Abstract
One of the theories involved in the etiology of Alzheimer's disease (AD) is the oxidative stress hypothesis. The amyloid beta-peptide (A beta), a hallmark in the pathogenesis of AD and the main component of senile plaques, generates free radicals in a metal-catalyzed reaction inducing neuronal cell death by a reactive oxygen species mediated process which damage neuronal membrane lipids, proteins and nucleic acids. Therefore, the interest in the protective role of different antioxidants in AD such as vitamin E, melatonin and estrogens is growing up. In this review we summarize data that support the involvement of oxidative stress as an active factor in A beta-mediated neuropathology, by triggering or facilitating neurodegeneration, through a wide range of molecular events that disturb neuronal cell homeostasis.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Alzheimer Disease / etiology
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Alzheimer Disease / immunology
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Alzheimer Disease / metabolism*
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Amyloid beta-Peptides / metabolism*
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Amyloid beta-Peptides / toxicity
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Animals
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Antioxidants / metabolism
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Antioxidants / pharmacology
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Apoptosis / drug effects
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Cell Death / drug effects
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Humans
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Membrane Lipids / metabolism
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Metals / metabolism
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Neuroprotective Agents / pharmacology
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Nucleic Acids / metabolism
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Oxidative Stress / drug effects
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Oxidative Stress / immunology
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Oxidative Stress / physiology*
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Proteins / metabolism
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Reactive Oxygen Species / metabolism
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Receptors, Cell Surface / metabolism
Substances
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Amyloid beta-Peptides
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Antioxidants
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Membrane Lipids
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Metals
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Neuroprotective Agents
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Nucleic Acids
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Proteins
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Reactive Oxygen Species
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Receptors, Cell Surface