Amyloid deposition is associated with c-Jun expression in Alzheimer's disease and amyloid angiopathy

Neuropathol Appl Neurobiol. 1996 Dec;22(6):521-6. doi: 10.1111/j.1365-2990.1996.tb01130.x.

Abstract

Since the PAD gene (also called promoter of Alzheimer's disease amyloid A4 precursor gene or amyloid beta-protein precursor promoter) has two AP-1 consensus sequences, and members of the Fos and Jun families are the major components of the transcription factor activator protein-1 (AP-1), we have investigated the localization of c-Fos and c-Jun immunoreactivity and its relationship to beta-amyloid deposition in the brains of patients with Alzheimer's disease and amyloid angiopathy. c-Jun, but not c-Fos, immunoreactivity is observed in the muscular layer of meningeal and cerebral blood vessels with amyloid angiopathy, and in the soma of glial cells and cellular processes of unknown origin surrounding beta-amyloid deposits in the brain. These results show that c-Jun may participate in the cascade of events leading to increased beta-APP (beta-amyloid precursor protein) production and beta-amyloid deposition in the brains of patients with Alzheimer's disease and amyloid angiopathy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / metabolism*
  • Amyloid beta-Protein Precursor / metabolism*
  • Cerebral Amyloid Angiopathy / metabolism*
  • Humans
  • Immunohistochemistry
  • Proto-Oncogene Proteins c-jun / metabolism*

Substances

  • Amyloid beta-Protein Precursor
  • Proto-Oncogene Proteins c-jun