Microtubule-associated protein tau forms insoluble neurofilamentous tangles (NFT) as one of the major histopathological hallmarks of Alzheimer’s disease (AD). Studies have emphasized that tau causes early functional deficits much before neurofilamentous aggregates develop. The redistribution of tau from the axon into the somatodendritic compartment of neurons and dendritic spines causes synaptic impairment, and then leads to the loss of synaptic contacts which correlates better with cognitive deficits in AD than amyloid-β (Aβ). In this review we discuss the underlying mechanisms by which tau mislocalizes to dendritic spines and contributes to synaptic dysfunction in AD. We also review the synergistic effect of tau and oligomeric forms of Aβ on promoting synaptic dysfunction in AD.

中文翻译：

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树突状/突触后tau蛋白和阿尔茨海默氏病的早期病理

微管相关蛋白tau形成不溶性神经丝缠结（NFT），这是阿尔茨海默氏病（AD）的主要组织病理学标志之一。研究强调，tau会在神经丝状聚集体发展之前就引起早期功能缺陷。tau从轴突重新分布到神经元和树突棘的躯体树突状区室中，导致突触损伤，然后导致突触接触的丧失，与淀粉样蛋白-β（Aβ）的认知缺陷相关性更好。在这篇综述中，我们讨论了tau错位于树突棘并促成AD突触功能障碍的潜在机制。我们还审查了tau和寡聚形式的Aβ对促进AD突触功能障碍的协同作用。