神经退行性变
发病机制
神经科学
疾病
病态的
机制(生物学)
生物
高磷酸化
医学
病理
细胞生物学
磷酸化
哲学
认识论
作者
Yan-Zhe Liao,Jing Ma,Jie-Zhi Dou
标识
DOI:10.1007/s12035-022-02847-x
摘要
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.
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