Evidence map›Paper›PMID 33776778›Full record

ReviewFrontiers in pharmacology2021

Neurodegenerative Disease and the NLRP3 Inflammasome.

Jonathan A Holbrook, Heledd H Jarosz-Griffiths, Emily Caseley, Samuel Lara-Reyna, James A Poulter, Caroline H Williams-Gray, Daniel Peckham, Michael F McDermott

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed
11.8field-weighted citation impact, top 1% 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

111 citing papers in PubMed, 183 citations in OpenAlex.

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51 more citing papers are in PubMed but not listed here.

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

8 authors at 5 institutions in 1 country.

Jonathan A HolbrookDepartment of Clinical Neurosciences, John Van Geest Centre for Brain Repair, University of Cambridge, Cambridge, United Kingdom.
Heledd H Jarosz-GriffithsLeeds Institute of Rheumatic and Musculoskeletal Medicine (LIRMM), University of Leeds, Leeds, United Kingdom.
Emily CaseleyLeeds Institute of Rheumatic and Musculoskeletal Medicine (LIRMM), University of Leeds, Leeds, United Kingdom.
Samuel Lara-ReynaInstitute of Microbiology and Infection, University of Birmingham, Birmingham, United Kingdom.
James A PoulterLeeds Institute of Rheumatic and Musculoskeletal Medicine (LIRMM), University of Leeds, Leeds, United Kingdom.
Caroline H Williams-GrayDepartment of Clinical Neurosciences, John Van Geest Centre for Brain Repair, University of Cambridge, Cambridge, United Kingdom.
Daniel PeckhamLeeds Institute of Medical Research at St. James's University Hospital, Leeds, United Kingdom.
Michael F McDermottLeeds Institute of Rheumatic and Musculoskeletal Medicine (LIRMM), University of Leeds, Leeds, United Kingdom.
Cystic Fibrosis Trust · GBNIHR Leeds Musculoskeletal Biomedical Research Unit · GBUniversity of Cambridge · GBUniversity of Birmingham · GBUniversity of Leeds · GB

Funding

Medical Research Council MC_PC_17230Medical Research Council MR/R007446/1Medical Research Council MR/T02044X/1
6 · The paper itself

Abstract

The prevalence of neurodegenerative disease has increased significantly in recent years, and with a rapidly aging global population, this trend is expected to continue. These diseases are characterised by a progressive neuronal loss in the brain or peripheral nervous system, and generally involve protein aggregation, as well as metabolic abnormalities and immune dysregulation. Although the vast majority of neurodegeneration is idiopathic, there are many known genetic and environmental triggers. In the past decade, research exploring low-grade systemic inflammation and its impact on the development and progression of neurodegenerative disease has increased. A particular research focus has been whether systemic inflammation arises only as a secondary effect of disease or is also a cause of pathology. The inflammasomes, and more specifically the NLRP3 inflammasome, a crucial component of the innate immune system, is usually activated in response to infection or tissue damage. Dysregulation of the NLRP3 inflammasome has been implicated in the progression of several neurodegenerative disorders, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, and prion diseases. This review aims to summarise current literature on the role of the NLRP3 inflammasome in the pathogenesis of neurodegenerative diseases, and recent work investigating NLRP3 inflammasome inhibition as a potential future therapy.

Indexed as

Alzheimer's diseaseinflammationneurodegenerative diseaseneuroinflammationNLRP3 inflammasomeParkinson’s disease

Identifiers

PMID33776778
PMCPMC7987926
OpenAlexW3133822785

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.