Abstract
The primal role that the amyloid-beta (Abeta) peptide has in the development of Alzheimer's disease is now almost universally accepted. It is also well recognized that Abeta exists in multiple assembly states, which have different physiological or pathophysiological effects. Although the classical view is that Abeta is deposited extracellularly, emerging evidence from transgenic mice and human patients indicates that this peptide can also accumulate intraneuronally, which may contribute to disease progression.
Publication types
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Research Support, N.I.H., Extramural
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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 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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Brain / metabolism*
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Brain / pathology
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Brain / physiopathology
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Extracellular Fluid / metabolism
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Humans
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Intracellular Fluid / metabolism*
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Plaque, Amyloid / genetics
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Plaque, Amyloid / metabolism*
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Plaque, Amyloid / pathology
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Proteasome Endopeptidase Complex / metabolism
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Synaptic Transmission / physiology
Substances
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Amyloid beta-Peptides
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Amyloid beta-Protein Precursor
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Proteasome Endopeptidase Complex