Li Jun-Wei, Zong Yu, Cao Xi-Peng, Tan Lin, Tan Lan
Department of Neurology, Qingdao Municipal Hospital, Dalian Medical University, Qingdao 266000, China.
Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao 266071, China.
Ann Transl Med. 2018 May;6(10):176. doi: 10.21037/atm.2018.04.22.
Alzheimer's disease (AD) is a chronic and progressive neurodegenerative disease of central nervous system (CNS). Nowadays, increasing evidence suggests that immune system plays a significant role in the mechanisms of AD's onset and progression. Microglia, the main participator in the immune system of CNS, is always regarded as a protector of our brain in a healthy state and also has a beneficial role in maintaining the homeostasis of CNS microenvironment. However, chronic and sustained stimulation can push microglia into the state termed priming. Primed microglia can induce the production of amyloid β (Aβ), tau pathology, neuroinflammation and reduce the release of neurotrophic factors, resulting in loss of normal neurons in quantity and function that has immense relationship with AD. The therapeutic strategies mainly aimed at modulating the microenvironment and microglial activity in CNS to delay progression and alleviate pathogenesis of AD. Overall, in this review, we highlight the mechanism of microglial priming, and discuss the profound relationship between microglial priming and AD. Besides, we also pay attention to the therapeutic strategies targeting at microglial priming.
阿尔茨海默病（AD）是一种慢性进行性中枢神经系统（CNS）神经退行性疾病。如今，越来越多的证据表明，免疫系统在AD的发病机制和进展中起着重要作用。小胶质细胞是CNS免疫系统的主要参与者，在健康状态下一直被视为我们大脑的保护者，并且在维持CNS微环境的稳态中也发挥着有益作用。然而，长期持续的刺激会使小胶质细胞进入所谓的预激状态。预激的小胶质细胞可诱导淀粉样β蛋白（Aβ）的产生、tau病理改变、神经炎症，并减少神经营养因子的释放，导致正常神经元在数量和功能上的丧失，这与AD密切相关。治疗策略主要旨在调节CNS中的微环境和小胶质细胞活性，以延缓AD的进展并减轻其发病机制。总体而言，在本综述中，我们重点介绍小胶质细胞预激的机制，并讨论小胶质细胞预激与AD之间的深远关系。此外，我们还关注针对小胶质细胞预激的治疗策略。
