Abstract
Neuronal oxidative stress occurs early in the progression of Alzheimer disease (AD), significantly before the development of the pathologic hallmarks, neurofibrillary tangles, and senile plaques. Study of Down syndrome, cases with autosomal dominant mutation, and sporadic AD all suggest amyloid-beta deposition and hyperphosphorylated tau function as compensatory responses and downstream adaptations to ensure that neuronal cells do not succumb to oxidative damage. Amyloid-beta and tau hyperphosphorylation also define vulnerable muscle cells in sporadic inclusion-body myositis (s-IBM). The role of the structural changes of s-IBM, as in AD, remains to be determined but may mark a critical response yielding a novel balance in oxidant homeostasis.
Publication types
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Comparative Study
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Adaptation, Physiological
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Alzheimer Disease / metabolism*
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Amyloid beta-Peptides / metabolism
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Cell Line, Tumor
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Down Syndrome / metabolism
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Drug Design
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Free Radical Scavengers / therapeutic use
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Heme Oxygenase-1 / genetics
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Heme Oxygenase-1 / metabolism
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Homeostasis
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Humans
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Mitochondria / metabolism
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Mitochondria, Muscle / metabolism
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Muscle Cells / metabolism
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Myositis, Inclusion Body / metabolism*
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Nerve Tissue Proteins / metabolism
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Neuroblastoma / pathology
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Neurons / metabolism
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Nootropic Agents / therapeutic use
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Oxidative Stress*
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Recombinant Fusion Proteins / physiology
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Transfection
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tau Proteins
Substances
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Amyloid beta-Peptides
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Free Radical Scavengers
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MAPT protein, human
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Nerve Tissue Proteins
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Nootropic Agents
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Recombinant Fusion Proteins
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tau Proteins
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Heme Oxygenase-1