Neurodegenerative diseases, including Alzheimer disease, Parkinson disease, amyotrophic lateral sclerosis, and multiple sclerosis, are chronic disorders of the CNS that are characterized by progressive neuronal dysfunction. These diseases have diverse clinical and pathological features and their pathogenetic mechanisms are not yet fully understood. Currently, widely accepted hypotheses include the accumulation of misfolded proteins, oxidative stress from reactive oxygen species, mitochondrial dysfunction, DNA damage, neurotrophin dysfunction, and neuroinflammatory processes. In the CNS of patients with neurodegenerative diseases, a variety of abnormally phosphorylated proteins play important roles in pathological processes such as neuroinflammation and intracellular accumulation of β-amyloid plaques and tau. In recent years, the roles of abnormal tyrosine phosphorylation of intracellular signaling molecules regulated by protein tyrosine kinases (PTKs) and protein tyrosine phosphatases (PTPs) in neurodegenerative diseases have attracted increasing attention. Here, we summarize the roles of signaling pathways related to protein tyrosine phosphorylation in the pathogenesis of neurodegenerative diseases and the progress of therapeutic studies targeting PTKs and PTPs that provide theoretical support for future studies on therapeutic strategies for these devastating and important neurodegenerative diseases.

中文翻译：

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神经退行性疾病中蛋白质酪氨酸的异常磷酸化。

神经退行性疾病，包括阿尔茨海默病、帕金森病、肌萎缩侧索硬化症和多发性硬化症，是中枢神经系统的慢性疾病，其特征是进行性神经元功能障碍。这些疾病具有多样的临床和病理特征，其发病机制尚未完全清楚。目前，广泛接受的假设包括错误折叠蛋白质的积累、活性氧的氧化应激、线粒体功能障碍、DNA 损伤、神经营养蛋白功能障碍和神经炎症过程。在神经退行性疾病患者的中枢神经系统中，多种异常磷酸化蛋白在神经炎症、细胞内β-淀粉样斑块和tau蛋白积聚等病理过程中发挥着重要作用。近年来，蛋白酪氨酸激酶（PTK）和蛋白酪氨酸磷酸酶（PTP）调控的细胞内信号分子酪氨酸异常磷酸化在神经退行性疾病中的作用日益受到关注。在此，我们总结了蛋白酪氨酸磷酸化相关信号通路在神经退行性疾病发病机制中的作用以及针对PTK和PTP的治疗研究进展，为未来研究这些破坏性且重要的神经退行性疾病的治疗策略提供理论支持。