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Front Aging Neurosci. 2010 May 21;2. doi: 10.3389/fnagi.2010.00013. eCollection 2010.

Synapses, synaptic activity and intraneuronal abeta in Alzheimer's disease.

Frontiers in aging neuroscience

Davide Tampellini, Gunnar K Gouras

Affiliations

  1. Department of Neurology and Neuroscience, Weill Cornell Medical College New York, NY, USA.

PMID: 20725518 PMCID: PMC2912028 DOI: 10.3389/fnagi.2010.00013

Abstract

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.

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

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