Abstract
After much initial debate for and against the role of amyloid in Alzheimer's disease (AD), mutations on the amyloid precursor protein (APP) and processing pathways that increase levels of the amyloid b peptide of 42 residues (Abeta42) have established that faulty function or processing of these proteins are responsible for AD pathogenesis. Given the neurotoxicity of aggregates of Ab42, the central role of this peptide in AD pathogenesis is self evident. In this article, I summarize the major pieces of evidence adduced to support the amyloid cascade hypothesis and point out their limitations.
MeSH terms
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Alzheimer Disease / genetics
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Alzheimer Disease / physiopathology*
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Amyloid / genetics
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Amyloid / physiology*
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Amyloid beta-Peptides / genetics*
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Amyloid beta-Peptides / physiology
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Amyloid beta-Peptides / toxicity
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Amyloid beta-Protein Precursor / genetics
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Animals
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Apolipoproteins E / metabolism
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Humans
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Immunization
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Immunotherapy
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Mice
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Mice, Transgenic
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Neurofibrillary Tangles / pathology
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Peptide Fragments / genetics*
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Peptide Fragments / toxicity
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tau Proteins / genetics
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tau Proteins / metabolism
Substances
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Amyloid
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Amyloid beta-Peptides
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Amyloid beta-Protein Precursor
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Apolipoproteins E
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Peptide Fragments
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amyloid beta-protein (1-42)
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tau Proteins