Unusual phenotypic alteration of beta amyloid precursor protein (betaAPP) maturation by a new Val-715 --> Met betaAPP-770 mutation responsible for probable early-onset Alzheimer's disease

Proc Natl Acad Sci U S A. 1999 Mar 30;96(7):4119-24. doi: 10.1073/pnas.96.7.4119.

Abstract

We have identified a novel beta amyloid precursor protein (betaAPP) mutation (V715M-betaAPP770) that cosegregates with early-onset Alzheimer's disease (AD) in a pedigree. Unlike other familial AD-linked betaAPP mutations reported to date, overexpression of V715M-betaAPP in human HEK293 cells and murine neurons reduces total Abeta production and increases the recovery of the physiologically secreted product, APPalpha. V715M-betaAPP significantly reduces Abeta40 secretion without affecting Abeta42 production in HEK293 cells. However, a marked increase in N-terminally truncated Abeta ending at position 42 (x-42Abeta) is observed, whereas its counterpart x-40Abeta is not affected. These results suggest that, in some cases, familial AD may be associated with a reduction in the overall production of Abeta but may be caused by increased production of truncated forms of Abeta ending at the 42 position.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Age of Onset
  • Alzheimer Disease / genetics*
  • Amino Acid Substitution
  • Amyloid beta-Peptides / biosynthesis*
  • Amyloid beta-Peptides / genetics
  • Amyloid beta-Protein Precursor / biosynthesis
  • Amyloid beta-Protein Precursor / genetics*
  • Cell Line
  • Female
  • Humans
  • Male
  • Methionine
  • Mutagenesis, Site-Directed
  • Pedigree
  • Phenotype
  • Point Mutation*
  • Recombinant Proteins / biosynthesis
  • Transfection
  • Valine

Substances

  • Amyloid beta-Peptides
  • Amyloid beta-Protein Precursor
  • Recombinant Proteins
  • Methionine
  • Valine