Evidence map›Paper›PMID 27979768›Full record

ReviewExperimental gerontology2017

A state of delirium: Deciphering the effect of inflammation on tau pathology in Alzheimer's disease.

Matthew Barron, Jane Gartlon, Lee A Dawson, Peter J Atkinson, Marie-Christine Pardon

Open access · hybridAbstract readReview
In one paragraph

Review in Experimental gerontology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

33 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. The innate immune response in tauopathies.European journal of immunology · 2023
    Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Intracerebral Infection withJournal of Alzheimer's disease reports · 2022
    Article
  19. 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

5 authors at 4 institutions in 2 countries.

Matthew BarronSchool of Life sciences, University of Nottingham, Queens Medical Centre, Nottingham NG7 2UH, UK.
Jane GartlonEisai Inc., 4 Corporate Drive, Andover, MA 01810, USA.
Lee A DawsonAstex Pharmaceuticals, 436 Cambridge Science Park Rd, Cambridge CB4 0QA, UK.
Peter J AtkinsonEisai Ltd., EMEA Knowledge Centre, Mosquito Way, Hatfield, Hertfordshire, AL10 9SN, UK.
Marie-Christine PardonSchool of Life sciences, University of Nottingham, Queens Medical Centre, Nottingham NG7 2UH, UK. Electronic address: marie.pardon@nottingham.ac.uk.
Eisai (United Kingdom) · GBEisai (United States) · USQueen's Medical Centre · GBUniversity of Nottingham · GB

Funding

Medical Research Council MR/K017853/1
6 · The paper itself

Abstract

Alzheimer's disease (AD), the predominant form of dementia, is highly correlated with the abnormal hyperphosphorylation and aggregation of tau. Immune responses are key drivers of AD and how they contribute to tau pathology in human disease remains largely unknown. This review summarises current knowledge on the association between inflammatory processes and tau pathology. While, preclinical evidence suggests that inflammation can indeed induce tau hyperphosphorylation at both pre- and post-tangles epitopes, a better understanding of whether this develops into advanced pathological features such as neurofibrillary tangles is needed. Microglial cells, the immune phagocytes in the central nervous system, appear to play a key role in regulating tau pathology, but the underlying mechanisms are not fully understood. Their activation can be detrimental via the secretion of pro-inflammatory mediators, particularly interleukin-1β, but also potentially beneficial through phagocytosis of extracellular toxic tau oligomers. Nevertheless, anti-inflammatory treatments in animal models were found protective, but whether or not they affect microglial phagocytosis of tau species is unknown. However, one major challenge to our understanding of the role of inflammation in the progression of tau pathology is the preclinical models used to address this question. They mostly rely on the use of septic doses of lipopolysaccharide that do not reflect the inflammatory conditions experienced AD patients, questioning whether the impact of inflammation on tau pathology in these models is dose-dependent and relevant to the human disease. The use of more translational models of inflammation corroborated with verification in clinical investigations are necessary to progress our understanding of the interplay between inflammation and tau pathology.

Indexed as

Protein Aggregation, PathologicalAlzheimer DiseaseAnimalsAnti-Inflammatory AgentsBrainHumansInflammationInflammation MediatorsNeuroprotective AgentsPhosphorylationSignal Transductiontau ProteinsAnti-Inflammatory AgentsInflammation MediatorsNeuroprotective Agentstau ProteinsAlzheimer's diseaseInflammationLipopolysaccharidePhosphorylationPreclinical modelsTau

Identifiers

PMID27979768
PMCPMC5479936
OpenAlexW2563010764

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.