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Ann N Y Acad Sci. 2000 Apr;903:335-44. doi: 10.1111/j.1749-6632.2000.tb06384.x.

Alterations of Alzheimer's disease in the HHS Vulnerability Disclosure

cholesterol-fed rabbit, including vascular

inflammation. Preliminary observations
D L Sparks 1 , Y M Kuo, A Roher, T Martin, R J Lukas

Affiliations
PMID: 10818523 DOI: 10.1111/j.1749-6632.2000.tb06384.x

Abstract
We determined the levels of endothelial inflammation using MECA-32 antibody and alpha 4
nicotinic receptor subunit densities employing [3H]epibatidine binding in the brains of Alzheimer's
disease (AD) patients, cholesterol-fed rabbits, and appropriate controls. We also assessed rabbit
brain for beta-amyloid levels and immunohistochemical localization, and for evidence of blood-
brain barrier breach using normally-excluded Evans Blue dye. Dietary cholesterol induced a twofold
increase in beta-amyloid concentration in rabbit hippocampal cortex, which may be related to the
appearance of beta-amyloid immunoreactivity in the neuropil. Epibatidine binding was significantly
decreased in AD superior frontal cortex, but unchanged in the superior frontal cortex of
cholesterol-fed rabbits. Increased vascular MECA-32 immunoreactivity occurred in AD and
cholesterol-fed rabbit brain. Evans Blue dye could be found in the parenchyma of cholesterol-fed
rabbits only, and appeared as pockets of dye surrounding small blood vessels. The data suggest
that vascular inflammation can lead to breach of the blood-brain barrier, which may produce
biochemical derangements in surrounding brain tissue that are conducive to production of beta-
amyloid.

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