Evidence map›Paper›PMID 29417336›Full record

ReviewJournal of neural transmission (Vienna, Austria : 1996)2018

Prion-like properties of disease-relevant proteins in amyotrophic lateral sclerosis.

S Bräuer, V Zimyanin, A Hermann

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of neural transmission (Vienna, Austria : 1996), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Antibody targeting TDP-43 mitigates pathogenic pathways induced by the cerebrospinal fluid of ALS.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Article
  4. Article
  5. Review
  6. Where and Why Modeling Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2021
    Review
  7. Diagnostics of Amyotrophic Lateral Sclerosis: Up to Date.Diagnostics (Basel, Switzerland) · 2021
    Review
  8. PrPFrontiers in molecular neuroscience · 2021
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
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

3 authors at 3 institutions in 1 country.

S BräuerDepartment of Neurology, Technische Universität Dresden, Fetscherstraße 74, 01307, Dresden, Germany.
V ZimyaninDepartment of Neurology, Technische Universität Dresden, Fetscherstraße 74, 01307, Dresden, Germany.
A HermannDepartment of Neurology, Technische Universität Dresden, Fetscherstraße 74, 01307, Dresden, Germany. Andreas.Hermann@uniklinikum-dresden.de.ORCID http://orcid.org/0000-0002-7364-7791
German Center for Neurodegenerative Diseases · DEStädtisches Klinikum Dresden · DETechnische Universität Dresden · DE

Funding

Helmholtz-Gemeinschaft VH-VI-510
6 · The paper itself

Abstract

The hallmark of age-related neurodegenerative diseases is the appearance of cellular protein deposits and spreading of this pathology throughout the central nervous system. Growing evidence has shown the involvement and critical role of proteins with prion-like properties in the formation of these characteristic cellular aggregates. Prion-like domains of such proteins with their proposed function in the organization of membraneless organelles are prone for misfolding and promoting further aggregation. Spreading of these toxic aggregates between cells and across tissues can explain the progression of clinical phenotypes and pathology in a stereotypical manner, characteristic for almost every neurodegenerative disease. Here, we want to review the current evidence for the role of prion-like mechanisms in classical neurodegenerative diseases and ALS in particular. We will also discuss an intriguingly central role of the protein TDP-43 in the majority of cases of this devastating disease.

Indexed as

Protein FoldingAmyotrophic Lateral SclerosisAnimalsDNA-Binding ProteinsHumansDNA-Binding ProteinsTARDBP protein, humanAmyotrophic lateral sclerosisDisease spreadingFUSMotor neuron diseaseNeurodegenerative diseasePrion-like propertiesStrainsTDP-43

Identifiers

PMID29417336
OpenAlexW2790532602

What OpenQuestion holds

Textmetadata
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.