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Ann Transl Med. 2018 May;6(10):176. doi: 10.21037/atm.2018.04.22.

Microglial priming in Alzheimer's disease.

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Department of Neurology, Qingdao Municipal Hospital, Dalian Medical University, Qingdao 266000, China.
Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao 266071, China.
Clinical Research Center, Qingdao Municipal Hospital, Qingdao University, Qingdao 266071, China.


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.


Alzheimer’s disease (AD); amyloid beta (Aβ); microglial priming; neuroinflammation; tau-protein

Conflict of interest statement

Conflicts of Interest: The authors have no conflicts of interest to declare.

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