Evidence map›Paper›PMID 23542689›Full record

ArticleNature neuroscience2013

Degeneration and impaired regeneration of gray matter oligodendrocytes in amyotrophic lateral sclerosis.

Shin H Kang, Ying Li, Masahiro Fukaya, Ileana Lorenzini, Don W Cleveland, Lyle W Ostrow, Jeffrey D Rothstein, Dwight E Bergles

Open access · greenAbstract read
In one paragraph

Article in Nature neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 351 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
351citing papers in PubMed, 1 pooled it
28.4field-weighted citation impact, top 1% 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

351 citing papers in PubMed, 1 synthesis or guideline pooled it, 572 citations in OpenAlex.

  1. A systematic review and functionalFrontiers in neuroscience · 2025
    Pooled it
  2. Trial
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  16. Article
  17. Neuronal TDP-43 regulates myelin formation via neurexin 1 mRNA stabilization.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  18. Aberrant Splicing Signatures Underpin Oligodendrocyte Damage in ALS and Neuron Loss in FTD.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  19. Article
  20. Regional Molecular Diversity in Chronic Spinal Cord Injury.Cellular and molecular neurobiology · 2026
    Article

291 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 2 countries.

Shin H KangThe Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Ying Li
Masahiro Fukaya
Ileana Lorenzini
Don W Cleveland
Lyle W Ostrow
Jeffrey D Rothstein
Dwight E Bergles
Johns Hopkins Medicine · USJohns Hopkins University · USKitasato University · JPUniversity of California, San Diego · US

Funding

NEURONAL FILAMENT SYNTHESIS, ASSEMBLY, AND FUNCTIONR01NS027036 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Bogdan Bintu, Don W Cleveland · 1989 to 2026
$11.8M
Neuronal vs. glial glutamate transport regulation in ALSR01NS033958 · NINDS · JOHNS HOPKINS UNIVERSITY · PI ROTHSTEIN, JEFFREY D · 1995 to 2013
$5.4M
Neurofilaments, SOD1 and Motor Neuron DiseasesR37NS027036 · NINDS · LUDWIG INSTITUTE FOR CANCER RES LTD · PI CLEVELAND, DON W · 2005 to 2011
$4.1M
Neuroscience Training ProgramT32EY017203 · NEI · JOHNS HOPKINS UNIVERSITY · PI BERGLES, DWIGHT E · 2005 to 2014
$2.9M
Neuronal Regulation of NG2 CellsR01NS051509 · NINDS · JOHNS HOPKINS UNIVERSITY · PI BERGLES, DWIGHT E · 2006 to 2010
$1.8M
NEI NIH HHS T32 EY017203NINDS NIH HHS NS051509NINDS NIH HHS NS27036NINDS NIH HHS NS33958NINDS NIH HHS R01 NS027036NINDS NIH HHS R01 NS033958NINDS NIH HHS R01 NS051509NINDS NIH HHS R37 NS027036Wellcome Trust 089701
6 · The paper itself

Abstract

Oligodendrocytes associate with axons to establish myelin and provide metabolic support to neurons. In the spinal cord of amyotrophic lateral sclerosis (ALS) mice, oligodendrocytes downregulate transporters that transfer glycolytic substrates to neurons and oligodendrocyte progenitors (NG2(+) cells) exhibit enhanced proliferation and differentiation, although the cause of these changes in oligodendroglia is unknown. We found extensive degeneration of gray matter oligodendrocytes in the spinal cord of SOD1 (G93A) ALS mice prior to disease onset. Although new oligodendrocytes were formed, they failed to mature, resulting in progressive demyelination. Oligodendrocyte dysfunction was also prevalent in human ALS, as gray matter demyelination and reactive changes in NG2(+) cells were observed in motor cortex and spinal cord of ALS patients. Selective removal of mutant SOD1 from oligodendroglia substantially delayed disease onset and prolonged survival in ALS mice, suggesting that ALS-linked genes enhance the vulnerability of motor neurons and accelerate disease by directly impairing the function of oligodendrocytes.

Indexed as

Amyotrophic Lateral SclerosisAnimalsAnimals, NewbornCell ProliferationCells, CulturedDisease Models, AnimalFunctional LateralityHumansMiceMice, TransgenicMotor CortexMyelin SheathNerve DegenerationNerve Fibers, MyelinatedNerve Tissue ProteinsOligodendrogliaNerve Tissue ProteinsReceptor, Platelet-Derived Growth Factor alpha

Identifiers

PMID23542689
PMCPMC3637847
OpenAlexW2166043619

What OpenQuestion holds

Textmetadata
LicenceTDM
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.