Department of Laboratory, The First People`s Hospital of Zhangjiagang City, Suzhou, Jiangsu, China.
Department of Neurosurgery, The First People`s Hospital of Zhangjiagang City, Suzhou, Jiangsu, China.
Curr Neuropharmacol. 2018;16(9):1348-1357. doi: 10.2174/1570159X16666180222165418.
The leucine-rich repeat kinase 2 (LRRK2) gene and α-synuclein gene (SNCA) are the key influencing factors of Parkinson's disease (PD). It is reported that dysfunction of LRRK2 may influence the accumulation of α-synuclein and its pathology to alter cellular functions and signaling pathways by the kinase activation of LRRK2. The accumulation of α-synuclein is one of the main stimulants of microglial activation. Microglia are macrophages that reside in the brain, and activation of microglia is believed to contribute to neuroinflammation and neuronal death in PD. Therefore, clarifying the complex relationship among LRRK2, α-synuclein and microglials could offer targeted clinical therapies for PD. Here, we provide an updated review focused on the discussion of the evidence supporting some of the key mechanisms that are important for LRRK2-dependent neurodegeneration in PD.
富含亮氨酸重复激酶 2（LRRK2）基因和α-突触核蛋白基因（SNCA）是帕金森病（PD）的关键影响因素。有报道称，LRRK2 的功能障碍可能通过 LRRK2 的激酶激活影响α-突触核蛋白的积累及其病理学，从而改变细胞功能和信号通路。α-突触核蛋白的积累是小胶质细胞激活的主要刺激因素之一。小胶质细胞是驻留在大脑中的巨噬细胞，小胶质细胞的激活被认为有助于 PD 中的神经炎症和神经元死亡。因此，阐明 LRRK2、α-突触核蛋白和小胶质细胞之间的复杂关系可能为 PD 提供有针对性的临床治疗方法。在这里，我们提供了一个更新的综述，重点讨论了支持一些关键机制的证据，这些机制对 PD 中 LRRK2 依赖性神经退行性变很重要。
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