Evidence map›Paper›PMID 32608162›Full record

ArticleAnnals of clinical and translational neurology2020

Neuronal RNA-binding protein dysfunction in multiple sclerosis cortex.

Hannah E Salapa, Catherine Hutchinson, Bogdan F Popescu, Michael C Levin

Open access · goldAbstract read
In one paragraph

Article in Annals of clinical and translational neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.1field-weighted citation impact, top 10% 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

25 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. RNArchitects: how hnRNPs shape neuronal landscapes.Brain : a journal of neurology · 2026
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  18. Regionally restricted modulation ofFrontiers in molecular neuroscience · 2022
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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

4 authors at 2 institutions in 1 country.

Hannah E SalapaDepartment of Anatomy, Physiology and Pharmacology & Cameco MS Neuroscience Research Center, College of Medicine, University of Saskatchewan, Saskatoon, SK, Canada.ORCID 0000-0001-7594-4514
Catherine HutchinsonOffice of the Saskatchewan Multiple Sclerosis Clinical Research Chair, University of Saskatchewan, Saskatoon, SK, Canada.
Bogdan F PopescuDepartment of Anatomy, Physiology and Pharmacology & Cameco MS Neuroscience Research Center, College of Medicine, University of Saskatchewan, Saskatoon, SK, Canada.
Michael C LevinDepartment of Anatomy, Physiology and Pharmacology & Cameco MS Neuroscience Research Center, College of Medicine, University of Saskatchewan, Saskatoon, SK, Canada.ORCID 0000-0002-3880-9193
Cameco (Canada) · CAUniversity of Saskatchewan · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveNeurodegeneration is thought to be the primary cause of neurological disability in multiple sclerosis (MS). Dysfunctional RNA-binding proteins (RBPs) including their mislocalization from nucleus to cytoplasm, stress granule formation, and altered RNA metabolism have been found to underlie neurodegeneration in amyotrophic lateral sclerosis and frontotemporal dementia. Yet, little is known about the role of dysfunctional RBPs in the pathogenesis of neurodegeneration in MS. As a follow-up to our seminal finding of altered RBP function in a single case of MS, we posited that there would be evidence of RBP dysfunction in cortical neurons in MS.

methodsCortical neurons from 12 MS and six control cases were analyzed by immunohistochemistry for heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1) and TAR-DNA-binding protein-43 (TDP-43). Seven distinct neuronal phenotypes were identified based on the nucleocytoplasmic staining of these RBPs. Statistical analyses were performed by analyzing each phenotype in relation to MS versus controls.

resultsAnalyses revealed a continuum of hnRNP A1 and TDP-43 nucleocytoplasmic staining was found in cortical neurons, from neurons with entirely nuclear staining with little cytoplasmic staining in contrast to those with complete nuclear depletion of RBPs concurrent with robust cytoplasmic staining. The neuronal phenotypes that showed the most nucleocytoplasmic mislocalization of hnRNP A1 and TDP-43 statistically distinguished MS from control cases (P < 0.01, P < 0.001, respectively).

interpretationThe discovery of hnRNP A1 and TDP-43 nucleocytoplasmic mislocalization in neurons in MS brain demonstrate that dysfunctional RBPs may play a role in neurodegeneration in MS, as they do in other neurological diseases.

Indexed as

AdultAgedCerebral CortexDNA-Binding ProteinsFemaleHeterogeneous Nuclear Ribonucleoprotein A1HumansMaleMiddle AgedMultiple SclerosisNeuronsRNA-Binding ProteinsDNA-Binding ProteinsHeterogeneous Nuclear Ribonucleoprotein A1hnRNPA1 protein, humanRNA-Binding ProteinsTARDBP protein, human

Identifiers

PMID32608162
PMCPMC7359129
OpenAlexW3040365468

What OpenQuestion holds

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Registered trials

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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.