Microglia Polarization From M1 to M2 in Neurodegenerative Diseases

Microglia-mediated neuroinflammation is a common feature of neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS). Microglia can be categorized into two opposite types: classical (M1) or alternative (M2...

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Published inFrontiers in aging neuroscience Vol. 14; p. 815347
Main Authors Guo, Shenrui, Wang, Hui, Yin, Yafu
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Research Foundation 16.02.2022
Frontiers Media S.A
Subjects
Online AccessGet full text
ISSN1663-4365
1663-4365
DOI10.3389/fnagi.2022.815347

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Abstract Microglia-mediated neuroinflammation is a common feature of neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS). Microglia can be categorized into two opposite types: classical (M1) or alternative (M2), though there’s a continuum of different intermediate phenotypes between M1 and M2, and microglia can transit from one phenotype to another. M1 microglia release inflammatory mediators and induce inflammation and neurotoxicity, while M2 microglia release anti-inflammatory mediators and induce anti-inflammatory and neuroprotectivity. Microglia-mediated neuroinflammation is considered as a double-edged sword, performing both harmful and helpful effects in neurodegenerative diseases. Previous studies showed that balancing microglia M1/M2 polarization had a promising therapeutic prospect in neurodegenerative diseases. We suggest that shifting microglia from M1 to M2 may be significant and we focus on the modulation of microglia polarization from M1 to M2, especially by important signal pathways, in neurodegenerative diseases.
AbstractList Microglia-mediated neuroinflammation is a common feature of neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS). Microglia can be categorized into two opposite types: classical (M1) or alternative (M2), though there’s a continuum of different intermediate phenotypes between M1 and M2, and microglia can transit from one phenotype to another. M1 microglia release inflammatory mediators and induce inflammation and neurotoxicity, while M2 microglia release anti-inflammatory mediators and induce anti-inflammatory and neuroprotectivity. Microglia-mediated neuroinflammation is considered as a double-edged sword, performing both harmful and helpful effects in neurodegenerative diseases. Previous studies showed that balancing microglia M1/M2 polarization had a promising therapeutic prospect in neurodegenerative diseases. We suggest that shifting microglia from M1 to M2 may be significant and we focus on the modulation of microglia polarization from M1 to M2, especially by important signal pathways, in neurodegenerative diseases.
Microglia-mediated neuroinflammation is a common feature of neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS). Microglia can be categorized into two opposite types: classical (M1) or alternative (M2), though there's a continuum of different intermediate phenotypes between M1 and M2, and microglia can transit from one phenotype to another. M1 microglia release inflammatory mediators and induce inflammation and neurotoxicity, while M2 microglia release anti-inflammatory mediators and induce anti-inflammatory and neuroprotectivity. Microglia-mediated neuroinflammation is considered as a double-edged sword, performing both harmful and helpful effects in neurodegenerative diseases. Previous studies showed that balancing microglia M1/M2 polarization had a promising therapeutic prospect in neurodegenerative diseases. We suggest that shifting microglia from M1 to M2 may be significant and we focus on the modulation of microglia polarization from M1 to M2, especially by important signal pathways, in neurodegenerative diseases.Microglia-mediated neuroinflammation is a common feature of neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS). Microglia can be categorized into two opposite types: classical (M1) or alternative (M2), though there's a continuum of different intermediate phenotypes between M1 and M2, and microglia can transit from one phenotype to another. M1 microglia release inflammatory mediators and induce inflammation and neurotoxicity, while M2 microglia release anti-inflammatory mediators and induce anti-inflammatory and neuroprotectivity. Microglia-mediated neuroinflammation is considered as a double-edged sword, performing both harmful and helpful effects in neurodegenerative diseases. Previous studies showed that balancing microglia M1/M2 polarization had a promising therapeutic prospect in neurodegenerative diseases. We suggest that shifting microglia from M1 to M2 may be significant and we focus on the modulation of microglia polarization from M1 to M2, especially by important signal pathways, in neurodegenerative diseases.
Microglia-mediated neuroinflammation is a common feature of neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS). Microglia can be categorized into two opposite types: classical (M1) or alternative (M2), though there’s a continuum of different intermediate phenotypes between M1 and M2, and microglia can transit from one phenotype to another. M1 microglia release inflammatory mediators and induce inflammation and neurotoxicity, while M2 microglia release anti-inflammatory mediators and induce anti-inflammatory and neuroprotectivity. Microglia-mediated neuroinflammation is considered as a double-edged sword, performing both harmful and helpful effects in neurodegenerative diseases. Previous studies showed that balancing microglia M1/M2 polarization had a promising therapeutic prospect in neurodegenerative diseases. We suggest that shifting microglia from M1 to M2 may be significative and we focus on the modulation of microglia polarization from M1 to M2, especially by important signal pathways, in neurodegenerative diseases.
Author Guo, Shenrui
Yin, Yafu
Wang, Hui
AuthorAffiliation Department of Nuclear Medicine, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine , Shanghai , China
AuthorAffiliation_xml – name: Department of Nuclear Medicine, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine , Shanghai , China
Author_xml – sequence: 1
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  surname: Guo
  fullname: Guo, Shenrui
– sequence: 2
  givenname: Hui
  surname: Wang
  fullname: Wang, Hui
– sequence: 3
  givenname: Yafu
  surname: Yin
  fullname: Yin, Yafu
BackLink https://www.ncbi.nlm.nih.gov/pubmed/35250543$$D View this record in MEDLINE/PubMed
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Keywords neurodegenerative diseases
Alzheimer’s disease
neuroinflammation
Parkinson’s disease
microglia polarization
Language English
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Reviewed by: Chun-Feng Liu, The Second Affiliated Hospital of Soochow University, China; Chiara Porro, University of Foggia, Italy
This article was submitted to Neuroinflammation and Neuropathy, a section of the journal Frontiers in Aging Neuroscience
Edited by: Daniel Ortuño-Sahagún, University of Guadalajara, Mexico
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Snippet Microglia-mediated neuroinflammation is a common feature of neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic...
Microglia-mediated neuroinflammation is a common feature of neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic...
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SubjectTerms Aging Neuroscience
Alzheimer's disease
Amyotrophic lateral sclerosis
Anti-inflammatory agents
Brain research
Brain-derived neurotrophic factor
Chemokines
Cytokines
Drugs
Genotype & phenotype
Growth factors
Homeostasis
Inflammation
Microglia
microglia polarization
Movement disorders
Multiple sclerosis
Nervous system
Neurodegenerative diseases
neuroinflammation
Neurons
Neurotoxicity
Nitric oxide
Parkinson's disease
Pathogenesis
Phenotypes
Polarization
Repair & maintenance
Signal transduction
Tumor necrosis factor-TNF
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Title Microglia Polarization From M1 to M2 in Neurodegenerative Diseases
URI https://www.ncbi.nlm.nih.gov/pubmed/35250543
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Volume 14
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