Evidence map›Paper›PMID 31011226›Full record

ArticleNature neuroscience2019

Bassoon proteinopathy drives neurodegeneration in multiple sclerosis.

Benjamin Schattling, Jan Broder Engler, Constantin Volkmann, Nicola Rothammer, Marcel S Woo, Meike Petersen, Iris Winkler, Max Kaufmann, Sina C Rosenkranz, Anna Fejtova and 12 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
–field-weighted citation impact
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

53 citing papers in PubMed.

  1. Article
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  4. Review
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  6. Article
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  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. The neuropathobiology of multiple sclerosis.Nature reviews. Neuroscience · 2024
    Review
  16. Article
  17. Article
  18. Article
  19. Behavioral and histological analyses of the mouseFrontiers in neuroscience · 2024
    Article
  20. 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

22 authors.

Benjamin Schattling *Institut für Neuroimmunologie und Multiple Sklerose, Zentrum für Molekulare Neurobiologie Hamburg, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany.ORCID http://orcid.org/0000-0001-8809-9073
Jan Broder Engler *Institut für Neuroimmunologie und Multiple Sklerose, Zentrum für Molekulare Neurobiologie Hamburg, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany.ORCID http://orcid.org/0000-0002-3169-2076
Constantin VolkmannInstitut für Neuroimmunologie und Multiple Sklerose, Zentrum für Molekulare Neurobiologie Hamburg, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany.
Nicola RothammerInstitut für Neuroimmunologie und Multiple Sklerose, Zentrum für Molekulare Neurobiologie Hamburg, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany.
Marcel S WooInstitut für Neuroimmunologie und Multiple Sklerose, Zentrum für Molekulare Neurobiologie Hamburg, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany.ORCID http://orcid.org/0000-0002-1306-2708
Meike PetersenZentrum für Molekulare Neurobiologie Hamburg, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany.
Iris WinklerInstitut für Neuroimmunologie und Multiple Sklerose, Zentrum für Molekulare Neurobiologie Hamburg, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany.
Max KaufmannInstitut für Neuroimmunologie und Multiple Sklerose, Zentrum für Molekulare Neurobiologie Hamburg, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany.ORCID http://orcid.org/0000-0002-1954-4425
Sina C RosenkranzInstitut für Neuroimmunologie und Multiple Sklerose, Zentrum für Molekulare Neurobiologie Hamburg, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany.ORCID http://orcid.org/0000-0002-5228-4266
Anna FejtovaLeibniz-Institute für Neurobiologie, Magdeburg, Germany.ORCID http://orcid.org/0000-0002-1815-4409
Ulrich ThomasLeibniz-Institute für Neurobiologie, Magdeburg, Germany.
Aparajita BoseInstitut für Neuroimmunologie und Multiple Sklerose, Zentrum für Molekulare Neurobiologie Hamburg, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany.
Simone BauerInstitut für Neuroimmunologie und Multiple Sklerose, Zentrum für Molekulare Neurobiologie Hamburg, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany.
Simone TrägerInstitut für Neuroimmunologie und Multiple Sklerose, Zentrum für Molekulare Neurobiologie Hamburg, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany.
Katharine K MillerZentrum für Molekulare Neurobiologie Hamburg, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany.
Wolfgang BrückInstitut für Neuropathologie, Universitätsmedizin Göttingen, Georg-August-Universität Göttingen, Göttingen, Germany.
Kent E DuncanZentrum für Molekulare Neurobiologie Hamburg, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany.
Gabriela SalinasTranskriptomanalyselabor, Institut für Entwicklungsbiochemie, Universitätsmedizin Göttingen, Georg-August-Universität Göttingen, Göttingen, Germany.
Peter SobaZentrum für Molekulare Neurobiologie Hamburg, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany.ORCID http://orcid.org/0000-0002-6163-4686
Eckart D GundelfingerLeibniz-Institute für Neurobiologie, Magdeburg, Germany.
Doron MerklerDepartment of Pathology and Immunology, Service of Clinical Pathology, Geneva Faculty of Medicine, Geneva, Switzerland.
Manuel A FrieseInstitut für Neuroimmunologie und Multiple Sklerose, Zentrum für Molekulare Neurobiologie Hamburg, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany. manuel.friese@zmnh.uni-hamburg.de.ORCID http://orcid.org/0000-0001-6380-2420

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is characterized by inflammatory insults that drive neuroaxonal injury. However, knowledge about neuron-intrinsic responses to inflammation is limited. By leveraging neuron-specific messenger RNA profiling, we found that neuroinflammation leads to induction and toxic accumulation of the synaptic protein bassoon (Bsn) in the neuronal somata of mice and patients with MS. Neuronal overexpression of Bsn in flies resulted in reduction of lifespan, while genetic disruption of Bsn protected mice from inflammation-induced neuroaxonal injury. Notably, pharmacological proteasome activation boosted the clearance of accumulated Bsn and enhanced neuronal survival. Our study demonstrates that neuroinflammation initiates toxic protein accumulation in neuronal somata and advocates proteasome activation as a potential remedy.

Indexed as

AnimalsDrosophilaHumansInflammationMiceMultiple SclerosisNerve DegenerationNerve Tissue ProteinsNeuronsSpinal CordNerve Tissue Proteins

Identifiers

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.