Abstract
The amyloid hypothesis has been the basis for most work on the pathogenesis of Alzheimer's disease. Recent clinical trials based on this hypothesis have been inconclusive. In this article I review the current status of the hypothesis and suggest that a major scientific need is to understand the normal function of amyloid-beta precursor protein (APP) and think how this may relate to the cell death in the disease process.
MeSH terms
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Alzheimer Disease / drug therapy*
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Alzheimer Disease / etiology*
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Alzheimer Disease / metabolism
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Alzheimer Vaccines / adverse effects
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Amyloid beta-Peptides / antagonists & inhibitors
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Amyloid beta-Peptides / immunology
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Amyloid beta-Peptides / metabolism*
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Amyloid beta-Protein Precursor / metabolism*
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Brain / drug effects*
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Brain / metabolism
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Brain / physiopathology*
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Cerebral Arteries / drug effects
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Cerebral Arteries / metabolism
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Cerebral Arteries / physiopathology
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Clinical Trials as Topic / methods
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Clinical Trials as Topic / standards
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Disease Progression
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Humans
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Nerve Degeneration / drug therapy
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Nerve Degeneration / metabolism
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Nerve Degeneration / physiopathology
Substances
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Alzheimer Vaccines
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Amyloid beta-Peptides
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Amyloid beta-Protein Precursor