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

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.

journal_name

Nat Neurosci

journal_title

Nature neuroscience

authors

Iadecola C,Zhang F,Niwa K,Eckman C,Turner SK,Fischer E,Younkin S,Borchelt DR,Hsiao KK,Carlson GA

doi

10.1038/5715

subject

Has Abstract

pub_date

1999-02-01 00:00:00

pages

157-61

issue

2

eissn

1097-6256

issn

1546-1726

journal_volume

2

pub_type

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