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Reviews in the Neurosciences

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Volume 29, Issue 8


CD200-, CX3CL1-, and TREM2-mediated neuron-microglia interactions and their involvements in Alzheimer’s disease

Lihang Zhang / Juan Xu / Jinchao Gao / Yuncheng Wu
  • Department of Neurology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, 100 Haining Road, Shanghai 200080, China
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
/ Ming Yin / Wenjuan Zhao
Published Online: 2018-05-05 | DOI: https://doi.org/10.1515/revneuro-2017-0084


Neurons and microglia are two major components in the central nervous system (CNS). The interactions between them play important roles in maintaining homeostasis of the brain. In recent years, substantial studies have focused on the interactions between neurons and microglia, revealing that microglia become reactive when the interactions are pathophysiologically interfered, usually accompanying neuronal injury, which is a common feature for Alzheimer’s disease (AD). Many molecules and factors participate in these physiological and pathological processes, either in a contact-dependent or a contact-independent manner. Accumulating studies have revealed that in the CNS, cluster of differentiation-200 (CD200) and fractalkine (CX3CL1) expressed mainly on neurons and triggering receptor expressed on myeloid cells 2 (TREM2) expressed mainly on microglia. These molecules can mediate neuron-microglia interactions in a contact-dependent manner and contribute to the pathogenesis of AD. Here, we review the expression, distribution, and function of CD200, CX3CL1, and TREM2 in regulating neuron-microglia interactions under physiological conditions as well as in AD.

Keywords: Alzheimer’s disease; CD200; CX3CL1; neuron-microglia interactions; TREM2


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About the article

Received: 2017-10-02

Accepted: 2018-03-06

Published Online: 2018-05-05

Published in Print: 2018-11-27

Conflict of interest statement: The authors declare that they have no conflict of interest.

Citation Information: Reviews in the Neurosciences, Volume 29, Issue 8, Pages 837–848, ISSN (Online) 2191-0200, ISSN (Print) 0334-1763, DOI: https://doi.org/10.1515/revneuro-2017-0084.

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