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Current Alzheimer Research

Editor-in-Chief

ISSN (Print): 1567-2050
ISSN (Online): 1875-5828

Oligomers of β-Amyloid Peptide Inhibit BDNF-Induced Arc Expression in Cultured Cortical Neurons

Author(s): Valentine Echeverria, Diego E. Berman and Ottavio Arancio

Volume 4 , Issue 5 , 2007

Page: [518 - 521] Pages: 4

DOI: 10.2174/156720507783018190

Price: $65

Abstract

The progressive memory loss observed in Alzheimers disease (AD) is accompanied by an increase in the levels of amyloid-β peptide (Aβ) and a block of synaptic plasticity. Both synaptic plasticity and memory require changes in the expression of synaptic proteins such as the activity-regulated cytoskeleton-associated protein, Arc (also termed Arg3.1). Using a model of synaptic plasticity in which BDNF increases Arc expression in cultured cortical neurons, we have found that an oligomeric form of Aβ strongly inhibits the BDNF-induced increase of Arc expression. Given that Aβ oligomers are likely to be involved in the synaptic dysfunction and cognitive impairment observed in amyloid depositing mouse models, we hypothesize that inhibition of Arc induction by BDNF contributes to the synaptic and memory deficits at early stages of AD.

Keywords: Synaptic plasticity, Arg3.1, Arc, Alzheimer's disease, LTP, BDNE


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