| Neurodegeneration, Alzheimer's disease, and beta-amyloid toxicity. | |
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MedLine Citation:
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PMID: 7997056 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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In its majority, Alzheimer's disease is sporadic and with late onset. Therefore, age-related disturbances in cellular metabolism may come into focus with respect to the etiopathogenesis of this neurodegenerative disorder. As a possible primary abnormal event in sporadic Alzheimer's disease, a desensitization of the neuronal insulin receptor and the subsequent deficits in ATP and acetylcholine are discussed with its impact on protein processing in general and beta-amyloid formation in particular, and neurotoxicity of the latter. |
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Authors:
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S Hoyer |
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Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: Life sciences Volume: 55 ISSN: 0024-3205 ISO Abbreviation: Life Sci. Publication Date: 1994 |
Date Detail:
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Created Date: 1995-01-18 Completed Date: 1995-01-18 Revised Date: 2005-11-16 |
Medline Journal Info:
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Nlm Unique ID: 0375521 Medline TA: Life Sci Country: ENGLAND |
Other Details:
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Languages: eng Pagination: 1977-83 Citation Subset: IM |
Affiliation:
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Department of Pathochemistry and General Neurochemistry, University of Heidelberg, FRG. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Alzheimer Disease
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physiopathology* Amyloid beta-Protein / biosynthesis, physiology* Animals Humans Nerve Degeneration / physiology* |
| Chemical | |
Reg. No./Substance:
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0/Amyloid beta-Protein |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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