Systemic overexpression of a C-terminal fragment of human amyloid beta-protein precursor causes accumulation of Alzheimer beta-amyloid fibrils in pancreas of transgenic mice

Gerontology. 1996:42 Suppl 1:48-56. doi: 10.1159/000213824.

Abstract

The deposition of amyloid beta-protein (A beta), derived from amyloid beta-protein precursor (beta APP), is a specific and early event in development of Alzheimer's disease. Transgenic mice carrying the carboxyl-terminus of beta APP gene linked to the cytomegalovirus enhancer/chicken beta-actin promoter sequence were studied. Deposition of amyloid fibrils, composing A beta, was observed in the transgenic pancreas, accompanied with cell degeneration. This result will provide a model to investigate the beta APP processing mechanism in vivo and a clue to generate possible A beta amyloidosis in animal brains.

MeSH terms

  • Actins / genetics
  • Alzheimer Disease / pathology*
  • Amyloid beta-Protein Precursor / metabolism*
  • Animals
  • Chickens / genetics
  • Cytomegalovirus / genetics
  • Enhancer Elements, Genetic
  • Gene Expression
  • Humans
  • Immunohistochemistry
  • Mice
  • Mice, Transgenic / genetics
  • Microscopy, Electron
  • Pancreas / metabolism*
  • Pancreas / pathology*
  • Peptide Fragments / metabolism*
  • Promoter Regions, Genetic
  • Transgenes

Substances

  • Actins
  • Amyloid beta-Protein Precursor
  • Peptide Fragments