Evidence map›Paper›PMID 27170209›Full record

ReviewExperimental neurology2016

Glial progenitor cell-based treatment of the childhood leukodystrophies.

M Joana Osorio, Steven A Goldman

Open access · greenAbstract readReview
In one paragraph

Review in Experimental neurology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

13 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
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  9. Review
  10. Article
  11. Article
  12. Review
  13. Progenitor cell-based treatment of glial disease.Progress in brain research · 2017
    Article
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 2 countries.

M Joana OsorioCenter for Translational Neuromedicine, University of Rochester Medical Center, Rochester, NY 14642, United States; Center for Basic and Translational Neuroscience, University of Copenhagen Faculty of Health and Medical Sciences, Copenhagen 2200, Denmark. Electronic address: joana.osorio@sund.ku.dk.
Steven A GoldmanCenter for Translational Neuromedicine, University of Rochester Medical Center, Rochester, NY 14642, United States; Center for Basic and Translational Neuroscience, University of Copenhagen Faculty of Health and Medical Sciences, Copenhagen 2200, Denmark. Electronic address: Steven_Goldman@urmc.rochester.edu.
University of Copenhagen · DKUniversity of Rochester Medical Center · US

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
An iPSC based humanized mouse model of dysmyelination in schizophreniaR01MH104701 · NIMH · UNIVERSITY OF ROCHESTER · PI GOLDMAN, STEVEN ALAN · 2014 to 2018
$2.1M
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 MH099578NIMH NIH HHS R01 MH104701NINDS NIH HHS R01 NS075345
6 · The paper itself

Abstract

The childhood leukodystrophies comprise a group of hereditary disorders characterized by the absence, malformation or destruction of myelin. These disorders share common clinical, radiological and pathological features, despite their diverse molecular and genetic etiologies. Oligodendrocytes and astrocytes are the major affected cell populations, and are either structurally impaired or metabolically compromised through cell-intrinsic pathology, or are the victims of mis-accumulated toxic byproducts of metabolic derangement. In either case, glial cell replacement using implanted tissue or pluripotent stem cell-derived human neural or glial progenitor cells may comprise a promising strategy for both structural remyelination and metabolic rescue. A broad variety of pediatric white matter disorders, including the primary hypomyelinating disorders, the lysosomal storage disorders, and the broader group of non-lysosomal metabolic leukodystrophies, may all be appropriate candidates for glial progenitor cell-based treatment. Nonetheless, a variety of specific challenges remain before this therapeutic strategy can be applied to children. These include timely diagnosis, before irreparable neuronal injury has ensued; understanding the natural history of the targeted disease; defining the optimal cell phenotype for each disorder; achieving safe and scalable cellular compositions; designing age-appropriate controlled clinical trials; and for autologous therapy of genetic disorders, achieving the safe genetic editing of pluripotent stem cells. Yet these challenges notwithstanding, the promise of glial progenitor cell-based treatment of the childhood myelin disorders offers hope to the many victims of this otherwise largely untreatable class of disease.

Indexed as

AnimalsCell- and Tissue-Based TherapyChildChild, PreschoolDemyelinating DiseasesHumansNeurogliaStem CellsCell therapyGlial progenitor cellsLeukodystrophiesMultiple sclerosisMyelinOligodendrocyte progenitor cellsPluripotent stem cellsRemyelinationStem cellsWhite matter

Identifiers

PMID27170209
PMCPMC5340082
OpenAlexW2349913782

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.