Induction of Alzheimer-like β-amyloid immunoreactivity in the brains of rabbits with dietary cholesterol

DL Sparks, SW Scheff, JC Hunsaker III, H Liu… - Experimental …, 1994 - Elsevier
DL Sparks, SW Scheff, JC Hunsaker III, H Liu, T Landers, DR Gross
Experimental neurology, 1994Elsevier
Abstract β-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 β-amyloid within 3 min after death. In animals
fed the experimental diet for 4, 6, and 8 weeks (postmorten interval< 3 min), there was an
increasingly mild-to-moderate-to-severe accumulation of intracellular immunolabeled β-
amyloid. Whether or not β-amyloid is causally linked to processes lending to dementia, it is …
Abstract
β-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 β-amyloid within 3 min after death. In animals fed the experimental diet for 4, 6, and 8 weeks (postmorten interval < 3 min), there was an increasingly mild-to-moderate-to-severe accumulation of intracellular immunolabeled β-amyloid. Whether or not β-amyloid is causally linked to processes lending 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 β-APP metabolism leading to Alzheimer-like β-amyloid accumulation xe03and extracellular deposition in brain.
Elsevier