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首页> 外文期刊>The European Journal of Neuroscience >Tau acts as a mediator for Alzheimer's disease-related synaptic deficits
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Tau acts as a mediator for Alzheimer's disease-related synaptic deficits

机译：Tau充当阿尔茨海默氏病相关突触缺陷的调解人

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摘要

The two histopathological hallmarks of Alzheimer's disease (AD) are amyloid plaques containing multiple forms of amyloid beta (Aβ) and neurofibrillary tangles containing phosphorylated tau proteins. As mild cognitive impairment frequently occurs long before the clinical diagnosis of AD, the scientific community has been increasingly interested in the roles of Aβ and tau in earlier cellular changes that lead to functional deficits. Therefore, great progress has recently been made in understanding how Aβ or tau causes synaptic dysfunction. However, the interaction between the Aβ and tau-initiated intracellular cascades that lead to synaptic dysfunction remains elusive. The cornerstone of the two-decade-old hypothetical amyloid cascade model is that amyloid pathologies precede tau pathologies. Although the premise of Aβ-tau pathway remains valid, the model keeps evolving as new signaling events are discovered that lead to functional deficits and neurodegeneration. Recent progress has been made in understanding Aβ-PrPC-Fyn-mediated neurotoxicity and synaptic deficits. Although still elusive, many novel upstream and downstream signaling molecules have been found to modulate tau mislocalization and tau hyperphosphorylation. Here we will discuss the mechanistic interactions between Aβ-PrPC-mediated neurotoxicity and tau-mediated synaptic deficits in an updated amyloid cascade model with calcium and tau as the central mediators.
机译：阿尔茨海默氏病（AD）的两个组织病理学标志是含有多种形式的β-淀粉样蛋白（Aβ）的淀粉样蛋白斑块和含有磷酸化tau蛋白的神经原纤维缠结。由于轻度认知功能障碍经常在AD临床诊断之前很久就发生，因此科学界对Aβ和tau在导致功能缺陷的早期细胞变化中的作用越来越感兴趣。因此，最近在理解Aβ或tau如何引起突触功能障碍方面已取得了很大的进展。然而，Aβ和tau引发的细胞内级联反应之间的相互作用导致突触功能障碍仍然难以捉摸。已有两个十年历史的假设淀粉样蛋白级联模型的基础是淀粉样蛋白病理先于tau病理。尽管Aβ-tau途径的前提仍然有效，但是随着发现导致功能缺陷和神经退行性变的新信号事件，该模型不断发展。在理解Aβ-PrPC-Fyn介导的神经毒性和突触缺陷方面取得了最新进展。尽管仍然难以捉摸，但是已经发现许多新颖的上游和下游信号传导分子调节tau错位和tau过度磷酸化。在这里，我们将讨论在以钙和tau为主要介质的最新淀粉样蛋白级联模型中，Aβ-PrPC介导的神经毒性与tau介导的突触缺陷之间的机制相互作用。

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