Evidence map›Paper›PMID 30261895›Full record

ArticleJournal of neuroinflammation2018

α1-antitrypsin mitigates NLRP3-inflammasome activation in amyloid β

Taraneh Ebrahimi, Marcus Rust, Sarah Nele Kaiser, Alexander Slowik, Cordian Beyer, Andreas Rembert Koczulla, Jörg B Schulz, Pardes Habib, Jan Philipp Bach

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

Article in Journal of neuroinflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

49 citing papers in PubMed, 69 citations in OpenAlex.

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  13. P2XBrain, behavior, and immunity · 2023
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  17. Non-canonical NLRC4 inflammasomes in astrocytes contribute to glioma malignancy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  18. Review
  19. NLRP3 inflammasome in neurodegenerative disease.Translational research : the journal of laboratory and clinical medicine · 2023
    Review
  20. Article
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

9 authors at 3 institutions in 1 country.

Taraneh EbrahimiDepartment of Neurology, RWTH Aachen University, Aachen, Germany.
Marcus RustDepartment of Neurology, RWTH Aachen University, Aachen, Germany.
Sarah Nele KaiserDepartment of Neurology, RWTH Aachen University, Aachen, Germany.
Alexander SlowikInstitute of Neuroanatomy, RWTH Aachen University, Aachen, Germany.
Cordian BeyerInstitute of Neuroanatomy, RWTH Aachen University, Aachen, Germany.
Andreas Rembert KoczullaDepartment of Internal Medicine, Pulmonary and Critical Care Medicine, University Medical Center Giessen and Marburg, Marburg, Germany.
Jörg B SchulzDepartment of Neurology, RWTH Aachen University, Aachen, Germany.
Pardes HabibDepartment of Neurology, RWTH Aachen University, Aachen, Germany.
Jan Philipp BachDepartment of Neurology, RWTH Aachen University, Aachen, Germany. jbach@ukaachen.de.ORCID http://orcid.org/0000-0002-6432-6187
RWTH Aachen University · DEForschungszentrum Jülich · DEUniversitätsklinikum Gießen und Marburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNeuroinflammation has an essential impact on the pathogenesis and progression of Alzheimer's disease (AD). Mostly mediated by microglia and astrocytes, inflammatory processes lead to degeneration of neuronal cells. The NLRP3-inflammasome (NOD-like receptor family, pyrin domain containing 3) is a key component of the innate immune system and its activation results in secretion of the proinflammatory effectors interleukin-1β (IL-1β) and interleukin-18 (IL-18). Under physiological conditions, cytosolic NLRP3-inflammsome is maintained in an inactive form, not able to oligomerize. Amyloid β

methodsPrimary cortical astrocytes from BALB/c mice were stimulated with Aβ

resultsOur study revealed that A1AT reduces Aβ

conclusionWe conclude that Aβ

Indexed as

alpha 1-AntitrypsinAmyloid beta-PeptidesAnimalsAnimals, NewbornAstrocytesBrainCalcium-Binding ProteinsCells, CulturedCytokinesDose-Response Relationship, DrugFuransGlial Fibrillary Acidic ProteinHeterocyclic Compounds, 4 or More RingsIndenesInflammasomesLipopolysaccharidesAif1 protein, mousealpha 1-AntitrypsinAmyloid beta-Peptidesamyloid beta-protein (1-42)Calcium-Binding ProteinsCytokinesFuransGlial Fibrillary Acidic ProteinHeterocyclic Compounds, 4 or More RingsIndenesInflammasomesLipopolysaccharidesL-Lactate DehydrogenaseMicrofilament ProteinsN-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamideNLR Family, Pyrin Domain-Containing 3 ProteinPeptide FragmentsSulfonamidesSulfonesTrypsin InhibitorsAlpha 1-antitrypsinAlzheimer’s diseaseAmyloid βAstrocytesInflammasomeNALP3NeuroinflammationNLRP3

Identifiers

PMID30261895
PMCPMC6158809
OpenAlexW2892919725

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.