The Role of TDP-43 in Neurodegenerative Disease
The Role of TDP-43 in Neurodegenerative Disease
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DOI：
10.1007/s12035-022-02847-x
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发表时间：
2022-05-02
影响因子：
5.1
通讯作者：
Dou, Jie-Zhi
中科院分区：
文献类型：
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作者：
Liao, Yan-Zhe;Ma, Jing;Dou, Jie-Zhi
近年来，越来越多的神经退行性疾病，如ALS、FTLD和AD，被发现有一个共同的病理特征，即通过过度磷酸化、泛素化和切割，TDP-43在细胞核内耗尽，TDP-43在细胞质中积聚。因此，这种神经退行性疾病也被称为TDP-43蛋白病。提示TDP-43在疾病的发病机制中起一定作用。目前的研究表明，TDP-43在神经退行性变中的病理生理机制非常复杂。本文就TDP-43的结构、主要生理功能、可能的发病机制以及TDP-43如何为治疗神经退行性疾病提供新的途径作一综述。
In recent years, more and more neurodegenerative diseases, such as ALS, FTLD and AD, have been found to share a common pathological feature, which is the depletion of TDP-43 in the nucleus and the accumulation of TDP-43 in the cytoplasm through hyperphosphorylation, ubiquitination and cleavage. Therefore, this kind of neurodegenerative disease is also called TDP-43 proteinopathy. This suggests that TDP-43 plays a role in the pathogenesis of disease. Current studies show that the pathophysiological mechanism of TDP-43 in neurodegeneration is very complex. In this review, we describe the structure of TDP-43, its main physiological functions, the possible pathogenesis and how TDP-43 provides a new pathway to treat neurodegenerative diseases.