Creutzfeldt-Jakob disease cosegregates with the codon 178Asn PRNP mutation in families of European origin

Ann Neurol. 1992 Mar;31(3):274-81. doi: 10.1002/ana.410310308.

Abstract

We recently discovered an amino acid-altering heterozygous mutation in codon 178 of the PRNP amyloid precursor gene in patients with familial Creutzfeldt-Jakob disease. This mutation is now shown to be associated with the occurrence of disease in 7 unrelated families of Western European origin, among which a total of 65 members are known to have died from Creutzfeldt-Jakob disease. The mutation was detected in each of 17 tested patients, including at least 1 affected member of each family, and in 16 of 36 of their first-degree relatives, but not in affected families with other mutations, patients with the nonfamilial form of the disease, or 83 healthy control individuals. Linkage analysis in two informative families yielded a lod score of 5.30, which, because no recombinants were found, strongly suggests that codon 178Asn is the actual disease mutation.

Publication types

  • Comparative Study

MeSH terms

  • Adult
  • Base Sequence
  • Codon
  • Creutzfeldt-Jakob Syndrome / ethnology
  • Creutzfeldt-Jakob Syndrome / genetics*
  • DNA Mutational Analysis
  • Europe / ethnology
  • Female
  • Genes
  • Genes, Dominant
  • Genetic Predisposition to Disease
  • Humans
  • Kuru / genetics
  • Lod Score
  • Male
  • Molecular Sequence Data
  • Mutation
  • Pedigree
  • Polymerase Chain Reaction
  • Polymorphism, Restriction Fragment Length
  • PrPC Proteins
  • Prions / genetics*
  • Prions / ultrastructure
  • Protein Conformation
  • Protein Precursors / genetics*
  • Protein Precursors / ultrastructure

Substances

  • Codon
  • PrPC Proteins
  • Prions
  • Protein Precursors