期刊
FRONTIERS IN NEUROLOGY
卷 9, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fneur.2018.00549
关键词
Alzheimer's disease; amyloid-beta peptide; protein tau; microglia; monocytes; chemokine receptors; chemokines; neuroinflammation
资金
- NIH [1RF1 AG051506, R01 AI119065]
- Portuguese Foundation for Science and Technology (FCT) [SFRH/BD/51677/2011, SFRH/BPD/120611/2016]
- FCT [SFRH/BPD/108312/2015]
- Fundação para a Ciência e a Tecnologia [SFRH/BD/51677/2011] Funding Source: FCT
Chemokines and their receptors have been shown to affect amyloid-beta (A beta) and tau pathologies in mouse models of Alzheimer's disease (AD) by regulating microglia and monocyte-associated neuroinflammation, microglial movement and monocyte recruitment into the brain. These cells in turn can promote and mediate Ab phagocytosis and degradation and tau phosphorylation. In this review we discuss published work in this field in mouse models of AD and review what is known about the contributions of microglial and monocyte chemokines and their receptors to amyloid and tau pathologies. We focus on the roles of the chemokine/chemokine receptor pairs CCL2/CCR2, CX3CL1/CX3CR1, CCL5/CCR5, CXCL10/CXCR3 and CXCL1/CXCR2, highlighting important knowledge gaps in this field. A full understanding of the functions of chemokines and their receptors in AD may guide the development of novel immunotherapies for this devastating disease.
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