Abstract：
The multiple hypothesis holds that the pathogenesis of Parkinson\'s disease (PD) requires many factors such as heredity, environment and ageing. Mutations in Leucine-rich repeat kinase 2 (LRRK2) are recognized the risk factors of PD, and closely related to sporadic and familial PD and can regulate a variety of cellular pathways and processes. An Increasing number of studies has shown that glial hyperactivation-mediated neuroinflammation participates in dopaminergic neuron degeneration and pathogenesis of PD. LRRK2 is essential to the regulaton of chronic inflammation, especially for the central nervous system. The review spotlights on the novel development of LRRK2 on microglia and astrocytes, and explore their potential therapeutic targets, in order to provide a new insights in PD. Key messages: What is already known on this topic The G2019S mutation of LRRK2 is now recognised as a pathogenic mutation in PD. Previous studies have focused on the relationship between neurons and LRRK2 G2019S. What this study adds Neuroinflammation mediated by LRRK2 G2019S of glial cells affects the progress and development of PD and attention must be paid to the role of LRRK2 G2019S in glial cells in PD. How this study might affect research, practice or policy Developing anti-inflammatory drugs from the perspective of LRRK2 G2019S of glial cells is a new direction for the treatment of PD.
摘要：
多重假说认为帕金森病(PD)的发病机制需要遗传、环境和老龄化。富含亮氨酸的重复激酶2（LRRK2）的突变被认为是PD的危险因素，与散发性和家族性PD密切相关，可以调节多种细胞通路和过程。越来越多的研究表明,神经胶质过度激活介导的神经炎症参与了多巴胺能神经元的变性和PD的发病机制。LRRK2对慢性炎症的调节至关重要，尤其是中枢神经系统。综述了LRRK2在小胶质细胞和星形胶质细胞上的新发展，探索他们潜在的治疗靶点，以便在PD中提供新的见解。关键信息：关于本主题的已知内容LRRK2的G2019S突变现在被认为是PD中的致病性突变。以往的研讨集中在神经元与LRRK2G2019S之间的关系。本研究增加了神经胶质细胞LRRK2G2019S介导的神经炎症影响PD的进展和发展，必须注意LRRK2G2019S在PD中神经胶质细胞中的作用。这项研究如何影响研究，实践或政策从神经胶质细胞LRRK2G2019S的角度开发抗炎药物是治疗PD的新方向。
