“应激反应”激酶通路在阿尔茨海默病进展中的作用。
Involvement of 'stress-response' kinase pathways in Alzheimer's disease progression.
作者信息
Mairet-Coello Georges, Polleux Franck
机构信息
The Scripps Research Institute, Dorris Neuroscience Center, Department of Molecular and Cellular Neuroscience, La Jolla, CA 92037-1000, USA.
The Scripps Research Institute, Dorris Neuroscience Center, Department of Molecular and Cellular Neuroscience, La Jolla, CA 92037-1000, USA.
出版信息
Curr Opin Neurobiol. 2014 Aug;27:110-7. doi: 10.1016/j.conb.2014.03.011. Epub 2014 Apr 5.
Abstract
Alzheimer's disease (AD) is the most prevalent cause of dementia, affecting more than 25 million people worldwide. Current models of the pathophysiological mechanisms of AD suggest that the accumulation of soluble oligomeric forms of amyloid-β (Aβ) peptides causes early loss of excitatory synapses and impairs synaptic plasticity. The signaling pathways mediating Aβ oligomer-induced impairment of synaptic plasticity and loss of excitatory synapses are only beginning to be unraveled. Here, we review recent evidence supporting the critical contribution of conserved 'stress-response' kinase pathways in AD progression.
摘要
阿尔茨海默病（AD）是痴呆最常见的病因，全球有超过2500万人受其影响。目前关于AD病理生理机制的模型表明，淀粉样β（Aβ）肽可溶性寡聚体形式的积累会导致兴奋性突触早期丧失并损害突触可塑性。介导Aβ寡聚体诱导的突触可塑性损害和兴奋性突触丧失的信号通路才刚刚开始被揭示。在此，我们综述了支持保守的“应激反应”激酶通路在AD进展中起关键作用的最新证据。
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