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SOD1 rescues cerebral endothelial dysfunction in mice overexpressing amyloid precursor protein

SOD1 rescues cerebral endothelial dysfunction in mice overexpressing amyloid precursor protein Peptides derived from proteolytic processing of the β–amyloid precursor protein (APP), including the amyloid–β 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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Nature Neuroscience Springer Journals

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References (52)

Publisher
Springer Journals
Copyright
Copyright © 1999 by Nature America Inc.
Subject
Biomedicine; Biomedicine, general; Neurosciences; Behavioral Sciences; Biological Techniques; Neurobiology; Animal Genetics and Genomics
ISSN
1097-6256
eISSN
1546-1726
DOI
10.1038/5715
Publisher site
See Article on Publisher Site

Abstract

Peptides derived from proteolytic processing of the β–amyloid precursor protein (APP), including the amyloid–β 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

Nature NeuroscienceSpringer Journals

Published: Feb 1, 1999

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