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阿尔茨海默病（AD）是非常普遍的神经变性性疾病并且是老年人痴呆的主要原因。AD患者的症状特点包括进行性的认知障碍、记忆丧失和行为障碍，与大脑中的病理变化密切相关。AD现成为全球最严重的健康和社会经济问题。在AD患者脑中神经纤维网或神经营养障碍的过程中存在tau蛋白的异常。tau 蛋白丧失其促微管组装的生物学功能, 导致细胞骨架的破坏、丝状物形成和神经缠结,轴突运输损害, 进而导致突触蛋白失去功能和神经退行性病变。其数量和结构的改变将会影响其功能而且会出现异常聚集。调节Tau 蛋白的异常聚集的分子机制主要是一些翻译后修饰使其结构及构象发生变化。因此，异常磷酸化和截断的 tau 蛋白作为tau 蛋白病理过程的关键机制而引起学者关注。本文描述了tau 蛋白的结构和功能及其在AD 中的主要病理变化，同时在本文中还涉及到磷酸化的tau 蛋白是神经元对氧化应激的代偿反应这一观点。对tau 蛋白进行更加全面的解读。

英文摘要:

Alzheimer's disease (AD) is a common neurodegenerative disease and a major cause of dementia. Its features include progressive symptoms of cognitive impairment, memory loss and behavior disorders in patients with AD, which are closely associated with pathological changes in the brain. Now AD has become the world's most serious health and social economic problems. In nerve fibres or nerve nutritional disorders in patients brain with AD tau proteins exist in the process of abnormal. Tau protein has lost its biological function that can promote microtubule assembly, which results in destruction of cytoskeletal filaments, formation and neuronal tangles of axonal transport damage, and leads to synaptic proteins lose function and neural degenerative diseases. Tau proteins facilitate the assembly of microtubules and stable, the number and structure changes will affect its function and gathered will appear abnormal. To adjust the Tau protein molecular mechanism of abnormal accumulation is mainly some modification after translation to make the structure and conformation change. As a result, abnormal phosphorylation and the truncation of the tau protein as the key mechanism of tau protein pathological process caused by the scholars attention. This paper describes the structure and function of the tau protein and its main pathological changes in AD and the idea that, Phosphorylated tau protein is neurons compensatory responses to oxidative stressis also involved in order to make a more comprehensive interpretation of the tau protein.

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