Evidence map›Paper›PMID 34884906›Full record

ReviewInternational journal of molecular sciences2021

Neuroinflammation as a Key Driver of Secondary Neurodegeneration Following Stroke?

Shannon M Stuckey, Lin Kooi Ong, Lyndsey E Collins-Praino, Renée J Turner

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

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed, 4 pooled it
8.7field-weighted citation impact, top 2% 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

85 citing papers in PubMed, 4 syntheses or guidelines pooled it, 141 citations in OpenAlex.

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25 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

4 authors at 2 institutions in 2 countries.

Shannon M StuckeyDiscipline of Anatomy and Pathology, School of Biomedicine, Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide 5005, Australia.ORCID 0000-0002-0446-7279
Lin Kooi OngSchool of Pharmacy, Monash University Malaysia, Subang Jaya 47500, Malaysia.ORCID 0000-0001-8664-0540
Lyndsey E Collins-PrainoDiscipline of Anatomy and Pathology, School of Biomedicine, Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide 5005, Australia.ORCID 0000-0002-4380-7600
Renée J TurnerDiscipline of Anatomy and Pathology, School of Biomedicine, Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide 5005, Australia.
The University of Adelaide · AUMonash University Malaysia · MY

Funding

NeuroSurgical Research Foundation 75123439Perpetual (Australia) 75123439
6 · The paper itself

Abstract

Ischaemic stroke involves the rapid onset of focal neurological dysfunction, most commonly due to an arterial blockage in a specific region of the brain. Stroke is a leading cause of death and common cause of disability, with over 17 million people worldwide suffering from a stroke each year. It is now well-documented that neuroinflammation and immune mediators play a key role in acute and long-term neuronal tissue damage and healing, not only in the infarct core but also in distal regions. Importantly, in these distal regions, termed sites of secondary neurodegeneration (SND), spikes in neuroinflammation may be seen sometime after the initial stroke onset, but prior to the presence of the neuronal tissue damage within these regions. However, it is key to acknowledge that, despite the mounting information describing neuroinflammation following ischaemic stroke, the exact mechanisms whereby inflammatory cells and their mediators drive stroke-induced neuroinflammation are still not fully understood. As a result, current anti-inflammatory treatments have failed to show efficacy in clinical trials. In this review we discuss the complexities of post-stroke neuroinflammation, specifically how it affects neuronal tissue and post-stroke outcome acutely, chronically, and in sites of SND. We then discuss current and previously assessed anti-inflammatory therapies, with a particular focus on how failed anti-inflammatories may be repurposed to target SND-associated neuroinflammation.

Indexed as

AnimalsAnti-Inflammatory AgentsClinical Trials as TopicGene Expression RegulationGene Regulatory NetworksHumansIschemic StrokeNeurodegenerative DiseasesNeuroinflammatory DiseasesAnti-Inflammatory Agentsanti-inflammatoriesastrocytescerebral ischaemiadementiainflammationmicroglianeuroprotectionstroketherapeutic

Identifiers

PMID34884906
PMCPMC8658328
OpenAlexW4200047141

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.