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首页> 外文期刊>The FEBS journal >Implication of calpain in neuronal apoptosis - A possible regulation of Alzheimer's disease
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Implication of calpain in neuronal apoptosis - A possible regulation of Alzheimer's disease

机译：钙蛋白酶在神经元凋亡中的意义-阿尔茨海默氏病的可能调节

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摘要

Apoptotic neuronal cell death is the cardinal feature of aging and neurodegenerative diseases, but its mechanisms remain obscure. Caspases, members of the cysteine protease family, are known to be critical effectors in central nervous system cellular apoptosis. More recently, the calcium-dependent proteases, calpains, have been implicated in cellular apoptotic processes. Indeed, several members of the Bcl-2 family of cell death regulators, nuclear transcription factors (p53) and caspases themselves are processed by calpains. Progressive regional loss of neurons underlies the irreversible pathogenesis of various neurodegenerative diseases such as Alzheimer's disease in adult brain. Alzheimer's disease is characterized by extracellular plaques of amyloid-beta peptide aggregates and intracellular neurofibrillary tangles composed of hyperphosphorylated tau leading to apoptotic cell death. In this review, we summarize the arguments showing that calpains modulate processes that govern the function and metabolism of these two key proteins in the pathogenesis of Alzheimer's disease. To conclude, this article reviews our understanding of calpain-dependent apoptotic neuronal cell death and the ability of these proteases to regulate intracellular signaling pathways leading to chronic neurodegenerative disorders such as Alzheimer's disease. Further research on these calpain-dependent mechanisms which promote or prevent cell apoptosis should help us to develop new approaches for preventing and treating neurodegenerative disorders.
机译：凋亡的神经元细胞死亡是衰老和神经退行性疾病的主要特征，但其机制仍然不清楚。半胱氨酸蛋白酶家族中的半胱天冬酶，在中枢神经系统细胞凋亡中起关键作用。最近，钙依赖性蛋白酶钙蛋白酶已参与细胞凋亡过程。实际上，钙蛋白酶处理了Bcl-2细胞死亡调节因子家族的几个成员，核转录因子（p53）和胱天蛋白酶本身。神经元的进行性区域性丧失是各种神经退行性疾病（例如成人大脑中的阿尔茨海默氏病）不可逆病机的基础。阿尔茨海默氏病的特征是淀粉样β肽聚集体的细胞外斑块和由高磷酸化tau组成的细胞内神经原纤维缠结导致凋亡细胞死亡。在这篇综述中，我们总结了表明钙蛋白酶调节阿尔茨海默氏病发病机理中控制这两个关键蛋白的功能和代谢的过程的论点。总而言之，本文回顾了我们对钙蛋白酶依赖性凋亡神经元细胞死亡的理解，以及这些蛋白酶调节导致慢性神经变性疾病（例如阿尔茨海默氏病）的细胞内信号传导途径的能力。这些促进或预防细胞凋亡的钙蛋白酶依赖性机制的进一步研究应有助于我们开发预防和治疗神经退行性疾病的新方法。

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