Evidence map›Paper›PMID 33351792›Full record

ArticlePLoS biology2020

Oligodendrocytes support axonal transport and maintenance via exosome secretion.

Carsten Frühbeis, Wen Ping Kuo-Elsner, Christina Müller, Kerstin Barth, Leticia Peris, Stefan Tenzer, Wiebke Möbius, Hauke B Werner, Klaus-Armin Nave, Dominik Fröhlich and 1 more

Open access · goldAbstract read
In one paragraph

Article in PLoS biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed, 1 pooled it
7.2field-weighted citation impact, top 2% 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

104 citing papers in PubMed, 1 synthesis or guideline pooled it, 174 citations in OpenAlex.

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  19. Extracellular RNAs as Messengers and Early Biomarkers in Neurodegeneration.International journal of molecular sciences · 2025
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44 more citing papers are in PubMed but not listed here.

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 3 institutions in 3 countries.

Carsten FrühbeisInstitute of Developmental Biology and Neurobiology, Johannes Gutenberg University of Mainz, Mainz, Germany.
Wen Ping Kuo-ElsnerInstitute of Developmental Biology and Neurobiology, Johannes Gutenberg University of Mainz, Mainz, Germany.ORCID 0000-0001-5424-5300
Christina MüllerInstitute of Developmental Biology and Neurobiology, Johannes Gutenberg University of Mainz, Mainz, Germany.
Kerstin BarthInstitute of Developmental Biology and Neurobiology, Johannes Gutenberg University of Mainz, Mainz, Germany.
Leticia PerisGrenoble Institut des Neurosciences, Université Grenoble Alpes, Inserm, U1216, Grenoble, France.ORCID 0000-0002-0668-1252
Stefan TenzerInstitute of Immunology, University Medical Center, Johannes Gutenberg University of Mainz, Mainz, Germany.ORCID 0000-0003-3034-0017
Wiebke MöbiusDepartment of Neurogenetics, Max Planck Institute of Experimental Medicine, Göttingen, Germany.ORCID 0000-0002-2902-7165
Hauke B WernerDepartment of Neurogenetics, Max Planck Institute of Experimental Medicine, Göttingen, Germany.
Klaus-Armin NaveDepartment of Neurogenetics, Max Planck Institute of Experimental Medicine, Göttingen, Germany.
Dominik FröhlichInstitute of Developmental Biology and Neurobiology, Johannes Gutenberg University of Mainz, Mainz, Germany.ORCID 0000-0002-9551-3620
Eva-Maria Krämer-AlbersInstitute of Developmental Biology and Neurobiology, Johannes Gutenberg University of Mainz, Mainz, Germany.ORCID 0000-0001-7994-1185
Johannes Gutenberg University Mainz · DEMax Planck Institute of Experimental Medicine · DEInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurons extend long axons that require maintenance and are susceptible to degeneration. Long-term integrity of axons depends on intrinsic mechanisms including axonal transport and extrinsic support from adjacent glial cells. The mechanisms of support provided by myelinating oligodendrocytes to underlying axons are only partly understood. Oligodendrocytes release extracellular vesicles (EVs) with properties of exosomes, which upon delivery to neurons improve neuronal viability in vitro. Here, we show that oligodendroglial exosome secretion is impaired in 2 mouse mutants exhibiting secondary axonal degeneration due to oligodendrocyte-specific gene defects. Wild-type oligodendroglial exosomes support neurons by improving the metabolic state and promoting axonal transport in nutrient-deprived neurons. Mutant oligodendrocytes release fewer exosomes, which share a common signature of underrepresented proteins. Notably, mutant exosomes lack the ability to support nutrient-deprived neurons and to promote axonal transport. Together, these findings indicate that glia-to-neuron exosome transfer promotes neuronal long-term maintenance by facilitating axonal transport, providing a novel mechanistic link between myelin diseases and secondary loss of axonal integrity.

Indexed as

AnimalsAxonal TransportAxonsExosomesExtracellular VesiclesFemaleHEK293 CellsHumansMaintenanceMaleMiceMice, Inbred C57BLMyelin SheathNeurogliaNeuronsOligodendroglia

Identifiers

PMID33351792
PMCPMC7787684
OpenAlexW3117185967

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.