微管相关蛋白tau磷酸化在阿尔茨海默病中的作用。

Q Engineering
Rong-Hong Ma, Yao Zhang, Xiao-Yue Hong, Jun-Fei Zhang, Jian-Zhi Wang, Gong-Ping Liu
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引用次数: 22

摘要

作为一种主要的微管相关蛋白,tau蛋白在促进微管组装和稳定微管方面发挥着重要作用。在阿尔茨海默病(AD)和其他tau病变中,异常过度磷酸化的tau蛋白聚集成成对的螺旋细丝,并以神经原纤维缠结的形式积聚在神经元中。蛋白激酶和蛋白磷酸酶的不平衡调节是tau过度磷酸化的直接原因。在各种激酶和磷酸酶中,糖原合成酶激酶-3β (GSK-3β)和蛋白磷酸酶2A (PP2A)是最受影响的。过度磷酸化的tau蛋白的积累诱导突触毒性和认知障碍。在这里,我们主要基于我们最近的发现回顾了可以调节GSK-3β或PP2A活性的上游因子或途径。我们还将讨论可能导致tau诱导突触毒性的机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Role of microtubule-associated protein tau phosphorylation in Alzheimer's disease.

As a major microtubule-associated protein, tau plays an important role in promoting microtubule assembly and stabilizing microtubules. In Alzheimer's disease (AD) and other tauopathies, the abnormally hyperphosphorylated tau proteins are aggregated into paired helical filaments and accumulated in the neurons with the form of neurofibrillary tangles. An imbalanced regulation in protein kinases and protein phosphatases is the direct cause of tau hyperphosphorylation. Among various kinases and phosphatases, glycogen synthase kinase-3β (GSK-3β) and protein phosphatase 2A (PP2A) are the most implicated. Accumulation of the hyperphosphorylated tau induces synaptic toxicity and cognitive impairments. Here, we review the upstream factors or pathways that can regulate GSK-3β or PP2A activity mainly based on our recent findings. We will also discuss the mechanisms that may underlie tau-induced synaptic toxicity.

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来源期刊
CiteScore
1.08
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3-8 weeks
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