Evidence map›Paper›PMID 31076648›Full record

ArticleScientific reports2019

Inhibition of tumour necrosis factor alpha in the R6/2 mouse model of Huntington's disease by etanercept treatment.

Jeffrey Pido-Lopez, Benedict Tanudjojo, Sahar Farag, Marie-Katrin Bondulich, Ralph Andre, Sarah J Tabrizi, Gillian P Bates

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

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 22% 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

15 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. 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

7 authors at 2 institutions in 1 country.

Jeffrey Pido-LopezHuntington's Disease Centre, Department of Neurodegenerative Disease and UK Dementia Research Institute, UCL Queen Square Institute of Neurology, University College London, London, WC1N 3BG, UK. j.pido@ucl.ac.uk.
Benedict TanudjojoHuntington's Disease Centre, Department of Neurodegenerative Disease and UK Dementia Research Institute, UCL Queen Square Institute of Neurology, University College London, London, WC1N 3BG, UK.
Sahar FaragHuntington's Disease Centre, Department of Neurodegenerative Disease and UK Dementia Research Institute, UCL Queen Square Institute of Neurology, University College London, London, WC1N 3BG, UK.
Marie-Katrin BondulichHuntington's Disease Centre, Department of Neurodegenerative Disease and UK Dementia Research Institute, UCL Queen Square Institute of Neurology, University College London, London, WC1N 3BG, UK.
Ralph AndreHuntington's Disease Centre, Department of Neurodegenerative Disease and UK Dementia Research Institute, UCL Queen Square Institute of Neurology, University College London, London, WC1N 3BG, UK.
Sarah J TabriziHuntington's Disease Centre, Department of Neurodegenerative Disease and UK Dementia Research Institute, UCL Queen Square Institute of Neurology, University College London, London, WC1N 3BG, UK.ORCID http://orcid.org/0000-0003-2716-2045
Gillian P BatesHuntington's Disease Centre, Department of Neurodegenerative Disease and UK Dementia Research Institute, UCL Queen Square Institute of Neurology, University College London, London, WC1N 3BG, UK. gillian.bates@ucl.ac.uk.ORCID http://orcid.org/0000-0002-4041-6305
UK Dementia Research Institute · GBJohn Radcliffe Hospital · GB

Funding

Medical Research Council MR/L02053X/1Medical Research Council MR/N00373X/1Wellcome Trust 200181/Z/15/Z
6 · The paper itself

Abstract

Huntington's disease (HD) is an inherited neurodegenerative disorder caused by the expansion of the CAG repeat in exon 1 of the huntingtin (HTT) gene, which results in a mutant protein with an extended polyglutamine tract. Inflammation occurs in both the brain and the periphery of HD patients and mouse models, with increases in brain and/or plasma levels of neurotoxic TNFα and several other proinflammatory cytokines. TNFα promotes the generation of many of these cytokines, such as IL6, which raises the possibility that TNFα is central to the inflammatory milieu associated with HD. A number of mouse studies have reported that the suppression of chronic immune activation during HD has beneficial consequences. Here, we investigated whether TNFα contributes to the peripheral inflammation that occurs in the R6/2 mouse model, and whether the in vivo blockade of TNFα, via etanercept treatment, can modify disease progression. We found that etanercept treatment normalised the elevated plasma levels of some cytokines. This did not modify the progression of certain behavioural measures, but slightly ameliorated brain weight loss, possibly related to a reduction in the elevated striatal level of soluble TNFα.

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalDisease Models, AnimalDown-RegulationEtanerceptExonsFemaleGene Expression RegulationHumansHuntingtin ProteinHuntington DiseaseMaleMiceMice, TransgenicTreatment OutcomeTumor Necrosis Factor-alphaAnti-Inflammatory Agents, Non-SteroidalEtanerceptHTT protein, humanHuntingtin ProteinTNF protein, humanTumor Necrosis Factor-alpha

Identifiers

PMID31076648
PMCPMC6510744
OpenAlexW2944156849

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.