Human amyloid-β1-42 applied in vivo inhibits the fast axonal transport of proteins in the sciatic nerve of rat

Peter Kasa, Henrietta Papp, Imre Kovacs, Monika Forgon, Botond Penke, Haruyasu Yamaguchi

Research output: Contribution to journalArticle

33 Citations (Scopus)


Human amyloid-β1-42 has been suggested to be a pathogenetic factor in Alzheimer's disease. The precise mechanism by which this peptide causes the degeneration of neurons in the affected brain is not yet fully understood. By using immunohistochemistry we explored the inhibitory effects of human amyloid-β1-42 applied in vivo on the fast axonal transport of acetylcholinesterase, the amyloid precursor protein, the vesicular acetylcholine transporter and synaptophysin in the sciatic nerve of rat. Our findings provide evidence for the in vivo neurotoxic effect of human amyloid- β peptide.

Original languageEnglish
Pages (from-to)117-119
Number of pages3
JournalNeuroscience Letters
Issue number1-2
Publication statusPublished - Jan 7 2000



  • Alzheimer's disease
  • Amyloid
  • Axonal transport
  • Immunohistochemistry
  • Neurotoxicity
  • Sciatic nerve

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this