Amyloid precursor protein accumulates in regions of neurodegeneration following focal cerebral ischemia in the rat

Brain Res. 1992 Oct 9;593(1):128-35. doi: 10.1016/0006-8993(92)91274-i.

Abstract

The distribution of beta-amyloid precursor protein (APP) was examined immunocytochemically in rats subjected to focal cerebral ischemia by permanent occlusion of the middle cerebral artery. At 4 and 7 days post-occlusion, APP immunoreactivity was preferentially localized within axonal swellings, dystrophic neurites and neuronal perikarya all along the periphery of the infarct. Immunolabeling was observed with antibodies generated against N-terminal, midregion, and C-terminal domains of APP. No immunoreactivity was observed with antisera directed against beta-amyloid protein (beta A4) itself. This pathological accumulation of APP is consistent with alterations of APP recently described in other models of neurodegeneration and implies a role for this protein in the response to CNS injury.

MeSH terms

  • Amyloid beta-Protein Precursor / metabolism*
  • Animals
  • Axons / metabolism
  • Axons / ultrastructure
  • Brain / metabolism*
  • Brain / pathology
  • Cerebral Arteries
  • Cerebral Infarction / metabolism
  • Cerebral Infarction / pathology
  • Immunohistochemistry
  • Ischemic Attack, Transient / metabolism*
  • Ischemic Attack, Transient / pathology
  • Male
  • Nerve Degeneration*
  • Neurites / metabolism
  • Neurites / ultrastructure
  • Neurons / metabolism
  • Neurons / pathology
  • Rats
  • Rats, Inbred SHR

Substances

  • Amyloid beta-Protein Precursor