Abstract
The distribution patterns of amyloid precursor protein (APP) fragments were studied immunocytochemically in the rat brain before, after 10 min ischemia and following treatment by idebenone. Six months after brain ischemia intense staining for APP appeared in extra- and intracellular space. These findings indicate that APP is involved in the degeneration process of brain neuronal and glial cells following ischemia-reperfusion injury and anti-oxidative therapy did not prevent and/or stop this phenomenon.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Alzheimer Disease / etiology*
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Amyloid beta-Protein Precursor / analysis
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Amyloid beta-Protein Precursor / metabolism*
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Amyloidosis / etiology
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Amyloidosis / prevention & control*
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Animals
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Antioxidants / therapeutic use*
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Benzoquinones / therapeutic use*
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Cell Death
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Drug Evaluation, Preclinical
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Extracellular Space / chemistry
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Female
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Free Radicals
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Heart Arrest / complications
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Hypoxia-Ischemia, Brain / drug therapy*
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Hypoxia-Ischemia, Brain / etiology
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Hypoxia-Ischemia, Brain / metabolism
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Hypoxia-Ischemia, Brain / pathology
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Intracellular Fluid / chemistry
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Neuroglia / pathology
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Neurons / pathology
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Neuroprotective Agents / therapeutic use*
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Oxidative Stress
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Rats
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Rats, Wistar
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Reperfusion Injury / drug therapy*
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Reperfusion Injury / etiology
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Reperfusion Injury / metabolism
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Reperfusion Injury / pathology
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Risk Factors
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Ubiquinone / analogs & derivatives
Substances
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Amyloid beta-Protein Precursor
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Antioxidants
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Benzoquinones
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Free Radicals
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Neuroprotective Agents
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Ubiquinone
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idebenone