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Exp Neurol. 1994 Mar;126(1):88-94. doi: 10.1006/exnr.1994.1044.

Induction of Alzheimer-like beta-amyloid HHS Vulnerability Disclosure

immunoreactivity in the brains of rabbits with

dietary cholesterol
D L Sparks 1 , S W Scheff, J C Hunsaker 3rd, H Liu, T Landers, D R Gross

Affiliations
PMID: 8157129 DOI: 10.1006/exnr.1994.1044

Abstract
beta-amyloid and ALZ-50 immunocytochemical reactivity were determined in the brains of rabbits
fed either a control or 2% cholesterol diet. Control rabbits demonstrated no accumulation of
intracellular immunolabeled beta-amyloid within 3 min after death. In animals fed the experimental
diet for 4, 6, and 8 weeks (postmortem interval < 3 min), there was an increasingly mild-to-
moderate-to-severe accumulation of intracellular immunolabeled beta-amyloid. Whether or not
beta-amyloid is causally linked to processes leading to dementia, it is related in some way to the
prime cause of human death; heart disease. Hypercholesterolemic rabbits may provide an animal
model to study altered beta-APP metabolism leading to Alzheimer-like beta-amyloid accumulation
xe03and extracellular deposition in brain.

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