Abstract
Six weeks after bilateral olfactory bulbectomy, a peptide with molecular weight of 4 kD was revealed in extracts of the neocortex and hippocampus from mice. Using monoclonal antibodies 4G8, this peptide was identified as beta-amyloid. Its level was significantly higher in the bulbectomized animals than in sham-operated mice. The bulbectomized mice displayed sharp impairment in spatial memory when tested in the Morris water maze. The results suggest that bulbectomy initiates in the brain a pathological process similar to human Alzheimer's disease in location, biochemistry, and behavioral manifestations.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Alzheimer Disease / etiology
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Alzheimer Disease / metabolism*
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Alzheimer Disease / physiopathology
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Amyloid beta-Peptides / analysis
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Amyloid beta-Peptides / metabolism*
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Animals
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Behavior, Animal / physiology
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Brain Chemistry*
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Disease Models, Animal
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Hippocampus / chemistry
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Hippocampus / metabolism*
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Humans
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Male
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Maze Learning / physiology
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Memory / physiology
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Mice
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Neocortex / chemistry
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Neocortex / metabolism*
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Olfactory Pathways / surgery
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Peptide Fragments / analysis
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Peptide Fragments / metabolism
Substances
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Amyloid beta-Peptides
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Peptide Fragments