Department of Neurobiology, School of Neurobiology, Biochemistry and Biophysics, Tel-Aviv University, Ramat-Aviv, Tel Aviv 69978, Israel.
Biomolecules. 2023 Sep 22;13(10):1435. doi: 10.3390/biom13101435.
Parkinson's disease (PD) is a devastating disease associated with accumulation of α-synuclein (α-Syn) within dopaminergic neurons, leading to neuronal death. PD is characterized by both motor and non-motor clinical symptoms. Several studies indicate that autophagy, an important intracellular degradation pathway, may be involved in different neurodegenerative diseases including PD. The autophagic process mediates the degradation of protein aggregates, damaged and unneeded proteins, and organelles, allowing their clearance, and thereby maintaining cell homeostasis. Impaired autophagy may cause the accumulation of abnormal proteins. Incomplete or impaired autophagy may explain the neurotoxic accumulation of protein aggregates in several neurodegenerative diseases including PD. Indeed, studies have suggested the contribution of impaired autophagy to α-Syn accumulation, the death of dopaminergic neurons, and neuroinflammation. In this review, we summarize the recent literature on the involvement of autophagy in PD pathogenesis.
帕金森病（PD）是一种毁灭性疾病，与多巴胺能神经元内α-突触核蛋白（α-Syn）的积累有关，导致神经元死亡。PD 的特征是既有运动症状又有非运动症状。几项研究表明，自噬是一种重要的细胞内降解途径，可能与包括 PD 在内的不同神经退行性疾病有关。自噬过程介导蛋白质聚集体、受损和不需要的蛋白质以及细胞器的降解，允许它们被清除，从而维持细胞内环境稳定。自噬受损可能导致异常蛋白质的积累。不完全或受损的自噬可能解释了包括 PD 在内的几种神经退行性疾病中蛋白质聚集体的神经毒性积累。事实上，研究表明自噬受损对α-Syn 积累、多巴胺能神经元死亡和神经炎症的贡献。在这篇综述中，我们总结了自噬在 PD 发病机制中的最新文献。
