Involvement of the nitric oxide pathway in synaptic dysfunction following amyloid elevation in Alzheimer's disease.
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.
Puzzo
Daniela
D
Department of Pathology, Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, New York, NY, USA. danypuzzo@yahoo.it
Palmeri
Agostino
A
Arancio
Ottavio
O
D000544:Alzheimer Disease / Q000378:metabolism* / Q000473:pathology; D016229:Amyloid beta-Peptides / Q000737:chemistry / Q000378:metabolism*; D000818:Animals; D017362:Cyclic AMP Response Element-Binding Protein / Q000378:metabolism; D006152:Cyclic GMP / Q000378:metabolism; D006624:Hippocampus / Q000473:pathology / Q000502:physiology*; D006801:Humans; D017774:Long-Term Potentiation / Q000502:physiology; D009473:Neuronal Plasticity / Q000502:physiology*; D009569:Nitric Oxide / Q000737:chemistry / Q000378:metabolism*; D013569:Synapses / Q000378:metabolism / Q000473:pathology*
D016229:Amyloid beta-Peptides; D017362:Cyclic AMP Response Element-Binding Protein; D009569:Nitric Oxide; D006152:Cyclic GMP