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Synapses, synaptic activity and intraneuronal Aβ in Alzheimer's disease

Journal

FRONTIERS IN AGING NEUROSCIENCE
Volume 2, Issue -, Pages -

Publisher

FRONTIERS MEDIA SA
DOI: 10.3389/fnagi.2010.00013

Keywords

Alzheimer disease; amyloid; amyloid precursor protein; synapse; synaptic plasticity; neprilysin; neuron; neurodegeneration

Funding

  1. Alzheimer's Association New Investigator Award
  2. Zenith Award
  3. National Institute of Health [AG027140, AG028174]

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beta-Amyloid peptide accumulation plays a central role in the pathogenesis of Alzheimer's disease. Aberrant beta-amyloid buildup in the brain has been shown to be present both in the extracellular space and within neurons. Synapses are important targets of beta-amyloid, and alterations in synapses better correlate with cognitive impairment than amyloid plaques or neurofibrillary tangles. The link between beta-amyloid and synapses became even tighter when it was discovered that beta-amyloid accumulates within synapses and that synaptic activity modulates beta-amyloid secretion. Currently, a central question in Alzheimer's disease research is what role synaptic activity plays in the disease process, and how specifically beta-amyloid is involved in the synaptic dysfunction that characterizes the disease.

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