Evidence map›Paper›PMID 33897596›Full record

ReviewFrontiers in neurology2021

Microglia-Derived Interleukin 23: A Crucial Cytokine in Alzheimer's Disease?

Louisa Nitsch, Linda Schneider, Julian Zimmermann, Marcus Müller

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in neurology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Immune-proteo-metabolomic changes link to Aβ and tau pathology in Alzheimer disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  3. Review
  4. Article
  5. Brain interleukins and Alzheimer's disease.Metabolic brain disease · 2025
    Review
  6. Article
  7. Roles of Cytokines in Alzheimer's Disease.International journal of molecular sciences · 2024
    Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. The homeostatic function of Regnase-2 restricts neuroinflammation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
    Article
  16. Article
  17. Article
  18. Article
  19. 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.

Louisa NitschDepartment of Neurology, University Hospital Bonn, Bonn, Germany.
Linda SchneiderDepartment of Surgery, University Hospital Bonn, Bonn, Germany.
Julian ZimmermannDepartment of Neurology, University Hospital Bonn, Bonn, Germany.
Marcus MüllerDepartment of Neurology, University Hospital Bonn, Bonn, Germany.
University Hospital Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuronal cell death, amyloid β plaque formation and development of neurofibrillary tangles are among the characteristics of Alzheimer's disease (AD). In addition to neurodegeneration, inflammatory processes such as activation of microglia and astrocytes are crucial in the pathogenesis and progression of AD. Cytokines are essential immune mediators of the immune response in AD. Recent data suggest a role of interleukin 23 (IL-23) and its p40 subunit in the pathogenesis of AD and corresponding animal models, in particular concerning microglia activation and amyloid β plaque formation. Moreover, in animal models, the injection of anti-p40 antibodies resulted in reduced amyloid β plaque formation and improved cognitive performance. Here, we discuss the pathomechanism of IL-23 mediated inflammation and its role in AD.

Indexed as

Alzheimer's diseaseantibody therapyinterleukin 23microglianeuroinflammation

Identifiers

PMID33897596
PMCPMC8058463
OpenAlexW3144321992

What OpenQuestion holds

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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.