Abstract
The amyloid precursor protein and the proteases cleaving this protein are important players in the pathogenesis of Alzheimer's disease via the generation of the amyloid peptide. Physiologically, the amyloid precursor protein is implied in axonal vesicular trafficking and the proteases are implicated in developmentally important signaling pathways, most significantly those involving regulated intramembrane proteolysis or RIP. We discuss the cell biology behind the amyloid and tangle hypothesis for Alzheimer's disease, drawing on the many links to the fields of cell biology and developmental biology that have been established in the recent years.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Alzheimer Disease / genetics
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Alzheimer Disease / metabolism*
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Alzheimer Disease / physiopathology
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Amyloid Precursor Protein Secretases
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Amyloid beta-Peptides / genetics
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Amyloid beta-Peptides / metabolism*
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Amyloid beta-Protein Precursor / genetics
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Amyloid beta-Protein Precursor / metabolism*
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Animals
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Aspartic Acid Endopeptidases
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Endopeptidases / genetics
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Endopeptidases / metabolism
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Humans
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Intracellular Membranes / metabolism*
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Membrane Glycoproteins / genetics
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Membrane Glycoproteins / metabolism
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Membrane Proteins / genetics
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Membrane Proteins / metabolism
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Neurons / metabolism*
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Neurons / pathology
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Peptide Hydrolases / genetics
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Peptide Hydrolases / metabolism*
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Presenilin-1
Substances
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Amyloid beta-Peptides
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Amyloid beta-Protein Precursor
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Membrane Glycoproteins
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Membrane Proteins
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PSEN1 protein, human
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Presenilin-1
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nicastrin protein
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Amyloid Precursor Protein Secretases
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Endopeptidases
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Peptide Hydrolases
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Aspartic Acid Endopeptidases
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BACE1 protein, human