Evidence map›Paper›PMID 37085528›Full record

ArticleScientific reports2023

Cortical glia in SOD1(G93A) mice are subtly affected by ALS-like pathology.

Tereza Filipi, Zuzana Matusova, Pavel Abaffy, Ondrej Vanatko, Jana Tureckova, Sarka Benesova, Monika Kubiskova, Denisa Kirdajova, Jakub Zahumensky, Lukas Valihrach and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

6 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Ferritin is closely associated with microglia in amyotrophic lateral sclerosis.Journal of neuropathology and experimental neurology · 2024
    Article
  5. Review
  6. Article
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

11 authors at 5 institutions in 1 country.

Tereza Filipi *Department of Cellular Neurophysiology, Institute of Experimental Medicine, Czech Academy of Sciences, Videnska 1083, 14220, Prague, Czech Republic.
Zuzana Matusova *Laboratory of Gene Expression, Institute of Biotechnology CAS, BIOCEV, Prumyslova 595, 25250, Vestec, Czech Republic.
Pavel AbaffyLaboratory of Gene Expression, Institute of Biotechnology CAS, BIOCEV, Prumyslova 595, 25250, Vestec, Czech Republic.
Ondrej VanatkoDepartment of Cellular Neurophysiology, Institute of Experimental Medicine, Czech Academy of Sciences, Videnska 1083, 14220, Prague, Czech Republic.
Jana TureckovaDepartment of Cellular Neurophysiology, Institute of Experimental Medicine, Czech Academy of Sciences, Videnska 1083, 14220, Prague, Czech Republic.
Sarka BenesovaLaboratory of Gene Expression, Institute of Biotechnology CAS, BIOCEV, Prumyslova 595, 25250, Vestec, Czech Republic.
Monika KubiskovaDepartment of Cellular Neurophysiology, Institute of Experimental Medicine, Czech Academy of Sciences, Videnska 1083, 14220, Prague, Czech Republic.
Denisa KirdajovaDepartment of Cellular Neurophysiology, Institute of Experimental Medicine, Czech Academy of Sciences, Videnska 1083, 14220, Prague, Czech Republic.
Jakub ZahumenskyDepartment of Functional Organization of Biomembranes, Institute of Experimental Medicine, Czech Academy of Sciences, Videnska 1083, 14220, Prague, Czech Republic.
Lukas ValihrachLaboratory of Gene Expression, Institute of Biotechnology CAS, BIOCEV, Prumyslova 595, 25250, Vestec, Czech Republic. lukas.valihrach@ibt.cas.cz.
Miroslava AnderovaDepartment of Cellular Neurophysiology, Institute of Experimental Medicine, Czech Academy of Sciences, Videnska 1083, 14220, Prague, Czech Republic. Miroslava.Anderova@iem.cas.cz.
Czech Academy of Sciences · CZCharles University · CZCzech Academy of Sciences, Institute of Experimental Medicine · CZCzech Academy of Sciences, Institute of Biotechnology · CZUniversity of Chemistry and Technology, Prague · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The role of glia in amyotrophic lateral sclerosis (ALS) is undeniable. Their disease-related activity has been extensively studied in the spinal cord, but only partly in the brain. We present herein a comprehensive study of glia in the cortex of SOD1(G93A) mice-a widely used model of ALS. Using single-cell RNA sequencing (scRNA-seq) and immunohistochemistry, we inspected astrocytes, microglia, and oligodendrocytes, in four stages of the disease, respecting the factor of sex. We report minimal changes of glia throughout the disease progression and regardless of sex. Pseudobulk and single-cell analyses revealed subtle disease-related transcriptional alterations at the end-stage in microglia and oligodendrocytes, which were supported by immunohistochemistry. Therefore, our data support the hypothesis that the SOD1(G93A) mouse cortex does not recapitulate the disease in patients, and we recommend the use of a different model for future studies of the cortical ALS pathology.

Indexed as

Amyotrophic Lateral SclerosisNeurogliaSuperoxide Dismutase-1AnimalsDisease Models, AnimalMiceMice, TransgenicMotor NeuronsSpinal CordSuperoxide DismutaseSuperoxide DismutaseSuperoxide Dismutase-1

Identifiers

PMID37085528
PMCPMC10121704
OpenAlexW4366742517

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.