Evidence map›Paper›PMID 28566429›Full record

ArticleScience translational medicine2017

Complement C3 deficiency protects against neurodegeneration in aged plaque-rich APP/PS1 mice.

Qiaoqiao Shi, Saba Chowdhury, Rong Ma, Kevin X Le, Soyon Hong, Barbara J Caldarone, Beth Stevens, Cynthia A Lemere

Open access · greenAbstract read
In one paragraph

Article in Science translational medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 345 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
345citing papers in PubMed, 2 pooled it
28.2field-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

345 citing papers in PubMed, 2 syntheses or guidelines pooled it, 582 citations in OpenAlex.

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285 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

8 authors at 3 institutions in 1 country.

Qiaoqiao ShiAnn Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Building for Transformative Medicine, 9th Floor, 60 Fenwood Road, Boston, MA 02115, USA.ORCID 0000-0003-4035-9272
Saba ChowdhuryAnn Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Building for Transformative Medicine, 9th Floor, 60 Fenwood Road, Boston, MA 02115, USA.ORCID 0000-0003-2945-7007
Rong MaAnn Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Building for Transformative Medicine, 9th Floor, 60 Fenwood Road, Boston, MA 02115, USA.ORCID 0000-0002-4644-805X
Kevin X LeAnn Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Building for Transformative Medicine, 9th Floor, 60 Fenwood Road, Boston, MA 02115, USA.ORCID 0000-0002-6879-8595
Soyon HongHarvard Medical School, Boston, MA 02115, USA.ORCID 0000-0002-5744-4871
Barbara J CaldaroneHarvard Medical School, Boston, MA 02115, USA.
Beth StevensHarvard Medical School, Boston, MA 02115, USA.ORCID 0000-0003-4226-1201
Cynthia A LemereAnn Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Building for Transformative Medicine, 9th Floor, 60 Fenwood Road, Boston, MA 02115, USA. clemere@bwh.harvard.edu.ORCID 0000-0002-2983-7870
Brigham and Women's Hospital · USBoston Children's Hospital · USHarvard University · US

Funding

Understanding and Mitigating Vascular Side-Effects Associated with Anti-Amyloid ImmunotherapyR01NS136122 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI CYNTHIA A LEMERE · 2024 to 2026
$2.5M
Generation of a Complement C3 Conditional Knockout MouseR21AG044713 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI LEMERE, CYNTHIA A · 2013 to 2014
$475k
NIA NIH HHS R21 AG044713NINDS NIH HHS R01 NS136122
6 · The paper itself

Abstract

The complement cascade not only is an innate immune response that enables removal of pathogens but also plays an important role in microglia-mediated synaptic refinement during brain development. Complement C3 is elevated in Alzheimer's disease (AD), colocalizing with neuritic plaques, and appears to contribute to clearance of Aβ by microglia in the brain. Previously, we reported that C3-deficient C57BL/6 mice were protected against age-related and region-specific loss of hippocampal synapses and cognitive decline during normal aging. Furthermore, blocking complement and downstream iC3b/CR3 signaling rescued synapses from Aβ-induced loss in young AD mice before amyloid plaques had accumulated. We assessed the effects of C3 deficiency in aged, plaque-rich APPswe/PS1dE9 transgenic mice (APP/PS1;

Indexed as

AgingAmyloid beta-Protein PrecursorAnimalsAstrocytesCognitive DysfunctionComplement C3CytokinesGliosisHippocampusMice, Inbred C57BLMice, KnockoutNerve DegenerationPlaque, AmyloidPresenilin-1SolubilitySynapsesAmyloid beta-Protein PrecursorComplement C3CytokinesPresenilin-1

Identifiers

PMID28566429
PMCPMC6936623
OpenAlexW2618794795

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.