing white matter disease is known to be caused by mutations in genes encoding subunits of the eukaryotic translation initiation factor 2B (eIF2B).

Purpose of the Study:

  • To investigate the genetic cause of Cree leukoencephalopathy.
  • To identify the specific molecular mechanisms underlying this rare neurological disorder.

Main Methods:

  • Neuropathological examination of affected individuals' brains to identify characteristic cellular phenotypes.
  • Genetic analysis, including sequencing of eIF2B family genes, to identify mutations in affected patients.

Main Results:

  • Brain tissue analysis revealed foamy cells with an oligodendroglial phenotype, consistent with central hypomyelination syndrome/vanishing white matter disease.
  • A homozygous missense mutation (R195H) in the epsilon-eIF2B subunit of the eukaryotic translation initiation factor 2B was identified in three patients from two Cree families.

Conclusions:

  • The identified homozygous missense mutation in epsilon-eIF2B is the likely cause of Cree leukoencephalopathy.
  • This finding establishes a genetic link between Cree leukoencephalopathy and mutations in the eIF2B complex, expanding the known spectrum of vanishing white matter disease.

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