Evidence map›Paper›PMID 33261147›Full record

ReviewInternational journal of molecular sciences2020

Danger-Sensing/Patten Recognition Receptors and Neuroinflammation in Alzheimer's Disease.

Anna Chiarini, Ubaldo Armato, Peng Hu, Ilaria Dal Prà

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. 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
3.5field-weighted citation impact, top 6% 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, 69 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Neuropsychiatric disease and treatment · 2026
    Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Role of NLRP3 Inflammasome in Chronic Pain and Alzheimer's Disease-A Review.Journal of biochemical and molecular toxicology · 2025
    Review
  15. Article
  16. Review
  17. Review
  18. 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

4 authors at 1 institution in 2 countries.

Anna ChiariniSection of Human Histology & Embryology, Department of Surgery, Dentistry, Pediatrics, and Gynecology, University of Verona, Verona, 37134 Venetia, Italy.
Ubaldo ArmatoSection of Human Histology & Embryology, Department of Surgery, Dentistry, Pediatrics, and Gynecology, University of Verona, Verona, 37134 Venetia, Italy.ORCID 0000-0002-7804-6143
Peng HuSection of Human Histology & Embryology, Department of Surgery, Dentistry, Pediatrics, and Gynecology, University of Verona, Verona, 37134 Venetia, Italy.
Ilaria Dal PràSection of Human Histology & Embryology, Department of Surgery, Dentistry, Pediatrics, and Gynecology, University of Verona, Verona, 37134 Venetia, Italy.ORCID 0000-0001-5523-4910
University of Verona · IT

Funding

European Union's Horizon 2020 Research and Innovation Program under the Marie Sklodowska-Curie Grant Agreement No. 754345.The Ministry of Italian University and Research FUR 2019
6 · The paper itself

Abstract

Fibrillar aggregates and soluble oligomers of both Amyloid-β peptides (Aβs) and hyperphosphorylated Tau proteins (p-Tau-es), as well as a chronic neuroinflammation are the main drivers causing progressive neuronal losses and dementia in Alzheimer's disease (AD). However, the underlying pathogenetic mechanisms are still much disputed. Several endogenous neurotoxic ligands, including Aβs, and/or p-Tau-es activate innate immunity-related danger-sensing/pattern recognition receptors (PPRs) thereby advancing AD's neuroinflammation and progression. The major PRR families involved include scavenger, Toll-like, NOD-like, AIM2-like, RIG-like, and CLEC-2 receptors, plus the calcium-sensing receptor (CaSR). This quite intricate picture stresses the need to identify the pathogenetically topmost Aβ-activated PRR, whose signaling would trigger AD's three main drivers and their intra-brain spread. In theory, the candidate might belong to any PRR family. However, results of preclinical studies using in vitro nontumorigenic human cortical neurons and astrocytes and in vivo AD-model animals have started converging on the CaSR as the pathogenetically upmost PRR candidate. In fact, the CaSR binds both Ca

Indexed as

Alzheimer DiseaseAnimalsBrainHumansInflammasomesInflammationNeurogliaReceptors, Pattern RecognitionInflammasomesReceptors, Pattern RecognitionAlzheimer’s diseasecalcium signalingdanger-sensing receptorsinflammasomesneuroinflammationpattern recognition receptors

Identifiers

PMID33261147
PMCPMC7731137
OpenAlexW3109691907

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.