Ionic effects of the Alzheimer's disease β-amyloid precursor protein and its metabolic fragments
Alzheimer's disease is a progressive dementia characterized in part by deposition of proteinaceous plaques in various areas of the brain. The main plaque protein component is β-amyloid, a metabolic product of the β-amyloid precursor protein. Substantial evidence has implicated β-amyloid (and ot...
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Published in | Trends in neurosciences (Regular ed.) Vol. 20; no. 2; pp. 67 - 72 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
Oxford
Elsevier Ltd
01.02.1997
Elsevier Science Elsevier Sequoia S.A |
Subjects | |
Online Access | Get full text |
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Summary: | Alzheimer's disease is a progressive dementia characterized in part by deposition of proteinaceous plaques in various areas of the brain. The main plaque protein component is β-amyloid, a metabolic product of the β-amyloid precursor protein. Substantial evidence has implicated β-amyloid (and other amyloidogenic fragments of the precursor protein) with the neurodegeneration observed in Alzheimer's disease. Recently, β-amyloid precursor protein and its amyloidogenic metabolic fragments have been shown to alter cellular ionic activity, either through interaction with existing channels or by
de novo channel formation. Such alteration in ionic homeostasis has also been linked with cellular toxicity and might provide a molecular mechanism underlying the neurodegeneration seen in Alzheimer's disease. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 |
ISSN: | 0166-2236 1878-108X |
DOI: | 10.1016/S0166-2236(96)10079-5 |