Abstract
In its earliest clinical phase, Alzheimer's disease characteristically produces a remarkably pure impairment of memory. Mounting evidence suggests that this syndrome begins with subtle alterations of hippocampal synaptic efficacy prior to frank neuronal degeneration, and that the synaptic dysfunction is caused by diffusible oligomeric assemblies of the amyloid beta protein.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Alzheimer Disease / pathology
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Alzheimer Disease / physiopathology*
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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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Brain / pathology
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Brain / physiopathology*
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Cognition
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Humans
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Long-Term Potentiation
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Membrane Proteins / genetics
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Memory
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Mice
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Mice, Transgenic
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Presenilin-1
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Synapses / physiology*
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Synapses / ultrastructure
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Synaptic Transmission
Substances
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Amyloid beta-Peptides
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Amyloid beta-Protein Precursor
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Membrane Proteins
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PSEN1 protein, human
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Presenilin-1