Tau的异常磷酸化与Tau病

doi:10.12677/IJPN.2017.62002

期刊菜单

Tau的异常磷酸化与Tau病
Abnormally Phosphorylated Tau and Tauopathies

DOI: 10.12677/IJPN.2017.62002, PDF, HTML, XML, 下载: 2,073 浏览: 5,293
作者: 陈亦刚：武汉科技大学医学院，湖北武汉
关键词: 蛋白质；Tau；异常磷酸化；Tau病；功能障碍；Protein； Tau； Abnormal Phosphorylation； Tauopathy； Dysfunction

摘要: Tau蛋白是脑内非常重要的微管相关蛋白。其异常磷酸化在神经退行性疾病中起重要的作用。Tau病是一种tau蛋白异常疾病的总称，即神经细胞内、神经胶质细胞内异常磷酸化tau蛋白蓄积的神经变性疾病。在tau蛋白某些区域的过度磷酸化可影响tau与微管的结合能力，更为严重的是，tau蛋白的过度磷酸化可促进和增强tau蛋白的聚集。许多证据表明，在阿尔茨海默病(AD)及其他tau蛋白引起的病理过程中tau蛋白的过度磷酸化可能发生在最早期。Tau蛋白发生过度磷酸化可能是蛋白激酶活性上调或磷酸酯酶活性下调造成。AD等神经退行性疾病的发生机制尚不明确。对tau蛋白的相关功能及调控机制进行深入的研究可能为了解神经退行性疾病的临床和病理生理机制提供某些新的思路，为此类疾病的早期诊断和治疗提供一定的依据。

Abstract: Tau is the very important microtuble-associated protein in the brain. Abnormally phosphorylated tau plays an important effect. Tauopathy is a total name of the diseases aroused by abnormal tau protein, being the neurodenatured diseases with the accumulation of abnormally phosphorylated tau in the neural cells and neuroglias. The hyper-phosphorylation at some regions of tau may affect the binding ability of tau with the microtuble, and being severer, the hyper-phosphorylation can improve and enhance the accumulation of tau. There are many evidences, that manifested the hyper-phosphorylation of tau protein may happen in the most early stage in the pathological courses of Alzheimer’s disease and the other diseases caused by the abnormal tau protein. Hyper-phosphorylation of tau protein can be caused by the up-regulation of the activity in the protein kinases or the down-regulation of the activity in the protein phosphatases. It is still not clear how do happen the neurodegenerative diseases such as AD and so on. The deep researches about the relative function and regulation-control mechanism of tau protein maybe provide some new thinking for us understanding the clinic and pathophysiological mechanism, and offer certain bases for the diagnosis and treatment in the early stage of the diseases.

文章引用：陈亦刚. Tau的异常磷酸化与Tau病[J]. 国际神经精神科学杂志, 2017, 6(2): 7-12. https://doi.org/10.12677/IJPN.2017.62002

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