Microglia Polarization in Alzheimer’s Disease: Mechanisms and a Potential Therapeutic Target

Qinqin Wang; Hongmei Yao; Wenyan Liu; Bailiu Ya; Hongju Cheng; Zhenkai Xing; Yili Wu; Yili Wu; Yili Wu

doi:10.3389/fnagi.2021.772717

Frontiers in Aging Neuroscience (Nov 2021)

Microglia Polarization in Alzheimer’s Disease: Mechanisms and a Potential Therapeutic Target

Qinqin Wang,
Hongmei Yao,
Wenyan Liu,
Bailiu Ya,
Hongju Cheng,
Zhenkai Xing,
Yili Wu,
Yili Wu,
Yili Wu

Affiliations

Qinqin Wang: Shandong Collaborative Innovation Center for Diagnosis, Treatment and Behavioral Interventions of Mental Disorders, Institute of Mental Health, Jining Medical University, Jining, China
Hongmei Yao: Affiliated Hospital of Jining Medical University, Jining, China
Wenyan Liu: Department of Physiology, College of Basic Medicine, Jining Medical University, Jining, China
Bailiu Ya: Department of Physiology, College of Basic Medicine, Jining Medical University, Jining, China
Hongju Cheng: Department of Physiology, College of Basic Medicine, Jining Medical University, Jining, China
Zhenkai Xing: Shandong Collaborative Innovation Center for Diagnosis, Treatment and Behavioral Interventions of Mental Disorders, Institute of Mental Health, Jining Medical University, Jining, China
Yili Wu: The Affiliated Kangning Hospital, Wenzhou Medical University, Wenzhou, China
Yili Wu: Key Laboratory of Alzheimer’s Disease of Zhejiang Province, Institute of Aging, School of Mental Health, Wenzhou Medical University, Wenzhou, China
Yili Wu: Oujiang Laboratory, Wenzhou, China

DOI: https://doi.org/10.3389/fnagi.2021.772717
Journal volume & issue: Vol. 13

Abstract

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Neuroinflammation regulated by microglia is one of the important factors involved in the pathogenesis of Alzheimer’s disease (AD). Activated microglia exhibited phenotypes termed as M1 and M2 phenotypes separately. M1 microglia contribute to the development of inflammation via upregulating pro-inflammatory cytokines, while M2 microglia exert anti-inflammation effects through enhancing the expression of anti-inflammation factors. Moreover, M1 and M2 microglia could be mutually transformed under various conditions. Both M1 and M2 microglia are implicated in AD. Amyloid-β (Aβ) and hyperphosphorylated tau are two major components of AD pathological hallmarks, neuritic plaques, and neurofibrillary tangles. Both Aβ and hyperphosphorylated tau were involved in microglial activation and subsequent inflammation, which further contribute to neuronal and synaptic loss in AD. In this review, we summarized the roles of M1 and M2 microglia in AD and underlying mechanisms, which will provide an insight into the role of microglia in the pathogenesis of AD and highlight the therapeutic potential of modulating microglia.

Published in Frontiers in Aging Neuroscience

ISSN: 1663-4365 (Online)
Publisher: Frontiers Media S.A.
Country of publisher: Switzerland
LCC subjects: Medicine: Internal medicine: Neurosciences. Biological psychiatry. Neuropsychiatry
Website: https://www.frontiersin.org/journals/aging-neuroscience

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Abstract

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