Evidence map›Paper›PMID 26322048›Full record

ReviewFrontiers in immunology2015

Complement in the Homeostatic and Ischemic Brain.

Ali Alawieh, Andrew Elvington, Stephen Tomlinson

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 1 pooled it
5.2field-weighted citation impact, top 5% 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

65 citing papers in PubMed, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.

  1. Pooled it
  2. Review
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  18. Neuroinflammation in Acute Ischemic and Hemorrhagic Stroke.Current neurology and neuroscience reports · 2023
    Review
  19. Article
  20. Article

5 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

3 authors at 1 institution in 1 country.

Ali AlawiehNeuroscience Institute, Department of Neurosciences, Medical University of South Carolina , Charleston, SC , USA.
Andrew ElvingtonDepartment of Pathology and Immunology, Washington University School of Medicine , St. Louis, MO , USA.
Stephen TomlinsonDepartment of Microbiology and Immunology, Ralph H. Johnson Veteran Affairs Medical Center, Medical University of South Carolina , Charleston, SC , USA.
Washington University in St. Louis · US

Funding

Treating Depression and Enhancing Locomotor Recovery Post-strokeP20GM109040 · NIGMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI KAUTZ, STEVEN A. · 2014 to 2024
$23.5M
Novel Therapies to Improve Functional Recovery After StrokeI01RX001141 · VA · RALPH H JOHNSON VA MEDICAL CENTER · PI TOMLINSON, STEPHEN · 2014 to 2022
–
NIGMS NIH HHS P20 GM109040RRD VA I01 RX001141
6 · The paper itself

Abstract

The complement system is a component of the immune system involved in both recognition and response to pathogens, and it is implicated in an increasing number of homeostatic and disease processes. It is well documented that reperfusion of ischemic tissue results in complement activation and an inflammatory response that causes post-reperfusion injury. This occurs following cerebral ischemia and reperfusion and triggers secondary damage that extends beyond the initial infarcted area, an outcome that has rationalized the use of complement inhibitors as candidate therapeutics after stroke. In the central nervous system, however, recent studies have revealed that complement also has essential roles in synaptic pruning, neurogenesis, and neuronal migration. In the context of recovery after stroke, these apparent divergent functions of complement may account for findings that the protective effect of complement inhibition in the acute phase after stroke is not always maintained in the subacute and chronic phases. The development of effective stroke therapies based on modulation of the complement system will require a detailed understanding of complement-dependent processes in both early neurodegenerative events and delayed neuro-reparatory processes. Here, we review the role of complement in normal brain physiology, the events initiating complement activation after cerebral ischemia-reperfusion injury, and the contribution of complement to both injury and recovery. We also discuss how the design of future experiments may better characterize the dual role of complement in recovery after ischemic stroke.

Indexed as

brain ischemiacomplementinnate immunityneuroprotectionreperfusion injurystroke

Identifiers

PMID26322048
PMCPMC4533015
OpenAlexW1877278762

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.