Impact Factor 3.508

Frontiers journals are at the top of citation and impact metrics

Mini Review ARTICLE Provisionally accepted The full-text will be published soon. Notify me

Front. Neurol. | doi: 10.3389/fneur.2018.00978

Microglia in Alzheimer’s disease: Risk factors and inflammation

  • 1Department of Neurology and Stroke Medicine, School of Medicine, Yokohama City University, Japan

Microglia are resident immune cells in the central nervous system (CNS) that originate from myeloid progenitor cells in the embryonic yolk sac and are maintained independently of circulating monocytes throughout life. In the healthy state, microglia are highly dynamic and control the environment by rapidly extending and retracting their processes. When the CNS is inflamed, microglia can give rise to macrophages, but the regulatory mechanisms underlying this process have not been fully elucidated. Recent genetic studies have suggested that microglial function is compromised in Alzheimer’s disease (AD), and that environmental factors such as diet and brain injury also affect microglial activation. In addition, studies of triggering receptor expressed on myeloid cells 2–deficiency in AD mice revealed heterogeneous microglial reactions at different disease stages, complicating the therapeutic strategy for AD. In this paper, we describe the relationship between genetic and environmental risk factors and the roles of microglia in AD pathogenesis, based on studies performed in human patients and animal models. We also discuss the mechanisms of inflammasomes and neurotransmitters in microglia, which accelerate the development of amyloid-β and tau pathology.

Keywords: Microglia, TBI (Traumatic Brain Injury), Inflammasomes, NLRP3, TREM2 (triggering receptor expressed on myeloid cells), Neuroinflammation, Glutamate

Received: 18 Sep 2018; Accepted: 30 Oct 2018.

Edited by:

Jun-ichi Kira, Kyushu University, Japan

Reviewed by:

Yasumasa Ohyagi, Ehime University, Japan
Katsuhisa Masaki, University of Chicago Medical Center, United States  

Copyright: © 2018 Katsumoto, Takeuchi, Takahashi and Tanaka. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Prof. Hideyuki Takeuchi, School of Medicine, Yokohama City University, Department of Neurology and Stroke Medicine, Yokohama, Kanagawa, Japan,