Abstract
Glutamate neurotoxicity may be an underlying pathological mechanism contributing to neuronal cell loss in a variety of conditions including Alzheimer's disease (AD). In this study, we examined whether the beta-amyloid protein found in the neuritic plaques of AD alters the susceptibility of neurons to excitotoxic damage. While mature cortical neurons exposed to beta-amyloid protein for 2-4 days did not appear to be damaged, their vulnerability to low-intensity exposure to glutamate, N-methyl-D-aspartate, and kainate increased, suggesting that this mechanism may contribute to the neurodegeneration seen in AD.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Alzheimer Disease / physiopathology
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Amyloid beta-Peptides / pharmacology*
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Animals
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Cell Survival / drug effects
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Cells, Cultured
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Cerebral Cortex / cytology
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Cerebral Cortex / drug effects*
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Cerebral Cortex / embryology
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Glutamates / toxicity
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Kainic Acid / toxicity
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L-Lactate Dehydrogenase / metabolism
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Mice
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N-Methylaspartate / toxicity
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Nerve Tissue Proteins / pharmacology*
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Neurons / drug effects*
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Neurotoxins / pharmacology*
Substances
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Amyloid beta-Peptides
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Glutamates
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Nerve Tissue Proteins
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Neurotoxins
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N-Methylaspartate
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L-Lactate Dehydrogenase
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Kainic Acid