Evidence map›Paper›PMID 29357880›Full record

ReviewJournal of neuroinflammation2018

The role of the complement system in traumatic brain injury: a review.

Adnan Hammad, Laura Westacott, Malik Zaben

Erratum issuedOpen access · goldAbstract readReview
In one paragraph

Review in Journal of neuroinflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 102 papers.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed
9.9field-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

102 citing papers in PubMed, 166 citations in OpenAlex.

  1. Review
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  4. Molecular characterization ofOpen veterinary journal · 2026
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42 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Adnan HammadSchool of Clinical Medicine, University of Cambridge, Cambridge, UK.
Laura WestacottNeuroscience and Mental Health Research Institute (NMHRI), School of Medicine, Cardiff University, Room 4FT 80E, 4th Floor, Heath Park, Cardiff, CF14 4XN, UK.
Malik ZabenNeuroscience and Mental Health Research Institute (NMHRI), School of Medicine, Cardiff University, Room 4FT 80E, 4th Floor, Heath Park, Cardiff, CF14 4XN, UK. zabenm@cardiff.ac.uk.ORCID http://orcid.org/0000-0002-7446-4532
Cardiff University · GBUniversity of Cambridge · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Traumatic brain injury (TBI) is an important cause of disability and mortality in the western world. While the initial injury sustained results in damage, it is the subsequent secondary cascade that is thought to be the significant determinant of subsequent outcomes. The changes associated with the secondary injury do not become irreversible until some time after the start of the cascade. This may present a window of opportunity for therapeutic interventions aiming to improve outcomes subsequent to TBI. A prominent contributor to the secondary injury is a multifaceted inflammatory reaction. The complement system plays a notable role in this inflammatory reaction; however, it has often been overlooked in the context of TBI secondary injury. The complement system has homeostatic functions in the uninjured central nervous system (CNS), playing a part in neurodevelopment as well as having protective functions in the fully developed CNS, including protection from infection and inflammation. In the context of CNS injury, it can have a number of deleterious effects, evidence for which primarily comes not only from animal models but also, to a lesser extent, from human post-mortem studies. In stark contrast to this, complement may also promote neurogenesis and plasticity subsequent to CNS injury. This review aims to explore the role of the complement system in TBI secondary injury, by examining evidence from both clinical and animal studies. We examine whether specific complement activation pathways play more prominent roles in TBI than others. We also explore the potential role of complement in post-TBI neuroprotection and CNS repair/regeneration. Finally, we highlight the therapeutic potential of targeting the complement system in the context of TBI and point out certain areas on which future research is needed.

Indexed as

AnimalsBrainBrain Injuries, TraumaticCell DifferentiationComplement ActivationComplement System ProteinsHumansSignal TransductionComplement System Proteins

Identifiers

PMID29357880
PMCPMC5778697
OpenAlexW2795085477

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.