Involvement of the Nitric Oxide Pathway in Synaptic Dysfunction Following Amyloid Elevation in Alzheimer's Disease

Overview

Journal Rev Neurosci

Publisher De Gruyter

Specialty Neurology

Date 2006 Dec 22

PMID 17180876

Citations 23

Authors

Daniela Puzzo

Agostino Palmeri

Ottavio Arancio

Affiliations

Soon will be listed here.

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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