Activation of neuronal extracellular receptor kinase (ERK) in Alzheimer disease links oxidative stress to abnormal phosphorylation
Activation of neuronal extracellular receptor kinase (ERK) in Alzheimer disease links oxidative stress to abnormal phosphorylation
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DOI：
10.1097/00001756-199908020-00035
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发表时间：
1999-08-02
期刊：
影响因子：
1.7
通讯作者：
Smith, MA
中科院分区：
文献类型：
--
作者：
Perry, G;Roder, H;Smith, MA
对氧化应激增加的反应可能是导致阿尔茨海默病（AD）不同细胞病理学的共同机制。支持这一假说的一个可能的联系是，AD最显著的特征之一是高度磷酸化的tau和神经丝蛋白的异常积累，这可能是由细胞外受体激酶（ERK）引起的，ERK的激活是氧化应激的一种常见反应。在这项研究中，我们证明了活化的ERK在AD的相同易损神经元中特异性增加，这些神经元是氧化损伤和异常磷酸化的部位。这些发现表明，可能由氧化应激引起的ERK失调可能在AD中观察到的细胞骨架蛋白磷酸化增加中发挥重要作用。神经报告10:2411-2415 (C) 1999 Lippincott Williams & Wilkins。
RESPONSES to increased oxidative stress may be the common mechanism responsible for the varied cytopathology of Alzheimer disease (AD). A possible link in support of this hypothesis is that one of the most striking features of AD, the abnormal accumulation of highly phosphorylated tau and neurofilament proteins, may be brought about by extracellular receptor kinase (ERK) whose activation is a common response to oxidative stress. In this study, we demonstrate that activated ERK is specifically increased in the same vulnerable neurons in AD that are the site of oxidative damage and abnormal phosphorylation. These findings suggest that ERK dysregulation, likely resulting from oxidative stress, could play an important role in the increased phosphorylation of cytoskeletal proteins observed in AD. NeuroReport 10:2411-2415 (C) 1999 Lippincott Williams & Wilkins.