Evidence map›Paper›PMID 34209586›Full record

ReviewInternational journal of molecular sciences2021

NLRP3 and Infections: β-Amyloid in Inflammasome beyond Neurodegeneration.

Giulia Sita, Agnese Graziosi, Patrizia Hrelia, Fabiana Morroni

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

24 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Cornuside alleviates cognitive impairments induced by AβAlzheimer's research & therapy · 2025
    Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Targeting NLRP3-Mediated Neuroinflammation in Alzheimer's Disease Treatment.International journal of molecular sciences · 2022
    Review
  20. Review
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

4 authors at 1 institution in 1 country.

Giulia SitaDepartment of Pharmacy and BioTechnology-FaBiT, University of Bologna-Alma Mater Studiorum, via Irnerio 48, 40126 Bologna, Italy.ORCID 0000-0001-6627-7078
Agnese GraziosiDepartment of Pharmacy and BioTechnology-FaBiT, University of Bologna-Alma Mater Studiorum, via Irnerio 48, 40126 Bologna, Italy.ORCID 0000-0002-4992-7902
Patrizia HreliaDepartment of Pharmacy and BioTechnology-FaBiT, University of Bologna-Alma Mater Studiorum, via Irnerio 48, 40126 Bologna, Italy.ORCID 0000-0002-8415-3711
Fabiana MorroniDepartment of Pharmacy and BioTechnology-FaBiT, University of Bologna-Alma Mater Studiorum, via Irnerio 48, 40126 Bologna, Italy.ORCID 0000-0001-6494-5968
University of Bologna · IT

Funding

Ministero dell'Istruzione, dell'Università e della Ricerca 2017MYJ5TH
6 · The paper itself

Abstract

Amyloid beta (Aβ)-induced abnormal neuroinflammation is recognized as a major pathological feature of Alzheimer's disease (AD), which results in memory impairment. Research exploring low-grade systemic inflammation and its impact on the development and progression of neurodegenerative disease has increased. A particular research focus has been whether systemic inflammation arises only as a secondary effect of disease, or it is also a cause of pathology. The inflammasomes, and more specifically the NLRP3 inflammasome, are crucial components of the innate immune system and are usually activated in response to infection or tissue damage. Although inflammasome activation plays critical roles against various pathogens in host defense, overactivation of inflammasome contributes to the pathogenesis of inflammatory diseases, including acute central nervous system (CNS) injuries and chronic neurodegenerative diseases, such as AD. This review summarizes the current literature on the role of the NLRP3 inflammasome in the pathogenesis of AD, and its involvement in infections, particularly SARS-CoV-2. NLRP3 might represent the crossroad between the hypothesized neurodegeneration and the primary COVID-19 infection.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsCoronavirusHumansImmunity, InnateInflammasomesMicrogliaNLR Family, Pyrin Domain-Containing 3 ProteinVirus DiseasesAmyloid beta-PeptidesInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinAlzheimer’s diseaseCOVID-19infectionsneurodegenerationneuroinflammationNLRP3

Identifiers

PMID34209586
PMCPMC8268482
OpenAlexW3174018508

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.