Evidence map›Paper›PMID 27001544›Full record

ReviewExperimental neurology2016

Targeting human oligodendrocyte progenitors for myelin repair.

Karen C Dietz, Jessie J Polanco, Suyog U Pol, Fraser J Sim

Abstract 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 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.5field-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

36 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. IncreasingBiological psychiatry global open science · 2025
    Article
  6. Wrap it up: myelination of transplanted neurons for repair.Frontiers in cellular neuroscience · 2025
    Review
  7. Article
  8. Article
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  13. Review
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  15. Review
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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

4 authors at 1 institution in 1 country.

Karen C DietzProgram in Neuroscience, Department of Pharmacology and Toxicology, School of Medicine and Biomedical Sciences, State University of New York at Buffalo, 3435 Main Street, 119 Farber Hall, Buffalo, NY 14214, United States. Electronic address: kdietz@buffalo.edu.
Jessie J PolancoProgram in Neuroscience, Department of Pharmacology and Toxicology, School of Medicine and Biomedical Sciences, State University of New York at Buffalo, 3435 Main Street, 119 Farber Hall, Buffalo, NY 14214, United States. Electronic address: jessiepo@buffalo.edu.
Suyog U PolProgram in Neuroscience, Department of Pharmacology and Toxicology, School of Medicine and Biomedical Sciences, State University of New York at Buffalo, 3435 Main Street, 119 Farber Hall, Buffalo, NY 14214, United States. Electronic address: suyogpol@buffalo.edu.
Fraser J SimProgram in Neuroscience, Department of Pharmacology and Toxicology, School of Medicine and Biomedical Sciences, State University of New York at Buffalo, 3435 Main Street, 119 Farber Hall, Buffalo, NY 14214, United States. Electronic address: fjsim@buffalo.edu.
University at Buffalo, State University of New York · US

Funding

Enabling Access to Cutting-Edge Biomedical and Behavioral ScienceR25GM095459 · NIGMS · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI DUBOCOVICH, MARGARITA L · 2012 to 2021
$4.4M
NIGMS NIH HHS R25 GM095459
6 · The paper itself

Abstract

Oligodendrocyte development has been studied for several decades, and has served as a model system for both neurodevelopmental and stem/progenitor cell biology. Until recently, the vast majority of studies have been conducted in lower species, especially those focused on rodent development and remyelination. In humans, the process of myelination requires the generation of vastly more myelinating glia, occurring over a period of years rather than weeks. Furthermore, as evidenced by the presence of chronic demyelination in a variety of human neurologic diseases, it appears likely that the mechanisms that regulate development and become dysfunctional in disease may be, in key ways, divergent across species. Improvements in isolation techniques, applied to primary human neural and oligodendrocyte progenitors from both fetal and adult brain, as well as advancements in the derivation of defined progenitors from human pluripotent stem cells, have begun to reveal the extent of both species-conserved signaling pathways and potential key differences at cellular and molecular levels. In this article, we will review the commonalities and differences in myelin development between rodents and man, describing the approaches used to study human oligodendrocyte differentiation and myelination, as well as heterogeneity within targetable progenitor pools, and discuss the advances made in determining which conserved pathways may be both modeled in rodents and translate into viable therapeutic strategies to promote myelin repair.

Indexed as

AnimalsCell DifferentiationCell TransplantationDemyelinating DiseasesHumansOligodendrogliaRegenerationStem CellsHuman cell implantationOligodendrocyte progenitorRemyelination

Identifiers

PMID27001544
PMCPMC5666574
OpenAlexW2298588974

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.