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Synapses, Synaptic Activity and Intraneuronal Aβ in Alzheimer's Disease

Authors
  • Tampellini, Davide1
  • Gouras, Gunnar K.1
  • 1 Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, NY, USA
Type
Published Article
Journal
Frontiers in Aging Neuroscience
Publisher
Frontiers Media SA
Publication Date
May 21, 2010
Volume
2
Identifiers
DOI: 10.3389/fnagi.2010.00013
Source
Frontiers
Keywords
Disciplines
  • Neuroscience
  • Review Article
License
Green

Abstract

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

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