Evidence map›Paper›PMID 25986556›Full record

ReviewCold Spring Harbor perspectives in biology2015

Glia Disease and Repair-Remyelination.

Robin J M Franklin, Steven A Goldman

Open access · bronzeAbstract readReview
In one paragraph

Review in Cold Spring Harbor perspectives in biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers.

0numbers the graph read from it
0cells of the map it votes in
111citing 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

111 citing papers in PubMed, 212 citations in OpenAlex.

  1. Article
  2. Review
  3. Natalizumab exacerbates astrocytopathy in NMOSD via blockade of endothelial VCAM1-astrocytic integrin α4 interaction.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Pmp2+ Schwann Cells Maintain the Survival of Large-Caliber Motor Axons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Functional myelin in cognition and neurodevelopmental disorders.Cellular and molecular life sciences : CMLS · 2024
    Review
  19. Article
  20. Review

51 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

2 authors at 2 institutions in 3 countries.

Robin J M FranklinWellcome Trust-Medical Research Council Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB3 0ES, United Kingdom.
Steven A GoldmanCenter for Translational Neuromedicine, University of Rochester Medical Center, Rochester, New York 14642 University of Copenhagen Faculty of Medicine, Copenhagen 2200, Denmark.
University of Copenhagen · DKWellcome/MRC Cambridge Stem Cell Institute · GB

Funding

A Humanized Mouse Model of Astrocytic Pathology in SchizophreniaR01MH099578 · NIMH · UNIVERSITY OF ROCHESTER · PI GOLDMAN, STEVEN ALAN, NEDERGAARD, MAIKEN · 2013 to 2017
$2.8M
Molecular Regulation of Human Glial Progenitor Cell-Based RemyelinationR01NS075345 · NINDS · UNIVERSITY OF ROCHESTER · PI GOLDMAN, STEVEN ALAN · 2011 to 2015
$1.7M
NIMH NIH HHS R01 MH099578NINDS NIH HHS R01 NS075345Wellcome Trust 97922
6 · The paper itself

Abstract

The inability of the mammalian central nervous system (CNS) to undergo spontaneous regeneration has long been regarded as a central tenet of neurobiology. However, although this is largely true of the neuronal elements of the adult mammalian CNS, save for discrete populations of granular neurons, the same is not true of its glial elements. In particular, the loss of oligodendrocytes, which results in demyelination, triggers a spontaneous and often highly efficient regenerative response, remyelination, in which new oligodendrocytes are generated and myelin sheaths are restored to denuded axons. Yet, remyelination in humans is not without limitation, and a variety of demyelinating conditions are associated with sustained and disabling myelin loss. In this review, we will review the biology of remyelination, including the cells and signals involved; describe when remyelination occurs and when and why it fails and the consequences of its failure; and discuss approaches for therapeutically enhancing remyelination in demyelinating diseases of both children and adults, both by stimulating endogenous oligodendrocyte progenitor cells and by transplanting these cells into demyelinated brain.

Indexed as

Nerve RegenerationAnimalsCell DifferentiationHumansMiceMyelin SheathNeurodegenerative DiseasesNeurogliaOligodendrogliaPluripotent Stem CellsSignal TransductionStem Cell Transplantation

Identifiers

PMID25986556
PMCPMC4484968
OpenAlexW1861300743

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.