Role of α-synuclein in microglia: autophagy and phagocytosis balance neuroinflammation in Parkinson’s disease

Background Parkinson’s disease (PD) is the second most common neurodegenerative disease, and is characterized by accumulation of α-synuclein (α-syn). Neuroinflammation driven by microglia is an important pathological manifestation of PD. α-Syn is a crucial marker of PD, and its accumulation leads to...

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Published inInflammation research Vol. 72; no. 3; pp. 443 - 462
Main Authors Lv, Qian-Kun, Tao, Kang-Xin, Wang, Xiao-Bo, Yao, Xiao-Yu, Pang, Meng-Zhu, Liu, Jun-Yi, Wang, Fen, Liu, Chun-Feng
Format Journal Article
LanguageEnglish
Published Cham Springer International Publishing 01.03.2023
Springer Nature B.V
Subjects
Accumulation
Allergology
alpha-Synuclein - genetics
alpha-Synuclein - metabolism
Apoptosis
Autophagy
Biomedical and Life Sciences
Biomedicine
Dermatology
Homeostasis
Humans
Immunology
Inflammasomes
Inflammasomes - metabolism
Inflammation
LRRK2 protein
Microglia
Microglia - metabolism
Movement disorders
Neurodegenerative diseases
Neurodegenerative Diseases - metabolism
Neurodegenerative Diseases - pathology
Neuroinflammatory Diseases
Neurology
NLR Family, Pyrin Domain-Containing 3 Protein - metabolism
PARK7 protein
Parkinson Disease - genetics
Parkinson Disease - metabolism
Parkinson Disease - pathology
Parkinson's disease
Pathogenesis
Phagocytosis
Pharmacology/Toxicology
Phenotypes
Review
Rheumatology
Synuclein
α-Synuclein
Neuroinflammation
Autophagy
Phagocytosis
Microglia
Online AccessGet full text

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Abstract Background Parkinson’s disease (PD) is the second most common neurodegenerative disease, and is characterized by accumulation of α-synuclein (α-syn). Neuroinflammation driven by microglia is an important pathological manifestation of PD. α-Syn is a crucial marker of PD, and its accumulation leads to microglia M1-like phenotype polarization, activation of NLRP3 inflammasomes, and impaired autophagy and phagocytosis in microglia. Autophagy of microglia is related to degradation of α-syn and NLRP3 inflammasome blockage to relieve neuroinflammation. Microglial autophagy and phagocytosis of released α-syn or fragments from apoptotic neurons maintain homeostasis in the brain. A variety of PD-related genes such as LRRK2 , GBA and DJ-1 also contribute to this stability process. Objectives Further studies are needed to determine how α-syn works in microglia. Methods A keyword-based search was performed using the PubMed database for published articles. Conclusion In this review, we discuss the interaction between microglia and α-syn in PD pathogenesis and the possible mechanism of microglial autophagy and phagocytosis in α-syn clearance and inhibition of neuroinflammation. This may provide a novel insight into treatment of PD.
AbstractList Parkinson's disease (PD) is the second most common neurodegenerative disease, and is characterized by accumulation of α-synuclein (α-syn). Neuroinflammation driven by microglia is an important pathological manifestation of PD. α-Syn is a crucial marker of PD, and its accumulation leads to microglia M1-like phenotype polarization, activation of NLRP3 inflammasomes, and impaired autophagy and phagocytosis in microglia. Autophagy of microglia is related to degradation of α-syn and NLRP3 inflammasome blockage to relieve neuroinflammation. Microglial autophagy and phagocytosis of released α-syn or fragments from apoptotic neurons maintain homeostasis in the brain. A variety of PD-related genes such as LRRK2, GBA and DJ-1 also contribute to this stability process.BACKGROUNDParkinson's disease (PD) is the second most common neurodegenerative disease, and is characterized by accumulation of α-synuclein (α-syn). Neuroinflammation driven by microglia is an important pathological manifestation of PD. α-Syn is a crucial marker of PD, and its accumulation leads to microglia M1-like phenotype polarization, activation of NLRP3 inflammasomes, and impaired autophagy and phagocytosis in microglia. Autophagy of microglia is related to degradation of α-syn and NLRP3 inflammasome blockage to relieve neuroinflammation. Microglial autophagy and phagocytosis of released α-syn or fragments from apoptotic neurons maintain homeostasis in the brain. A variety of PD-related genes such as LRRK2, GBA and DJ-1 also contribute to this stability process.Further studies are needed to determine how α-syn works in microglia.OBJECTIVESFurther studies are needed to determine how α-syn works in microglia.A keyword-based search was performed using the PubMed database for published articles.METHODSA keyword-based search was performed using the PubMed database for published articles.In this review, we discuss the interaction between microglia and α-syn in PD pathogenesis and the possible mechanism of microglial autophagy and phagocytosis in α-syn clearance and inhibition of neuroinflammation. This may provide a novel insight into treatment of PD.CONCLUSIONIn this review, we discuss the interaction between microglia and α-syn in PD pathogenesis and the possible mechanism of microglial autophagy and phagocytosis in α-syn clearance and inhibition of neuroinflammation. This may provide a novel insight into treatment of PD.
Background Parkinson’s disease (PD) is the second most common neurodegenerative disease, and is characterized by accumulation of α-synuclein (α-syn). Neuroinflammation driven by microglia is an important pathological manifestation of PD. α-Syn is a crucial marker of PD, and its accumulation leads to microglia M1-like phenotype polarization, activation of NLRP3 inflammasomes, and impaired autophagy and phagocytosis in microglia. Autophagy of microglia is related to degradation of α-syn and NLRP3 inflammasome blockage to relieve neuroinflammation. Microglial autophagy and phagocytosis of released α-syn or fragments from apoptotic neurons maintain homeostasis in the brain. A variety of PD-related genes such as LRRK2 , GBA and DJ-1 also contribute to this stability process. Objectives Further studies are needed to determine how α-syn works in microglia. Methods A keyword-based search was performed using the PubMed database for published articles. Conclusion In this review, we discuss the interaction between microglia and α-syn in PD pathogenesis and the possible mechanism of microglial autophagy and phagocytosis in α-syn clearance and inhibition of neuroinflammation. This may provide a novel insight into treatment of PD.
Parkinson's disease (PD) is the second most common neurodegenerative disease, and is characterized by accumulation of α-synuclein (α-syn). Neuroinflammation driven by microglia is an important pathological manifestation of PD. α-Syn is a crucial marker of PD, and its accumulation leads to microglia M1-like phenotype polarization, activation of NLRP3 inflammasomes, and impaired autophagy and phagocytosis in microglia. Autophagy of microglia is related to degradation of α-syn and NLRP3 inflammasome blockage to relieve neuroinflammation. Microglial autophagy and phagocytosis of released α-syn or fragments from apoptotic neurons maintain homeostasis in the brain. A variety of PD-related genes such as LRRK2, GBA and DJ-1 also contribute to this stability process. Further studies are needed to determine how α-syn works in microglia. A keyword-based search was performed using the PubMed database for published articles. In this review, we discuss the interaction between microglia and α-syn in PD pathogenesis and the possible mechanism of microglial autophagy and phagocytosis in α-syn clearance and inhibition of neuroinflammation. This may provide a novel insight into treatment of PD.
BackgroundParkinson’s disease (PD) is the second most common neurodegenerative disease, and is characterized by accumulation of α-synuclein (α-syn). Neuroinflammation driven by microglia is an important pathological manifestation of PD. α-Syn is a crucial marker of PD, and its accumulation leads to microglia M1-like phenotype polarization, activation of NLRP3 inflammasomes, and impaired autophagy and phagocytosis in microglia. Autophagy of microglia is related to degradation of α-syn and NLRP3 inflammasome blockage to relieve neuroinflammation. Microglial autophagy and phagocytosis of released α-syn or fragments from apoptotic neurons maintain homeostasis in the brain. A variety of PD-related genes such as LRRK2, GBA and DJ-1 also contribute to this stability process.ObjectivesFurther studies are needed to determine how α-syn works in microglia.MethodsA keyword-based search was performed using the PubMed database for published articles.ConclusionIn this review, we discuss the interaction between microglia and α-syn in PD pathogenesis and the possible mechanism of microglial autophagy and phagocytosis in α-syn clearance and inhibition of neuroinflammation. This may provide a novel insight into treatment of PD.
Author Liu, Chun-Feng
Lv, Qian-Kun
Liu, Jun-Yi
Wang, Xiao-Bo
Pang, Meng-Zhu
Wang, Fen
Yao, Xiao-Yu
Tao, Kang-Xin
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– sequence: 2
  givenname: Kang-Xin
  surname: Tao
  fullname: Tao, Kang-Xin
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  givenname: Xiao-Bo
  surname: Wang
  fullname: Wang, Xiao-Bo
  organization: Jiangsu Key Laboratory of Neuropsychiatric Diseases and Institute of Neuroscience, Soochow University
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  givenname: Xiao-Yu
  surname: Yao
  fullname: Yao, Xiao-Yu
  organization: Department of Neurology and Clinical Research Center of Neurological Disease, The Second Affiliated Hospital of Soochow University, Jiangsu Key Laboratory of Neuropsychiatric Diseases and Institute of Neuroscience, Soochow University
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  givenname: Jun-Yi
  surname: Liu
  fullname: Liu, Jun-Yi
  organization: Department of Neurology, Dushu Lake Hospital Affiliated to Soochow University
– sequence: 7
  givenname: Fen
  surname: Wang
  fullname: Wang, Fen
  email: wangfen_1982@126.com
  organization: Department of Neurology and Clinical Research Center of Neurological Disease, The Second Affiliated Hospital of Soochow University, Jiangsu Key Laboratory of Neuropsychiatric Diseases and Institute of Neuroscience, Soochow University
– sequence: 8
  givenname: Chun-Feng
  surname: Liu
  fullname: Liu, Chun-Feng
  email: liuchunfeng@suda.edu.cn
  organization: Department of Neurology and Clinical Research Center of Neurological Disease, The Second Affiliated Hospital of Soochow University, Jiangsu Key Laboratory of Neuropsychiatric Diseases and Institute of Neuroscience, Soochow University
BackLink https://www.ncbi.nlm.nih.gov/pubmed/36598534$$D View this record in MEDLINE/PubMed
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Keywords α-Synuclein
Neuroinflammation
Autophagy
Phagocytosis
Microglia
Language English
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PublicationSubtitle Official Journal of: The International Association of Inflammation Societies + The European Histamine Research Society
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Snippet Background Parkinson’s disease (PD) is the second most common neurodegenerative disease, and is characterized by accumulation of α-synuclein (α-syn)....
Parkinson's disease (PD) is the second most common neurodegenerative disease, and is characterized by accumulation of α-synuclein (α-syn). Neuroinflammation...
BackgroundParkinson’s disease (PD) is the second most common neurodegenerative disease, and is characterized by accumulation of α-synuclein (α-syn)....
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SubjectTerms Accumulation
Allergology
alpha-Synuclein - genetics
alpha-Synuclein - metabolism
Apoptosis
Autophagy
Biomedical and Life Sciences
Biomedicine
Dermatology
Homeostasis
Humans
Immunology
Inflammasomes
Inflammasomes - metabolism
Inflammation
LRRK2 protein
Microglia
Microglia - metabolism
Movement disorders
Neurodegenerative diseases
Neurodegenerative Diseases - metabolism
Neurodegenerative Diseases - pathology
Neuroinflammatory Diseases
Neurology
NLR Family, Pyrin Domain-Containing 3 Protein - metabolism
PARK7 protein
Parkinson Disease - genetics
Parkinson Disease - metabolism
Parkinson Disease - pathology
Parkinson's disease
Pathogenesis
Phagocytosis
Pharmacology/Toxicology
Phenotypes
Review
Rheumatology
Synuclein
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Title Role of α-synuclein in microglia: autophagy and phagocytosis balance neuroinflammation in Parkinson’s disease
URI https://link.springer.com/article/10.1007/s00011-022-01676-x
https://www.ncbi.nlm.nih.gov/pubmed/36598534
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