Evidence map›Paper›PMID 36598534›Full record

ReviewInflammation research : official journal of the European Histamine Research Society ... [et al.]2023

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

Qian-Kun Lv, Kang-Xin Tao, Xiao-Bo Wang, Xiao-Yu Yao, Meng-Zhu Pang, Jun-Yi Liu, Fen Wang, Chun-Feng Liu

Abstract readReview
PubMed Publisher
In one paragraph

Review in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
11.7field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

61 citing papers in PubMed, 96 citations in OpenAlex.

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  4. ProteinJournal of pharmaceutical analysis · 2026
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1 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Qian-Kun LvDepartment of Neurology and Clinical Research Center of Neurological Disease, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China.
Kang-Xin TaoJiangsu Key Laboratory of Neuropsychiatric Diseases and Institute of Neuroscience, Soochow University, Suzhou, 215123, China.
Xiao-Bo WangJiangsu Key Laboratory of Neuropsychiatric Diseases and Institute of Neuroscience, Soochow University, Suzhou, 215123, China.
Xiao-Yu YaoDepartment of Neurology and Clinical Research Center of Neurological Disease, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China.
Meng-Zhu PangJiangsu Key Laboratory of Neuropsychiatric Diseases and Institute of Neuroscience, Soochow University, Suzhou, 215123, China.
Jun-Yi LiuDepartment of Neurology, Dushu Lake Hospital Affiliated to Soochow University, Suzhou, China.
Fen WangDepartment of Neurology and Clinical Research Center of Neurological Disease, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China. wangfen_1982@126.com.
Chun-Feng LiuDepartment of Neurology and Clinical Research Center of Neurological Disease, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China. liuchunfeng@suda.edu.cn.
Soochow University · CNSecond Affiliated Hospital of Soochow University · CN

Funding

Jiangsu Provincial Key Research and Development Program BE2018658National Natural Science Foundation of China 82071420Science and Technology Program of Suzhou SLJ2021010
6 · The paper itself

Abstract

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.

Indexed as

Neurodegenerative DiseasesParkinson Diseasealpha-SynucleinAutophagyHumansInflammasomesMicrogliaNeuroinflammatory DiseasesNLR Family, Pyrin Domain-Containing 3 ProteinPhagocytosisalpha-SynucleinInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinSNCA protein, humanAutophagyMicrogliaNeuroinflammationPhagocytosisα-Synuclein

Identifiers

PMID36598534
OpenAlexW4313488897

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.