Evidence map›Paper›PMID 28676934›Full record

ReviewJournal of neural transmission (Vienna, Austria : 1996)2018

Type-I interferon pathway in neuroinflammation and neurodegeneration: focus on Alzheimer's disease.

Juliet M Taylor, Zachery Moore, Myles R Minter, Peter J Crack

Open access · greenAbstract readReview
PubMed Publisher
In one paragraph

Review in Journal of neural transmission (Vienna, Austria : 1996), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.

  1. Pooled it
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  12. Adenosine and adenosine receptors in metabolic imbalance-related neurological issues.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2024
    Review
  13. JAK1/2 Regulates Synergy Between Interferon Gamma and Lipopolysaccharides in Microglia.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024
    Article
  14. Review
  15. Article
  16. Review
  17. Mitochondrial DNA and Inflammation in Alzheimer's Disease.Current issues in molecular biology · 2023
    Review
  18. Review
  19. Article
  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 2 institutions in 2 countries.

Juliet M TaylorNeuropharmacology Laboratory, Department of Pharmacology and Therapeutics, The University of Melbourne, Parkville, VIC, Australia.
Zachery MooreNeuropharmacology Laboratory, Department of Pharmacology and Therapeutics, The University of Melbourne, Parkville, VIC, Australia.
Myles R MinterDepartment of Neurobiology, The University of Chicago, Chicago, IL, 60637, USA.
Peter J CrackNeuropharmacology Laboratory, Department of Pharmacology and Therapeutics, The University of Melbourne, Parkville, VIC, Australia. pcrack@unimelb.edu.au.ORCID 0000-0002-5030-0330
The University of Melbourne · AUUniversity of Chicago · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Past research in Alzheimer's disease (AD) has largely been driven by the amyloid hypothesis; the accompanying neuroinflammation seen in AD has been assumed to be consequential and not disease modifying or causative. However, recent data from both clinical and preclinical studies have established that the immune-driven neuroinflammation contributes to AD pathology. Key evidence for the involvement of neuroinflammation in AD includes enhanced microglial and astroglial activation in the brains of AD patients, increased pro-inflammatory cytokine burden in AD brains, and epidemiological evidence that chronic non-steroidal anti-inflammatory drug use prior to disease onset leads to a lower incidence of AD. Identifying critical mediators controlling this neuroinflammation will prove beneficial in developing anti-inflammatory therapies for the treatment of AD. The type-I interferons (IFNs) are pleiotropic cytokines that control pro-inflammatory cytokine secretion and are master regulators of the innate immune response that impact on disorders of the central nervous system. This review provides evidence that the type-I IFNs play a critical role in the exacerbation of neuroinflammation and actively contribute to the progression of AD.

Indexed as

Alzheimer DiseaseAnimalsBrainHumansInflammationInterferon Type INerve DegenerationInterferon Type IAlzheimer’s diseaseAmyloidAstrocytesMicrogliaNeurodegenerationNeuroinflammationType-I interferon

Identifiers

PMID28676934
OpenAlexW2730836138

What OpenQuestion holds

Textmetadata
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.