Abstract
Beta-amyloid, the 39-43 amino acid peptide fragment originating from amyloid precursor protein, is today, generally accepted as the biological entity responsible for causing the debilitating human disorder Alzheimer's disease. Understanding the exact biological effects of beta-amyloid in vitro and in vivo is clearly important to provide therapeutic strategies for the disease. Recent in vitro studies have focused on the production of reactive oxygen species by aggregating beta-amyloid, but the cellular effects of beta-amyloid induced reactive oxygen species production have not been fully elucidated.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Alzheimer Disease / metabolism*
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Amyloid beta-Peptides / chemistry
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Amyloid beta-Peptides / pharmacology*
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Catalase / metabolism
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Cell Line, Tumor
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Glutathione Reductase / metabolism
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Glutathione Transferase / metabolism
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Humans
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Neuroblastoma / enzymology
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Neuroblastoma / metabolism
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Neuroblastoma / ultrastructure
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Oxidative Stress / drug effects*
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Peptide Fragments / chemistry
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Peptide Fragments / pharmacology*
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Superoxide Dismutase / metabolism
Substances
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Amyloid beta-Peptides
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Peptide Fragments
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amyloid beta-protein (1-40)
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Catalase
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Superoxide Dismutase
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Glutathione Reductase
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Glutathione Transferase