SOD1 rescues cerebral endothelial dysfunction in mice overexpressing amyloid precursor protein Academic Article uri icon

Overview

MeSH Major

  • Amyloid beta-Protein Precursor
  • Cerebrovascular Circulation
  • Superoxide Dismutase

abstract

  • Peptides derived from proteolytic processing of the beta-amyloid precursor protein (APP), including the amyloid-beta peptide, are important for the pathogenesis of Alzheimer's dementia. We found that transgenic mice overexpressing APP have a profound and selective impairment in endothelium-dependent regulation of the neocortical microcirculation. Such endothelial dysfunction was not found in transgenic mice expressing both APP and superoxide dismutase-1 (SOD1) or in APP transgenics in which SOD was topically applied to the cerebral cortex. These cerebrovascular effects of peptides derived from APP processing may contribute to the alterations in cerebral blood flow and to neuronal dysfunction in Alzheimer's dementia.

publication date

  • February 1999

Research

keywords

  • Academic Article

Identity

Language

  • eng

Digital Object Identifier (DOI)

  • 10.1038/5715

PubMed ID

  • 10195200

Additional Document Info

start page

  • 157

end page

  • 61

volume

  • 2

number

  • 2