Evidence map›Paper›PMID 30061661›Full record

ArticleScientific reports2018

In vivo neutralization of the protagonist role of macrophages during the chronic inflammatory stage of Huntington's disease.

Jeffrey Pido-Lopez, Ralph Andre, Agnesska C Benjamin, Nadira Ali, Sahar Farag, Sarah J Tabrizi, Gillian P Bates

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.0field-weighted citation impact, top 29% 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

22 citing papers in PubMed, 48 citations in OpenAlex.

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  4. Animal models of Huntington's disease. Pros and cons.Brain, behavior, & immunity - health · 2025
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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

7 authors at 1 institution in 1 country.

Jeffrey Pido-LopezHuntington's Disease Centre, Department of Neurodegenerative Disease and Dementia Research Institute, UCL Institute of Neurology, University College London, London, WC1N 3BG, UK. j.pido@ucl.ac.uk.
Ralph AndreHuntington's Disease Centre, Department of Neurodegenerative Disease and Dementia Research Institute, UCL Institute of Neurology, University College London, London, WC1N 3BG, UK.
Agnesska C BenjaminHuntington's Disease Centre, Department of Neurodegenerative Disease and Dementia Research Institute, UCL Institute of Neurology, University College London, London, WC1N 3BG, UK.ORCID 0000-0001-9220-4702
Nadira AliHuntington's Disease Centre, Department of Neurodegenerative Disease and Dementia Research Institute, UCL Institute of Neurology, University College London, London, WC1N 3BG, UK.
Sahar FaragHuntington's Disease Centre, Department of Neurodegenerative Disease and Dementia Research Institute, UCL Institute of Neurology, University College London, London, WC1N 3BG, UK.
Sarah J TabriziHuntington's Disease Centre, Department of Neurodegenerative Disease and Dementia Research Institute, UCL Institute of Neurology, University College London, London, WC1N 3BG, UK.ORCID 0000-0003-2716-2045
Gillian P BatesHuntington's Disease Centre, Department of Neurodegenerative Disease and Dementia Research Institute, UCL Institute of Neurology, University College London, London, WC1N 3BG, UK. gillian.bates@ucl.ac.uk.ORCID 0000-0002-4041-6305
UK Dementia Research Institute · GB

Funding

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

Abstract

Neurodegenerative diseases, characterised by the progressive and selective neuronal death in the central nervous system, are frequently accompanied by an activated immune system. In Huntington's disease (HD), clinical and animal studies show evidence of immune activity, along with hyper-reactive monocyte/macrophage responses, while application of immunosuppressive regimens have imparted beneficial effects to HD mice. These findings suggest a contributory role of the immune system in HD pathology, with immune-based interventions offering a potential therapeutic strategy. Herein, we show that peripheral and CNS immune system activity increased with disease progression in HD mouse models and defined the phenotype of the immune response. Additionally, the depletion of monocytes and macrophages in vivo, via clodronate liposome treatment, revealed a major contributory role of these innate immune cells to the chronic inflammatory milieu observed during the course of the disease. This suggests that peripheral immunomodulatory strategies targeting monocytes and macrophages could be relevant for HD.

Indexed as

AnimalsBrainChronic DiseaseClodronic AcidCytokinesDendritic CellsFemaleHuntington DiseaseInflammationLiposomesMacrophagesMaleMice, Inbred C57BLSpleenClodronic AcidCytokinesLiposomes

Identifiers

PMID30061661
PMCPMC6065433
OpenAlexW2884874570

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.