β-Amyloid (1-42) peptide impairs blood-brain barrier function after intracarotid infusion in rats

Gábor Jancsó, Ferenc Domoki, Péter Sántha, József Varga, János Fischer, Krisztina Orosz, Botond Penke, Attila Becskei, Mária Dux, Lajos Tóth

Research output: Contribution to journalArticle

59 Citations (Scopus)

Abstract

The effects of intracarotid infusions of β-amyloid (1-42) peptide was studied on the permeability of brain vessels. Using a quantitative Evans blue method a dose-dependent increase of brain tissue albumin content was established following intracarotid injections of the peptide. Cerebral vessels of increased permeability were also demonstrated with a vital 'staining' technique. Lectin histochemistry revealed an almost complete abolition of specific lectin binding sites of affected endothelial cells. The findings indicate a significant deterioration by β-amyloid (1-42) peptide of blood-brain barrier function and suggest that this may result from endothelial damage. It is assumed that altered permeability of cerebral vessels may be involved in the development of brain pathologies associated with Alzheimer's disease.

Original languageEnglish
Pages (from-to)139-141
Number of pages3
JournalNeuroscience Letters
Volume253
Issue number2
DOIs
Publication statusPublished - Sep 4 1998

Keywords

  • Alzheimer's disease
  • Blood-brain barrier
  • Cerebral vessel
  • Lectin binding
  • Permeability
  • Vascular labelling
  • β-Amyloid (1-42) peptide

ASJC Scopus subject areas

  • Neuroscience(all)

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