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Nat Neurosci. 1999 Feb;2(2):157-61.

SOD1 rescues cerebral endothelial dysfunction in mice overexpressing amyloid precursor protein.

Author information

1
Department of Neurology, University of Minnesota, Minneapolis 55455, USA. iadec001@tc.umn.edu

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.

PMID:
10195200
DOI:
10.1038/5715
[Indexed for MEDLINE]

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