Evidence map›Paper›PMID 33239010›Full record

ReviewJournal of neuroinflammation2020

The good, the bad, and the opportunities of the complement system in neurodegenerative disease.

Nicole D Schartz, Andrea J Tenner

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

Review in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 177 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
177citing papers in PubMed, 2 pooled it
12.8field-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

177 citing papers in PubMed, 2 syntheses or guidelines pooled it, 279 citations in OpenAlex.

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117 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

2 authors at 1 institution in 1 country.

Nicole D SchartzDepartment of Molecular Biology and Biochemistry, University of California Irvine, 3205 McGaugh Hall, Irvine, CA, 92697, USA.
Andrea J TennerDepartment of Molecular Biology and Biochemistry, University of California Irvine, 3205 McGaugh Hall, Irvine, CA, 92697, USA. atenner@uci.edu.ORCID http://orcid.org/0000-0003-3000-024X
University of California, Irvine · US

Funding

Defining the Mechanistic Link between C5aR1 signaling and cognitive loss in Alzheimer's diseasesR01AG060148 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI MORTAZAVI, SEYED ALI, TENNER, ANDREA JOAN · 2018 to 2021
$2.6M
Modulating Polarization of Glial Cells in AD mouse models by a Complement Receptor AntagonistR21AG061746 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI TENNER, ANDREA JOAN · 2019 to 2020
$425k
Alzheimer's Association AARFD-20-677771NIA NIH HHS NIA R21 061746NIA NIH HHS R01 AG060148NIA NIH HHS R21 AG061746NIH HHS NIA R01 060148
6 · The paper itself

Abstract

The complement cascade is a critical effector mechanism of the innate immune system that contributes to the rapid clearance of pathogens and dead or dying cells, as well as contributing to the extent and limit of the inflammatory immune response. In addition, some of the early components of this cascade have been clearly shown to play a beneficial role in synapse elimination during the development of the nervous system, although excessive complement-mediated synaptic pruning in the adult or injured brain may be detrimental in multiple neurogenerative disorders. While many of these later studies have been in mouse models, observations consistent with this notion have been reported in human postmortem examination of brain tissue. Increasing awareness of distinct roles of C1q, the initial recognition component of the classical complement pathway, that are independent of the rest of the complement cascade, as well as the relationship with other signaling pathways of inflammation (in the periphery as well as the central nervous system), highlights the need for a thorough understanding of these molecular entities and pathways to facilitate successful therapeutic design, including target identification, disease stage for treatment, and delivery in specific neurologic disorders. Here, we review the evidence for both beneficial and detrimental effects of complement components and activation products in multiple neurodegenerative disorders. Evidence for requisite co-factors for the diverse consequences are reviewed, as well as the recent studies that support the possibility of successful pharmacological approaches to suppress excessive and detrimental complement-mediated chronic inflammation, while preserving beneficial effects of complement components, to slow the progression of neurodegenerative disease.

Indexed as

AnimalsComplement ActivationComplement System ProteinsHumansNeurodegenerative DiseasesNeuroprotective AgentsComplement System ProteinsNeuroprotective AgentsAlzheimer’s diseaseComplementEpilepsyMicrogliaMultiple sclerosisNeurodegenerationNeuroprotectionStrokeToll-like receptorsTraumatic brain injury

Identifiers

PMID33239010
PMCPMC7690210
OpenAlexW3109073748

What OpenQuestion holds

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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.