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

  • Lihang Zhang , Juan Xu , Jinchao Gao , Yuncheng Wu , Ming Yin EMAIL logo und Wenjuan Zhao EMAIL logo
Veröffentlicht/Copyright: 5. Mai 2018
Veröffentlichen auch Sie bei De Gruyter Brill

Abstract

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.

Acknowledgements

This study is supported by a grant from the Natural Science Foundation of China (Funder Id: 10.13039/501100001809, grant no. 81471232) and the Biomedical Multidisciplinary Program of Shanghai Jiao Tong University (YG2014MS31).

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

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Received: 2017-10-02
Accepted: 2018-03-06
Published Online: 2018-05-05
Published in Print: 2018-11-27

©2018 Walter de Gruyter GmbH, Berlin/Boston

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