Puzzo Daniela, Palmeri Agostino, Arancio Ottavio
Department of Pathology, Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, New York, NY, USA.
Rev Neurosci. 2006;17(5):497-523. doi: 10.1515/revneuro.2006.17.5.497.
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.
β-淀粉样蛋白（Aβ）是一种被认为在阿尔茨海默病（AD）中起关键作用的肽，为了阐明其参与AD发病机制的机制，它已引起了科学界的关注。人们发现Aβ会显著损害海马体长期增强效应（LTP），LTP是一种被广泛研究的突触可塑性细胞模型，被认为是学习和记忆的基础。本综述的总体目的是确定一氧化氮（NO）/环鸟苷酸（cGMP）/环磷酸腺苷（cAMP）反应元件结合蛋白（CREB）信号通路在β-淀粉样蛋白诱导的海马体基础神经传递和突触可塑性变化中的作用，海马体是大脑颞叶内对记忆存储至关重要的结构。
