Evidence map›Paper›PMID 33898514›Full record

ArticleFrontiers in molecular biosciences2021

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

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

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in molecular biosciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 10% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
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  8. Neutrophils: a new target for postoperative cognitive dysfunction.Apoptosis : an international journal on programmed cell death · 2025
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  19. The innate immune response in tauopathies.European journal of immunology · 2023
    Review
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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 3 institutions in 1 country.

Gabriela Canalli KretzschmarLaboratory of Human Molecular Genetics, Postgraduate Program in Genetics, Department of Genetics, Federal University of Paraná (UFPR), Belém, Brazil.
Valéria Bumiller-BiniLaboratory of Human Molecular Genetics, Postgraduate Program in Genetics, Department of Genetics, Federal University of Paraná (UFPR), Belém, Brazil.
Miguel Angelo Gasparetto FilhoLaboratory of Human Molecular Genetics, Postgraduate Program in Genetics, Department of Genetics, Federal University of Paraná (UFPR), Belém, Brazil.
Yohan Ricci ZontaMedical School of Botucatu, Laboratory of Immunopathology and Infectious Agents-LIAI, UNIPEX-Experimental Research Unity, Sector 5, São Paulo State University (UNESP), Botucatu, Brazil.
Kaio Shu Tsyr YuMedical School of Botucatu, Laboratory of Immunopathology and Infectious Agents-LIAI, UNIPEX-Experimental Research Unity, Sector 5, São Paulo State University (UNESP), Botucatu, Brazil.
Ricardo Lehtonen R de SouzaLaboratory of Polymorphism and Linkage, Department of Genetics, Federal University of Paraná, Curitiba, Brazil.
Luciane Alarcão Dias-MelicioMedical School of Botucatu, Laboratory of Immunopathology and Infectious Agents-LIAI, UNIPEX-Experimental Research Unity, Sector 5, São Paulo State University (UNESP), Botucatu, Brazil.
Angelica Beate Winter BoldtLaboratory of Human Molecular Genetics, Postgraduate Program in Genetics, Department of Genetics, Federal University of Paraná (UFPR), Belém, Brazil.
Universidade Federal do Paraná · BRCentro Universitário de João Pessoa · BRUniversidade Estadual Paulista (Unesp) · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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,

Indexed as

Alzheimer's DiseaseC1qC5acomplement systemCR1inflammationneutrophil extracellular traps

Identifiers

PMID33898514
PMCPMC8060499
OpenAlexW3156712093

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.