Abstract
Inflammatory and oxidative events are up-regulated in the brain of AD patients. It has been reported that in animal models of AD, exposure to aluminum (Al) or copper (Cu) enhanced oxidative events and accumulation of amyloid beta (Abeta) peptides. The present study was designed to evaluate the effect of a 3-month exposure of mice to copper sulfate (8 microM), aluminum lactate (10 or 100 microM), or a combination of the salts. Results suggest that although Al or Cu may independently initiate inflammatory or oxidative events, they may function cooperatively to increase APP levels.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Aluminum / toxicity*
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Alzheimer Disease / etiology
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Amyloid beta-Peptides / analysis
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Amyloid beta-Protein Precursor / analysis
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Animals
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Brain / drug effects*
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Brain / metabolism
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Copper / toxicity*
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Inflammation / chemically induced*
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Interleukin-1 / biosynthesis
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Interleukin-4 / biosynthesis
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Lipid Peroxidation
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Male
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Mice
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Mice, Inbred C3H
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Mice, Inbred C57BL
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Oxidation-Reduction
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Tumor Necrosis Factor-alpha / biosynthesis
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Water Supply / analysis*
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Water Supply / standards
Substances
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Amyloid beta-Peptides
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Amyloid beta-Protein Precursor
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Interleukin-1
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Tumor Necrosis Factor-alpha
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Interleukin-4
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Copper
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Aluminum