Pelizaeus-Merzbacher-like disease: exclusion of the proteolipid protein locus and documentation of a new locus on Xq

Neurology. 1997 Sep;49(3):824-32. doi: 10.1212/wnl.49.3.824.

Abstract

A large X-linked kindred with Pelizaeus-Merzbacher like disease (Pelizaeus-Merzbacher disease [PMD] lacking a proteolipid protein [PLP] mutation) was studied for linkage to 34 X-chromosome short tandem repeat polymorphism markers. Recombinational events excluded linkage to PLP and supported linkage to a 9.4-cM critical region more than 10 cM away from PLP on the X chromosome. A maximum 2-point lod score of 3.91 was observed for DXS441 at theta = 0.0. Neuropathologic study of one affected male showed intact myelin. The data thus support a different etiology for a disease that clinically resembles PMD, distinguishable phenotypically only by degree of myelin involvement. Other patients with the clinical diagnosis of PMD but without PLP mutations could have mutations at this new locus.

Publication types

  • Case Reports
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Brain / pathology
  • Child
  • Child, Preschool
  • Diffuse Cerebral Sclerosis of Schilder / epidemiology
  • Diffuse Cerebral Sclerosis of Schilder / genetics*
  • Diffuse Cerebral Sclerosis of Schilder / pathology
  • Family
  • Genetic Linkage
  • Genetic Markers
  • Humans
  • Infant
  • Magnetic Resonance Imaging
  • Male
  • Mutation
  • Myelin Proteolipid Protein / genetics*
  • Pedigree
  • Phenotype
  • Recombinant Proteins / genetics
  • X Chromosome / genetics

Substances

  • Genetic Markers
  • Myelin Proteolipid Protein
  • Recombinant Proteins