Failure to detect missense mutations in the S182 gene in a series of late-onset Alzheimer's disease cases

Neurosci Lett. 1995 Dec 8;201(2):188-90. doi: 10.1016/0304-3940(95)12170-6.

Abstract

The possibility of an interaction of multiple genes has been speculated in pathogenesis of Alzheimer's disease (AD). Because we have recently cloned a novel gene S182 bearing five different missense mutations which segregate with early-onset familial AD, we sought the frequency of these mutations in familial and sporadic late-onset AD to clarify the incidence of these mutations in the disease. The current study showed lack of these mutations in 118 independent subjects affected with late-onset Alzheimer's disease.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Aged
  • Alzheimer Disease / genetics*
  • Base Sequence
  • Cloning, Molecular
  • DNA Primers
  • Genes
  • Humans
  • Membrane Proteins / genetics*
  • Molecular Sequence Data
  • Mutation / genetics*
  • Mutation / physiology
  • Polymerase Chain Reaction
  • Presenilin-1

Substances

  • DNA Primers
  • Membrane Proteins
  • PSEN1 protein, human
  • Presenilin-1