Evidence map›Paper›PMID 26302698›Full record

ReviewPediatric neurology2015

Brain Injury in the Preterm Infant: New Horizons for Pathogenesis and Prevention.

Stephen A Back

Open access · greenAbstract readReview
In one paragraph

Review in Pediatric neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 2 pooled it
20.1field-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

60 citing papers in PubMed, 2 syntheses or guidelines pooled it, 107 citations in OpenAlex.

  1. Pooled it
  2. MRI-based brain volumes of preterm infants at term: a systematic review and meta-analysis.Archives of disease in childhood. Fetal and neonatal edition · 2022
    Pooled it
  3. Article
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  6. Review
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  8. [Effects of α1-antitrypsin on motor function in mice with immature brain white matter injury].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2024
    Article
  9. Review
  10. Article
  11. Article
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  14. 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

1 author at 1 institution in 1 country.

Stephen A BackDepartment of Pediatrics, Oregon Health & Science University, Portland, Oregon; Department of Neurology, Oregon Health & Science University, Portland, Oregon. Electronic address: backs@ohsu.edu.
Oregon Health & Science University · US

Funding

White Matter Damage in Age-Related Cognitive DeclineR01AG031892 · NIA · UNIVERSITY OF WASHINGTON · PI MONTINE, THOMAS J · 2009 to 2016
$6.1M
Role of Extracellular Matrix in Hypoxic-Ischemic Perinatal White Matter InjuryR01NS054044 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI BACK, STEPHEN ARTHUR · 2006 to 2021
$4.8M
Cellular Mechanisms of Fetal White Matter InjuryR01NS045737 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI BACK, STEPHEN ARTHUR · 2003 to 2019
$3.7M
Cellular mechanisms of fetal white matter injuryR37NS045737 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI BACK, STEPHEN ARTHUR · 2007 to 2013
$2.7M
AGING AND THE MUCOSAL IMMUNE RESPONSER01AG003189 · NIA · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI KAGNOFF, MARTIN FREDERICK · 1985 to 1985
–
NIA NIH HHS 1R01AG03189NIA NIH HHS R01 AG031892NINDS NIH HHS 1R01NS054044NINDS NIH HHS R01 NS045737NINDS NIH HHS R01 NS054044NINDS NIH HHS R37 NS045737NINDS NIH HHS R37NS045737-06S1/06S2
6 · The paper itself

Abstract

Preterm neonates are surviving with a milder spectrum of motor and cognitive disabilities that appear to be related to widespread disturbances in cell maturation that target cerebral gray and white matter. Whereas the preterm brain was previously at high risk for destructive lesions, preterm survivors now commonly display less severe injury that is associated with aberrant regeneration and repair responses that result in reduced cerebral growth. Impaired cerebral white matter growth is related to myelination disturbances that are initiated by acute death of premyelinating oligodendrocytes, but are followed by rapid regeneration of premyelinating oligodendrocytes that fail to normally mature to myelinating cells. Although immature neurons are more resistant to cell death than mature neurons, they display widespread disturbances in maturation of their dendritic arbors and synapses, which further contributes to impaired cerebral growth. Thus, even more mild cerebral injury involves disrupted repair mechanisms in which neurons and premyelinating oligodendrocytes fail to fully mature during a critical window in development of neural circuitry. These recently recognized distinct forms of cerebral gray and white matter dysmaturation raise new diagnostic challenges and suggest new therapeutic strategies to promote brain growth and repair.

Indexed as

Infant, PrematureAnimalsBrainBrain DiseasesBrain InjuriesHumansInfant, Newbornastrocytegliagray matterhypoxia-ischemiamyelinationoligodendrocyteprematuritywhite matter

Identifiers

PMID26302698
PMCPMC4550810
OpenAlexW2034154061

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.