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Neutrophil Extracellular Traps: A Perspective of Neuroinflammation and Complement Activation in Alzheimer's Disease.

作者信息

Kretzschmar Gabriela Canalli, Bumiller-Bini Valéria, Gasparetto Filho Miguel Angelo, Zonta Yohan Ricci, Yu Kaio Shu Tsyr, de Souza Ricardo Lehtonen R, Dias-Melicio Luciane Alarcão, Boldt Angelica Beate Winter

机构信息

Laboratory of Human Molecular Genetics, Postgraduate Program in Genetics, Department of Genetics, Federal University of Paraná (UFPR), Belém, Brazil.

Medical School of Botucatu, Laboratory of Immunopathology and Infectious Agents-LIAI, UNIPEX-Experimental Research Unity, Sector 5, São Paulo State University (UNESP), Botucatu, Brazil.

出版信息

Front Mol Biosci. 2021 Apr 8;8:630869. doi: 10.3389/fmolb.2021.630869. eCollection 2021.


DOI:10.3389/fmolb.2021.630869
PMID:33898514
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8060499/
Abstract

Complement system (CS) components are associated with Alzheimer's disease (AD), the commonest cause of dementia in the world. Neutrophils can be attracted to amyloid-β plaques by several pro-inflammatory factors, including the complement anaphylatoxin C5a. They may release neutrophil extracellular traps (NETs), which are chromatin nets associated with myeloperoxidase, elastase, and other enzymes. Some CS molecules, such as C5a, C1q, and CR1, are associated with increased neutrophil recruitment and NETs release. However, the relationship between CS molecules and NETs in AD is poorly understood. In this work, we detected higher NET concentrations in plasma and serum of Brazilian AD patients, than in elderly controls (medians = 2.78 [2.07-6.19] vs. 2.23 [0.33-4.14] ng/mL, = 0.0005). We discussed these results within the context of our former findings on complement and AD and the context of the literature on complement and NET release, suggesting both as possible therapeutic targets to prevent the progress of the disease.

摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a13c/8060499/3867935a5586/fmolb-08-630869-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a13c/8060499/e73785a21511/fmolb-08-630869-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a13c/8060499/3867935a5586/fmolb-08-630869-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a13c/8060499/e73785a21511/fmolb-08-630869-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a13c/8060499/3867935a5586/fmolb-08-630869-g002.jpg

相似文献

[1]
Neutrophil Extracellular Traps: A Perspective of Neuroinflammation and Complement Activation in Alzheimer's Disease.

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[4]
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[5]
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[6]
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[7]
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[8]
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[9]
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[10]
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本文引用的文献

[1]
The Important Interface Between Apolipoprotein E and Neuroinflammation in Alzheimer's Disease.

Front Immunol. 2020

[2]
First Report of CR1 Polymorphisms and Soluble CR1 Levels Associated with Late Onset Alzheimer's Disease (LOAD) in Latin America.

J Mol Neurosci. 2020-9

[3]
Neutrophil Extracellular Trap Induced Dendritic Cell Activation Leads to Th1 Polarization in Type 1 Diabetes.

Front Immunol. 2020

[4]
Complement-Mediated Events in Alzheimer's Disease: Mechanisms and Potential Therapeutic Targets.

J Immunol. 2020-1-15

[5]
The emerging role of neutrophils in neurodegeneration.

Immunobiology. 2020-1

[6]
Complement dysregulation in the central nervous system during development and disease.

Semin Immunol. 2019-11-7

[7]
The complement cascade in Alzheimer's disease: a systematic review and meta-analysis.

Mol Psychiatry. 2021-10

[8]
Proteomic analysis of peripheral blood polymorphonuclear cells (PBMCs) reveals alteration of neutrophil extracellular trap (NET) components in uncontrolled diabetes.

Mol Cell Biochem. 2019-7-4

[9]
Neutrophil extracellular traps generation and degradation in patients with granulomatosis with polyangiitis and systemic lupus erythematosus.

Autoimmunity. 2019-5

[10]
A Novel Assay for Neutrophil Extracellular Trap Formation Independently Predicts Disseminated Intravascular Coagulation and Mortality in Critically Ill Patients.

Am J Respir Crit Care Med. 2019-10-1

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