Evidence map›Paper›PMID 31907273›Full record

ReviewJournal of immunology (Baltimore, Md. : 1950)2020

Complement-Mediated Events in Alzheimer's Disease: Mechanisms and Potential Therapeutic Targets.

Andrea J Tenner

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

Review in Journal of immunology (Baltimore, Md. : 1950), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 3 pooled it
5.7field-weighted citation impact, top 3% 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

64 citing papers in PubMed, 3 syntheses or guidelines pooled it, 99 citations in OpenAlex.

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4 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

1 author at 1 institution in 1 country.

Andrea J TennerDepartment of Molecular Biology and Biochemistry, University of California Irvine, Irvine, CA 92697; atenner@uci.edu.ORCID 0000-0003-3000-024X
University of California, Irvine · US

Funding

TISSUE REPOSITORY COREP01AG000538 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI LAFERLA, FRANK M · 1985 to 2018
$24.8M
COMPLEMENT AND INFLAMMATORY FACTORS IN AD PATHOGENESISR01NS035144 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI TENNER, ANDREA JOAN · 1997 to 2014
$4.2M
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
NIA NIH HHS P01 AG000538NIA NIH HHS R01 AG060148NIA NIH HHS R21 AG061746NINDS NIH HHS R01 NS035144
6 · The paper itself

Abstract

An estimated 5.7 million Americans suffer from Alzheimer's disease in the United States, with no disease-modifying treatments to prevent or treat cognitive deficits associated with the disease. Genome-wide association studies suggest that an enhancement of clearance mechanisms and/or promotion of an anti-inflammatory response may slow or prevent disease progression. Increasing awareness of distinct roles of complement components in normal brain development and function and in neurodegenerative disorders align with complement-mediated responses, and thus, thorough understanding of these molecular pathways is needed to facilitate successful therapeutic design. Both beneficial and detrimental effects of C1q as well as contributions to local inflammation by C5a-C5aR1 signaling in brain highlight the need for precision of therapeutic design. The potential benefit of β-amyloid clearance from the circulation via CR1-mediated mechanisms is also reviewed. Therapies that suppress inflammation while preserving protective effects of complement could be tested now to slow the progression of this debilitating disease.

Indexed as

Alzheimer DiseaseAnimalsBrainComplement System ProteinsHumansComplement System Proteins

Identifiers

PMID31907273
PMCPMC6951444
OpenAlexW2998859017

What OpenQuestion holds

Textmetadata
LicenceTDM
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.