Abstract
Dietary factors may play a role in Alzheimer's disease (AD) pathogenesis. In an effort to recapitulate some of the synaptic protein changes observed in the disease, AD transgenic and wild-type mice were fed either a normal or pro-oxidant diet for 3 months from three months of age. Pro-oxidant diet treatment resulted in altered expression of vesicular glutamate transporter-1 and glutamine synthetase, suggesting changes in glutamatergic synaptic function, and increased expression of urokinase plasminogen activator receptor, possibly reflecting oxidative stress.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Alzheimer Disease / diet therapy*
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Alzheimer Disease / genetics
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Alzheimer Disease / metabolism
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Amyloid beta-Protein Precursor / genetics
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Animals
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Dietary Supplements
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Disease Models, Animal
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Gene Expression Regulation / drug effects*
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Gene Expression Regulation / genetics
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Glutamate-Ammonia Ligase / metabolism
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Humans
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Mice
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Mice, Transgenic
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Mutation / genetics
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Oxidants / administration & dosage*
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Presenilin-1 / genetics
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Receptors, Urokinase Plasminogen Activator / metabolism
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Synaptophysin / metabolism
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Vesicular Glutamate Transport Protein 1 / metabolism*
Substances
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Amyloid beta-Protein Precursor
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Oxidants
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PSEN1 protein, human
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Presenilin-1
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Receptors, Urokinase Plasminogen Activator
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SLC17A7 protein, human
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Synaptophysin
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Vesicular Glutamate Transport Protein 1
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Glutamate-Ammonia Ligase