Evidence map›Paper›PMID 30686733›Full record

ArticleNeuron2019

Calcium Influx through Plasma-Membrane Nanoruptures Drives Axon Degeneration in a Model of Multiple Sclerosis.

Maarten E Witte, Adrian-Minh Schumacher, Christoph F Mahler, Jan P Bewersdorf, Jonas Lehmitz, Alexander Scheiter, Paula Sánchez, Philip R Williams, Oliver Griesbeck, Ronald Naumann and 2 more

Abstract read
In one paragraph

Article in Neuron, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing 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

48 citing papers in PubMed.

  1. Review
  2. Article
  3. Multiple sclerosis: molecular pathogenesis and therapeutic intervention.Signal transduction and targeted therapy · 2025
    Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. From progression to progress: The future of multiple sclerosis.Journal of central nervous system disease · 2024
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors.

Maarten E WitteInstitute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität München, Marchioninistraße 15, 81377 Munich, Germany; Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Großhaderner Strasse 9, 82152 Planegg Martinsried, Germany.
Adrian-Minh SchumacherInstitute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität München, Marchioninistraße 15, 81377 Munich, Germany; Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Großhaderner Strasse 9, 82152 Planegg Martinsried, Germany.
Christoph F MahlerInstitute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität München, Marchioninistraße 15, 81377 Munich, Germany; Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Großhaderner Strasse 9, 82152 Planegg Martinsried, Germany.
Jan P BewersdorfInstitute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität München, Marchioninistraße 15, 81377 Munich, Germany; Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Großhaderner Strasse 9, 82152 Planegg Martinsried, Germany.
Jonas LehmitzInstitute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität München, Marchioninistraße 15, 81377 Munich, Germany; Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Großhaderner Strasse 9, 82152 Planegg Martinsried, Germany; Institute of Neuronal Cell Biology, Technische Universität München, Biedersteiner Straße 29, 80802 Munich, Germany.
Alexander ScheiterInstitute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität München, Marchioninistraße 15, 81377 Munich, Germany; Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Großhaderner Strasse 9, 82152 Planegg Martinsried, Germany; Institute of Neuronal Cell Biology, Technische Universität München, Biedersteiner Straße 29, 80802 Munich, Germany.
Paula SánchezInstitute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität München, Marchioninistraße 15, 81377 Munich, Germany; Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Großhaderner Strasse 9, 82152 Planegg Martinsried, Germany.
Philip R WilliamsInstitute of Neuronal Cell Biology, Technische Universität München, Biedersteiner Straße 29, 80802 Munich, Germany.
Oliver GriesbeckMax-Planck Institute of Neurobiology, Am Klopferspitz 18, 82152 Planegg-Martinsried, Germany.
Ronald NaumannMax-Planck Institute of Molecular Cell Biology and Genetics, Pfotenhauerstrasse 108, 01307 Dresden, Germany.
Thomas MisgeldInstitute of Neuronal Cell Biology, Technische Universität München, Biedersteiner Straße 29, 80802 Munich, Germany; Munich Cluster for Systems Neurology (SyNergy), Feodor-Lynen-Straße 17, 81377 Munich, Germany; German Center for Neurodegenerative Diseases (DZNE), Feodor-Lynen-Straße 17, 81377 Munich, Germany; Center of Integrated Protein Science (CIPSM), Butenandtstraße 5-13, 81377 Munich, Germany. Electronic address: thomas.misgeld@tum.de.
Martin KerschensteinerInstitute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität München, Marchioninistraße 15, 81377 Munich, Germany; Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Großhaderner Strasse 9, 82152 Planegg Martinsried, Germany; Munich Cluster for Systems Neurology (SyNergy), Feodor-Lynen-Straße 17, 81377 Munich, Germany. Electronic address: martin.kerschensteiner@med.uni-muenchen.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Axon loss determines persistent disability in multiple sclerosis patients. Here, we use in vivo calcium imaging in a multiple sclerosis model to show that cytoplasmic calcium levels determine the choice between axon loss and survival. We rule out the endoplasmic reticulum, glutamate excitotoxicity, and the reversal of the sodium-calcium exchanger as sources of intra-axonal calcium accumulation and instead identify nanoscale ruptures of the axonal plasma membrane as the critical path of calcium entry.

Indexed as

AnimalsAxonsCalciumCell MembraneFemaleIon TransportMaleMiceMultiple SclerosisCalciumaxon degenerationcalcium imagingexperimental autoimmune encephalomyelitisin vivo microscopymultiple sclerosisplasma membrane

Identifiers

PMID30686733
PMCPMC6389591

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.