Evidence map›Paper›PMID 26116759›Full record

ReviewNeuropharmacology2016

Pharmacological approaches to intervention in hypomyelinating and demyelinating white matter pathology.

Li-Jin Chew, Cynthia A DeBoy

Open access · greenAbstract readReview
In one paragraph

Review in Neuropharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

15 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. White Matter and Neuroprotection in Alzheimer's Dementia.Molecules (Basel, Switzerland) · 2020
    Review
  7. Executive Dysfunction Early Postnatal Biomarkers among Children Born Extremely Preterm.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2019
    Article
  8. Review
  9. Circulating biomarkers in extremely preterm infants associated with ultrasound indicators of brain damage.European journal of paediatric neurology : EJPN : official journal of the European Paediatric Neurology Society · 2018
    Observational
  10. Article
  11. Observational
  12. Observational
  13. Article
  14. Review
  15. 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 1 country.

Li-Jin ChewCenter for Neuroscience Research, Children's Research Institute, Children's National Medical Center, Washington, DC, USA. Electronic address: LChew@childrensnational.org.
Cynthia A DeBoyBiology Department, Trinity Washington University, Washington, DC, USA.
Children's National · USTrinity Washington University · US

Funding

Characterization of Sox17 as a Regulator of Oligodendrocyte Cell DifferentiationR01NS056427 · NINDS · CHILDREN'S RESEARCH INSTITUTE · PI VITTORIO GALLO, VITTORIO GALLO VITTORIO GALLO · 2007 to 2011
$1.8M
Long term consequences of white matter damage by perinatal hyperoxia.R21NS078731 · NINDS · CHILDREN'S RESEARCH INSTITUTE · PI VITTORIO GALLO, VITTORIO GALLO VITTORIO GALLO · 2012 to 2013
$460k
NINDS NIH HHS R01 NS056427NINDS NIH HHS R21 NS078731
6 · The paper itself

Abstract

White matter disease afflicts both developing and mature central nervous systems. Both cell intrinsic and extrinsic dysregulation result in profound changes in cell survival, axonal metabolism and functional performance. Experimental models of developmental white matter (WM) injury and demyelination have not only delineated mechanisms of signaling and inflammation, but have also paved the way for the discovery of pharmacological approaches to intervention. These reagents have been shown to enhance protection of the mature oligodendrocyte cell, accelerate progenitor cell recruitment and/or differentiation, or attenuate pathological stimuli arising from the inflammatory response to injury. Here we highlight reports of studies in the CNS in which compounds, namely peptides, hormones, and small molecule agonists/antagonists, have been used in experimental animal models of demyelination and neonatal brain injury that affect aspects of excitotoxicity, oligodendrocyte development and survival, and progenitor cell function, and which have been demonstrated to attenuate damage and improve WM protection in experimental models of injury. The molecular targets of these agents include growth factor and neurotransmitter receptors, morphogens and their signaling components, nuclear receptors, as well as the processes of iron transport and actin binding. By surveying the current evidence in non-immune targets of both the immature and mature WM, we aim to better understand pharmacological approaches modulating endogenous oligodendroglia that show potential for success in the contexts of developmental and adult WM pathology. This article is part of the Special Issue entitled 'Oligodendrocytes in Health and Disease'.

Indexed as

Brain InjuriesAnimalsAnti-Inflammatory AgentsCell DifferentiationDemyelinating DiseasesDisease Models, AnimalHumansNerve RegenerationWhite MatterAnti-Inflammatory AgentsAdultBrain injuryDevelopmentNeonatalOligodendrocytesPharmaceuticalRegenerationRemyelinationRepair

Identifiers

PMID26116759
PMCPMC4690794
OpenAlexW750923683

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.