Abstract
Little is known about the metabolic process of tau and tau-derived substances. Alz-50- and tau 2-immunoreactivities in intracellular granules of neurons were observed in regions surrounding infarcted foci in the human cerebral cortex. Ultrastructurally, these granules in the fresh infarcted region exhibited primary lysosome-like structures, while those in old infarctions were lipofuscin. These findings indicate that tau is metabolized within lysosomes in neurons damaged by ischemic injury in human cortical penumbra. Alz-50-positive granules were more prominent in fresh infarction than in old infarction. After undergoing degradation and modification, altered tau might remain, at least partially, in secondary lysosomes.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Aged
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Aged, 80 and over
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Antigens / analysis*
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Antigens / immunology
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Brain Ischemia / metabolism
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Brain Ischemia / pathology
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Cerebral Cortex / metabolism*
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Cerebral Cortex / pathology
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Cerebral Cortex / ultrastructure
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Cerebral Infarction / metabolism*
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Cerebral Infarction / pathology
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Cytoplasmic Granules / chemistry
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Cytoplasmic Granules / metabolism
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Cytoplasmic Granules / ultrastructure
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Humans
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Immunohistochemistry
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Lipofuscin / analysis
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Lysosomes / chemistry
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Lysosomes / metabolism*
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Lysosomes / ultrastructure
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Microscopy, Immunoelectron
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Neurons / metabolism*
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Neurons / pathology
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Neurons / ultrastructure
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Time Factors
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tau Proteins / chemistry
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tau Proteins / immunology
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tau Proteins / metabolism*
Substances
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Alzheimer's disease antigen
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Antigens
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Lipofuscin
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tau Proteins