Microglia Polarization From M1 to M2 in Neurodegenerative Diseases

被引:474
作者
Guo, Shenrui [1 ]
Wang, Hui [1 ]
Yin, Yafu [1 ]
机构
[1] Shanghai Jiao Tong Univ, Xinhua Hosp, Dept Nucl Med, Sch Med, Shanghai, Peoples R China
来源
FRONTIERS IN AGING NEUROSCIENCE | 2022年 / 14卷
基金
中国国家自然科学基金;
关键词
neurodegenerative diseases; neuroinflammation; Alzheimer's disease; Parkinson's disease; microglia polarization; NF-KAPPA-B; NONSTEROIDAL ANTIINFLAMMATORY DRUGS; ALZHEIMERS-DISEASE; MOUSE MODEL; M1/M2; POLARIZATION; BRAIN INFLAMMATION; PREVENTION TRIAL; INNATE IMMUNITY; MOTOR-NEURONS; NADPH OXIDASE;
D O I
10.3389/fnagi.2022.815347
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
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.
引用
收藏
页数:16
相关论文
共 167 条
[1]   Aspirin in Alzheimer's disease (AD2000): a randomised open-label trial [J].
不详 .
LANCET NEUROLOGY, 2008, 7 (01) :41-49
[2]   PPARγ signaling and metabolism: the good, the bad and the future [J].
Ahmadian, Maryam ;
Suh, Jae Myoung ;
Hah, Nasun ;
Liddle, Christopher ;
Atkins, Annette R. ;
Downes, Michael ;
Evans, Ronald M. .
NATURE MEDICINE, 2013, 19 (05) :557-566
[3]   Clemastine Confers Neuroprotection and Induces an Anti-Inflammatory Phenotype in SOD1G93A Mouse Model of Amyotrophic Lateral Sclerosis [J].
Apolloni, Savina ;
Fabbrizio, Paola ;
Parisi, Chiara ;
Amadio, Susanna ;
Volonte, Cinzia .
MOLECULAR NEUROBIOLOGY, 2016, 53 (01) :518-531
[4]   Spinal cord pathology is ameliorated by P2X7 antagonism in a SOD1-mutant mouse model of amyotrophic lateral sclerosis [J].
Apolloni, Savina ;
Amadio, Susanna ;
Parisi, Chiara ;
Matteucci, Alessandra ;
Potenza, Rosa L. ;
Armida, Monica ;
Popoli, Patrizia ;
D'Ambrosi, Nadia ;
Volonte, Cinzia .
DISEASE MODELS & MECHANISMS, 2014, 7 (09) :1101-1109
[5]   17p-Estradiol Reduces Demyelination in Cuprizone-fed Mice by Promoting M2 Microglia Polarity and Regulating NLRP3 Inflammasome [J].
Aryanpour, Roya ;
Zibara, Kazem ;
Pasbakhsh, Parichehr ;
Jame'ei, Seyyed Behnamodin ;
Namjoo, Zeinab ;
Ghanbari, Amir ;
Mahmoudi, Reza ;
Amani, Showan ;
Kashani, Iraj Ragerdi .
NEUROSCIENCE, 2021, 463 :116-127
[6]   Progesterone therapy induces an M1 to M2 switch in microglia phenotype and suppresses NLRP3 inflammasome in a cuprizone-induced demyelination mouse model [J].
Aryanpour, Roya ;
Pasbakhsh, Parichehr ;
Zibara, Kazem ;
Namjoo, Zeinab ;
Boroujeni, Fatemeh Beigi ;
Shahbeigi, Saeed ;
Kashani, Iraj Ragerdi ;
Beyer, Cordian ;
Zendehdel, Adib .
INTERNATIONAL IMMUNOPHARMACOLOGY, 2017, 51 :131-139
[7]   NADPH oxidase: An update [J].
Babior, BM .
BLOOD, 1999, 93 (05) :1464-1476
[8]   NSAID use and risk of Parkinson disease: a population-based case-control study [J].
Becker, C. ;
Jick, S. S. ;
Meier, C. R. .
EUROPEAN JOURNAL OF NEUROLOGY, 2011, 18 (11) :1336-1342
[9]   The complex language of chromatin regulation during transcription [J].
Berger, Shelley L. .
NATURE, 2007, 447 (7143) :407-412
[10]   ALS:: A disease of motor neurons and their nonneuronal neighbors [J].
Boillee, Sverine ;
Vande Velde, Christine ;
Cleveland, Don W. .
NEURON, 2006, 52 (01) :39-59