摘要帕金森病是最常见的与年龄相关的神经退行性病，影响患者的生活质量，给社会和家庭带来巨大负担。帕金森病典型的病理学特征为α-突触核蛋白（α-syn）在中脑黑质-纹状体区的异常聚集，造成多巴胺能神经元死亡。然而，随着研究的深入，发现α-syn介导星形胶质细胞功能异常导致血脑屏障破坏和小胶质细胞介导炎性因子的释放与帕金森病的发病机制有关。因此，将神经元、胶质细胞、血管作为一个神经血管单元整体开展研究能够更好地反映疾病的病理生理环境，揭示其发病机制。已有研究发现α-syn可通过朊蛋白样、隧道纳米管、外泌体等方式传播，与帕金森病的发生发展密切相关。随着Braak病理分期的提出和早期帕金森病前瞻性队列研究结果的公布，提示外周α-syn向中枢传播可能是介导帕金森病发生发展的另一重要途径。针对α-syn异常聚集和传播的研究可为帕金森病的发病机制提供新的思路，为帕金森病的疾病修饰治疗提供新的靶点。文中就α-syn的异常聚集与传播在帕金森病发病机制中的作用进行综述。

abstractsParkinson′s disease (PD) is the most common age-related neurodegenerative disease, which has the effects on the patients′ quality of life and brings a huge burden to the society and family. The pathological feature of PD is the abnormal accumulation of alpha-synuclein (α-syn) in the brain of substantia nigra-striatum, mediating the death of dopaminergic neurons. However, further studies have found that α-syn mediates the abnormal function of astrocytes leading to the destruction of the blood-brain barrier and the release of inflammatory factors caused by microglia, which are related to the pathogenesis of PD. Therefore, neurons, glial cells, and blood vessels as a whole named neurovascular unit can better reflect the pathophysiological environment of PD and reveal the PD pathogenesis. Studies have detected the ways of α-syn transmission, such as prion-like, tunneling nanotubes, exosomes, are connected with the pathogenesis and progression of PD. The Braak stage and the prospective cohort of early PD provide a view that the peripheral α-syn to the central nervous system may be an another important way to mediate the pathogenesis and progression of PD. The research about the abnormal aggregation and spread of α-syn can provide the new theory for the pathogenesis of PD and the new disease modifying therapy of PD. This article reviews the role of abnormal aggregation and transmission of α-syn in the pathogenesis of PD.