In:
Annals of the New York Academy of Sciences, Wiley, Vol. 903, No. 1 ( 2000-04), p. 335-344
Abstract:
A bstract : We determined the levels of endothelial inflammation using MECA‐32 antibody and a4 nicotinic receptor subunit densities employing [ 3 H]epibatidine binding in the brains of Alzheimer's disease (AD) patients, cholesterol‐fed rabbits, and appropriate controls. We also assessed rabbit brain for β‐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 β‐amyloid concentration in rabbit hippocampal cortex, which may be related to the appearance of β‐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 β‐amyloid.
Type of Medium:
Online Resource
ISSN:
0077-8923
,
1749-6632
DOI:
10.1111/nyas.2000.903.issue-1
DOI:
10.1111/j.1749-6632.2000.tb06384.x
Language:
English
Publisher:
Wiley
Publication Date:
2000
detail.hit.zdb_id:
2834079-6
detail.hit.zdb_id:
211003-9
detail.hit.zdb_id:
2071584-5
SSG:
11
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