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Updated: Jul 18, 2026

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices
Published on: July 14, 2010
Involvement of the nitric oxide pathway in synaptic dysfunction following amyloid elevation in Alzheimer's disease
Daniela Puzzo1, Agostino Palmeri, Ottavio Arancio
1Department of Pathology, Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, New York, NY, USA. danypuzzo@yahoo.it
Abstract:
Amyloid-beta (Abeta), a peptide thought to play a crucial role in Alzheimer's disease (AD), has attracted scientific interest with the aim of characterizing the mechanisms by which it is involved in AD pathogenesis. Abeta has been found to markedly impair hippocampal long-term potentiation (LTP), a widely studied cellular model of synaptic plasticity that is thought to underlie learning and memory. The overall purpose of this review is to define the role of the nitric oxide (NO)/cGMP/cAMP-regulatory element binding (CREB) pathway in beta-amyloid-induced changes of basal neurotransmission and synaptic plasticity in the hippocampus, a structure within the temporal lobe of the brain critical for memory storage.
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