Evidence map›Paper›PMID 33323383›Full record

ArticleCancer research2021

Glia-Selective Deletion of Complement

Mineh Markarian, Robert P Krattli, Jabra D Baddour, Leila Alikhani, Erich Giedzinski, Manal T Usmani, Anshu Agrawal, Janet E Baulch, Andrea J Tenner, Munjal M Acharya

Open access · bronzeAbstract readComment
In one paragraph

Article in Cancer research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 9% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.

  1. Pooled it
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  11. [C1q-neutralizing antibodies improves postpartum depressive-like behaviors in mice by regulating the C1q/C3 pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
    Article
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  15. Immune checkpoint inhibition perturbs neuro-immune homeostasis and impairs cognitive function.Journal of experimental & clinical cancer research : CR · 2025
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Mineh Markarian *Department of Radiation Oncology, University of California, Irvine, California.ORCID 0000-0001-5887-6775
Robert P Krattli *Department of Radiation Oncology, University of California, Irvine, California.
Jabra D BaddourDepartment of Radiation Oncology, University of California, Irvine, California.
Leila AlikhaniDepartment of Radiation Oncology, University of California, Irvine, California.
Erich GiedzinskiDepartment of Radiation Oncology, University of California, Irvine, California.
Manal T UsmaniDepartment of Radiation Oncology, University of California, Irvine, California.
Anshu AgrawalDepartment of Medicine, University of California, Irvine, California.ORCID 0000-0002-3323-9152
Janet E BaulchDepartment of Radiation Oncology, University of California, Irvine, California.ORCID 0000-0002-1078-6946
Andrea J TennerDepartment of Molecular Biology and Biochemistry, University of California, Irvine, California.ORCID 0000-0003-3000-024X
Munjal M AcharyaDepartment of Radiation Oncology, University of California, Irvine, California. macharya@uci.edu.ORCID 0000-0002-7767-5642
University of California, Irvine · US

Funding

Univ.of Calif., Irvine Cancer Center Support GrantP30CA062203 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI Melanie Funes · 1994 to 2026
$57.9M
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
NCI NIH HHS P30 CA062203NIA NIH HHS R01 AG060148
6 · The paper itself

Abstract

The adverse neurocognitive sequelae following clinical radiotherapy (RT) for central nervous system (CNS) malignancies are often long-lasting without any clinical recourse. Despite recent progress, the cellular mechanisms mediating RT-induced cognitive deficits (RICD) are poorly understood. The complement system is an immediate sensor of a disturbed inflammatory environment and a potent mediator of gliosis with a range of nonimmune functions in the CNS, including synaptic pruning, which is detrimental if dysregulated. We hypothesize that complement-mediated changes in glial cell function significantly contribute to RICD. The underlying alterations in CNS complement cascade proteins (C1q, C3), TLR4, and colabeling with glia (IBA1, GFAP) were examined using gene expression, immunofluorescence, and

Indexed as

Cognitive DysfunctionComplement C1qAnimalsCognitionMiceMicrogliaNeurogliaComplement C1q

Identifiers

PMID33323383
PMCPMC8137520
OpenAlexW3112281857

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.