Evidence map›Paper›PMID 30861188›Full record

ArticleGlia2019

Transforming growth factor-beta renders ageing microglia inhibitory to oligodendrocyte generation by CNS progenitors.

Roey Baror, Björn Neumann, Michael Segel, Kevin J Chalut, Stephen P J Fancy, Dorothy P Schafer, Robin J M Franklin

Open access · hybridAbstract read
In one paragraph

Article in Glia, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 7% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. The molecular asynchrony of single cells.bioRxiv : the preprint server for biology · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Aging microglia.Cellular and molecular life sciences : CMLS · 2023
    Review
  16. Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  17. Review
  18. Review
  19. Review
  20. 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

7 authors at 3 institutions in 2 countries.

Roey BarorWellcome-MRC Stem Cell Institute, University of Cambridge, Cambridge, United Kingdom.
Björn NeumannWellcome-MRC Stem Cell Institute, University of Cambridge, Cambridge, United Kingdom.
Michael SegelWellcome-MRC Stem Cell Institute, University of Cambridge, Cambridge, United Kingdom.
Kevin J ChalutWellcome-MRC Stem Cell Institute, University of Cambridge, Cambridge, United Kingdom.
Stephen P J FancyDepartment of Paediatrics, University California San Francisco, San Francisco, California.
Dorothy P SchaferDepartment of Neurobiology and the Brudnik Neuropsychiatric Institute, University of Massachusetts Medical School, Worcester, Massachusetts.
Robin J M FranklinWellcome-MRC Stem Cell Institute, University of Cambridge, Cambridge, United Kingdom.ORCID 0000-0001-6522-2104
Wellcome/MRC Cambridge Stem Cell Institute · GBUniversity of California, San Francisco · USUniversity of Massachusetts Chan Medical School · US

Funding

Vasculature provides the substrate for oligodendrocyte progenitor migration in development and diseaseR01NS097551 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI FANCY, STEPHEN PHILIP JAMES · 2017 to 2021
$1.7M
Medical Research Council MC_PC_12009NINDS NIH HHS R01 NS097551
6 · The paper itself

Abstract

It is now well-established that the macrophage and microglial response to CNS demyelination influences remyelination by removing myelin debris and secreting a variety of signaling molecules that influence the behaviour of oligodendrocyte progenitor cells (OPCs). Previous studies have shown that changes in microglia contribute to the age-related decline in the efficiency of remyelination. In this study, we show that microglia increase their expression of the proteoglycan NG2 with age, and that this is associated with an altered micro-niche generated by aged, but not young, microglia that can divert the differentiation OPCs from oligodendrocytes into astrocytes in vitro. We further show that these changes in ageing microglia are generated by exposure to high levels of TGFβ. Thus, our findings suggest that the rising levels of circulating TGFβ known to occur with ageing contribute to the age-related decline in remyelination by impairing the ability of microglia to promote oligodendrocyte differentiation from OPCs, and therefore could be a potential therapeutic target to promote remyelination.

Indexed as

Age FactorsAnimalsAnimals, NewbornCell DifferentiationCells, CulturedCellular SenescenceCentral Nervous SystemDose-Response Relationship, DrugMicrogliaOligodendrocyte Precursor CellsOligodendrogliaRatsRats, Sprague-DawleyTransforming Growth Factor betaTransforming Growth Factor betaageingextracellular matrixmicrogliaoligodendrocyteprogenitor cells

Identifiers

PMID30861188
PMCPMC6563458
OpenAlexW2921725925

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.