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帕金森病发病机制至今未明，近几年研究发现，线粒体依赖性PCD通路的激活在PD 发病过程中是不可缺少的, 不同形态学表现的细胞死亡形式在帕金森病发病过程中可以共同存在，而所有的这些细胞死亡都归因于PCD 共同的上游通路的激活。 PCD 通路不仅仅是指线粒体介导的caspase 依赖性凋亡，还包括非caspase 依赖性细胞非凋亡性死亡，比如细胞坏死。这不仅仅是概念上的延伸，更为我们在帕金森病神经保护性治疗上提供了更多的靶点，有助于寻求神经保护的新方法和延缓神经退行性疾病的进程. 抗凋亡治疗已经成为帕金森病等神经退行性疾病治疗的新热点，已经证实，caspase 抑制剂能够通过抑制caspase 的激活，阻止细胞退行性病变。那么将位于caspase 执行者上游的Bax 作为靶点，抑制Bax 的激活与转位，能够产生更为持久显著的神经保护作用。本文综述了近年来相关研究进展。

英文摘要:

The mechanism of Parkinson's disease (PD) has not been clarified. Recent studies found that activation of mitochondrion-dependent programmed cell death (PCD) pathways is indispensable to the demise of dopaminergic neurons in PD. The co-existence of different morphological forms of cell death attributed to the activation of the common upstream pathways was detected in PD. PCD, not only refer to mitochondrial caspase-dependent apoptosis, but also caspase-independent apoptosis, such as cell necrosis. The extension of concept provides more therapeutic targets in neural-protective treatment for PD, contributing to the prevention of the development of the neurodegenerative diseases. Now, more and more attention has been focused on anti-apoptosis therapy for neurodegenerative diseases, PD included. Many studies has demonstrated that inhibitor of caspase prevent the activation of caspase, and neurodegenerative disorders. Bax, located in the upstream of caspase, the executor of apoptosis, is set as the therapeutic target. More obvious neuro-protection may be achieved by the application of Bax-inhibiting Peptide (BIP), which inhibits the activation and translocation of Bax. This article reviews recent research progress on PD and PCD.

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