Involvement of 'stress-response' kinase pathways in Alzheimer's disease progression.

Involvement of 'stress-response' kinase pathways in Alzheimer's disease progression.
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DOI:
10.1016/j.conb.2014.03.011
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发表时间:
2014-08
影响因子:
5.7
通讯作者:
Polleux F
Polleux F
中科院分区:
医学2区
文献类型:
--
作者:
Mairet-Coello G;Polleux F

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阿尔茨海默病(AD)是痴呆症最常见的原因,全世界有超过2500万人受到影响。目前AD病理生理机制的模型表明,淀粉样蛋白A(Aβ,Aβ)多肽的聚集导致兴奋性突触的早期丧失,损害突触的可塑性。介导Aβ寡聚体引起的突触可塑性受损和兴奋性突触丢失的信号通路才刚刚开始解开。在这里,我们回顾了最近的证据支持保守的‘应激-反应’激酶通路在AD进展中的关键作用。
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.
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