Abstract
Accumulation of beta-amyloid protein (Abeta) in the extracellular space of the brain has been hypothesized to be a culprit in the pathogenesis of Alzheimer's disease. In this issue of Neuron, Cirrito et al. describe a series of experiments demonstrating that extracellular Abeta levels are directly modulated by neuronal and synaptic activity.
MeSH terms
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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 / metabolism*
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Animals
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Aspartic Acid Endopeptidases
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Brain / metabolism*
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Brain / physiopathology
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Endopeptidases / metabolism
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Extracellular Fluid / metabolism
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Humans
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Plaque, Amyloid / metabolism
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Presynaptic Terminals / metabolism*
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Synaptic Transmission / physiology*
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Synaptic Vesicles / metabolism
Substances
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Amyloid beta-Peptides
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Amyloid Precursor Protein Secretases
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Endopeptidases
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Aspartic Acid Endopeptidases
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BACE1 protein, human