Evidence map›Paper›PMID 26546966›Full record

ReviewBrain research2016

Oligodendrocyte progenitor programming and reprogramming: Toward myelin regeneration.

Alejandro Lopez Juarez, Danyang He, Q Richard Lu

Open access · greenAbstract readReview
In one paragraph

Review in Brain research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
3.8field-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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.

  1. Pooled it
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  17. The Current Challenges for Drug Discovery in CNS Remyelination.International journal of molecular sciences · 2021
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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

3 authors at 1 institution in 1 country.

Alejandro Lopez JuarezDepartment of Pediatrics, Divisions of Experimental Hematology and Cancer Biology & Developmental Biology, Cincinnati Children׳s Hospital Medical Center, Cincinnati, OH 45229, USA.
Danyang HeDepartment of Pediatrics, Divisions of Experimental Hematology and Cancer Biology & Developmental Biology, Cincinnati Children׳s Hospital Medical Center, Cincinnati, OH 45229, USA.
Q Richard LuDepartment of Pediatrics, Divisions of Experimental Hematology and Cancer Biology & Developmental Biology, Cincinnati Children׳s Hospital Medical Center, Cincinnati, OH 45229, USA. Electronic address: richard.lu@cchmc.org.
Cincinnati Children's Hospital Medical Center · US

Funding

Molecular Mechanisms of Oligodendrocyte Differentiation and MyelinationR01NS072427 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI LU, QING R · 2010 to 2018
$3.6M
Chromatin remodeling control of myelination and remyelinationR01NS075243 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI LU, QING R · 2012 to 2018
$2.6M
A Novel Model of Medulloblastoma to Define Cancer Pathways and Molecular TargetsR01NS078092 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI LU, QING R · 2012 to 2016
$1.7M
NINDS NIH HHS R01 NS072427NINDS NIH HHS R01 NS075243NINDS NIH HHS R01 NS078092
6 · The paper itself

Abstract

Demyelinating diseases such as multiple sclerosis (MS) are among the most disabling and cost-intensive neurological disorders. The loss of myelin in the central nervous system, produced by oligodendrocytes (OLs), impairs saltatory nerve conduction, leading to motor and cognitive deficits. Immunosuppression therapy has a limited efficacy in MS patients, arguing for a paradigm shift to strategies that target OL lineage cells to achieve myelin repair. The inhibitory microenvironment in MS lesions abrogates the expansion and differentiation of resident OL precursor cells (OPCs) into mature myelin-forming OLs. Recent studies indicate that OPCs display a highly plastic ability to differentiate into alternative cell lineages under certain circumstances. Thus, understanding the mechanisms that maintain and control OPC fate and differentiation into mature OLs in a hostile, non-permissive lesion environment may open new opportunities for regenerative therapies. In this review, we will focus on 1) the plasticity of OPCs in terms of their developmental origins, distribution, and differentiation potentials in the normal and injured brain; 2) recent discoveries of extrinsic and intrinsic factors and small molecule compounds that control OPC specification and differentiation; and 3) therapeutic potential for motivation of neural progenitor cells and reprogramming of differentiated cells into OPCs and their likely impacts on remyelination. OL-based therapies through activating regenerative potentials of OPCs or cell replacement offer exciting opportunities for innovative strategies to promote remyelination and neuroprotection in devastating demyelinating diseases like MS. This article is part of a Special Issue entitled SI:NG2-glia(Invited only).

Indexed as

AnimalsCellular ReprogrammingHumansOligodendrogliaRegenerationStem CellsMyelinationOligodendrocytePlasticityProgenitorRemyelination

Identifiers

PMID26546966
PMCPMC5119932
OpenAlexW1901736351

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.