Evidence map›Paper›PMID 36012243›Full record

ReviewInternational journal of molecular sciences2022

Targeting NLRP3-Mediated Neuroinflammation in Alzheimer's Disease Treatment.

Julia Barczuk, Natalia Siwecka, Weronika Lusa, Wioletta Rozpędek-Kamińska, Ewa Kucharska, Ireneusz Majsterek

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

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
5.0field-weighted citation impact, top 3% 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

43 citing papers in PubMed, 62 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Frontiers in pharmacology · 2026
    Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Review
  19. 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

6 authors at 2 institutions in 1 country.

Julia BarczukDepartment of Clinical Chemistry and Biochemistry, Medical University of Lodz, 90-419 Lodz, Poland.
Natalia SiweckaDepartment of Clinical Chemistry and Biochemistry, Medical University of Lodz, 90-419 Lodz, Poland.ORCID 0000-0002-0308-580X
Weronika LusaDepartment of Clinical Chemistry and Biochemistry, Medical University of Lodz, 90-419 Lodz, Poland.
Wioletta Rozpędek-KamińskaDepartment of Clinical Chemistry and Biochemistry, Medical University of Lodz, 90-419 Lodz, Poland.ORCID 0000-0001-9206-1203
Ewa KucharskaDepartment of Gerontology, Geriatrics and Social Work, Jesuit University Ignatianum, 31-501 Krakow, Poland.
Ireneusz MajsterekDepartment of Clinical Chemistry and Biochemistry, Medical University of Lodz, 90-419 Lodz, Poland.
Medical University of Lodz · PLAkademia Ignatianum w Krakowie · PL

Funding

Medical University of Lodz 503/5-108-05/503-51-001-19-00
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common cause of dementia in the general population and, to date, constitutes a major therapeutic challenge. In the pathogenesis of AD, aggregates of amyloid β (Aβ) and neurofibrillary tangles (NFTs) containing Tau-microtubule-associated protein (tau) are known to trigger a neuroinflammatory response with subsequent formation of an inflammasome. In particular, the NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome is thought to play a crucial role in AD-related pathology. While the mechanisms for NLRP3 activation are not fully understood, it has been demonstrated that, after detection of protein aggregates, NLRP3 induces pro-inflammatory cytokines, such as interleukin 18 (IL-18) or interleukin 1β (IL-1β), that further potentiate AD progression. Specific inhibitors of NLRP3 that exhibit various mechanisms to attenuate the activity of NLRP3 have been tested in in vivo studies and have yielded promising results, as shown by the reduced level of tau and Aβ aggregates and diminished cognitive impairment. Herein, we would like to summarize the current state of knowledge on NLRP3 inflammasome priming, activation, and its actual role in AD pathogenesis, and to characterize the NLRP3 inhibitors that have been studied most and their impact on AD-related pathology.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesHumansInflammasomesNeuroinflammatory DiseasesNLR Family, Pyrin Domain-Containing 3 ProteinAmyloid beta-PeptidesInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinAlzheimer’s diseaseAlzheimer’s disease treatmentamyloid βneurofibrillary tanglesNOD-like receptor pyrin domain-containing 3NOD-like receptor pyrin domain-containing 3 inflammasomeNOD-like receptor pyrin domain-containing 3 inhibitors

Identifiers

PMID36012243
PMCPMC9409081
OpenAlexW4290973279

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.