蛋白质酪氨酸磷酸酶
神经退行性变
信号转导
磷酸化
突触可塑性
发病机制
细胞生物学
磷酸酶
生物
阿尔茨海默病
酪氨酸磷酸化
神经科学
τ蛋白
疾病
生物化学
医学
免疫学
内科学
受体
作者
Xia Zhao,Xiong Li,Lingyu She,Liwei Li,Ping Huang,Guang Liang
标识
DOI:10.1016/j.biopha.2022.113188
摘要
Protein tyrosine phosphatases (PTPs) are important regulator of neuronal signal transduction and a growing number of PTPs have been implicated in Alzheimer’s disease (AD). In the brains of patients with AD, there are a variety of abnormally phosphorylated proteins, which are closely related to the abnormal expression and activity of PTPs. β-Amyloid plaques (Aβ) and hyperphosphorylated tau protein are two pathological hallmarks of AD, and their accumulation ultimately leads to neurodegeneration. Studies have shown that protein phosphorylation signaling pathways mediates intracellular accumulation of Aβ and tau during AD development and are involved in synaptic plasticity and other stress responses. Here, we summarized the roles of PTPs related to the pathogenesis of AD and analyzed their therapeutic potential in AD.
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