Human oligodendroglial development

Relationship to periventricular leukomalacia

H. C. Kinney, Stephen Back

Research output: Contribution to journalArticle

140 Citations (Scopus)

Abstract

Periventricular leukomalacia in the premature infant is a lesion of cerebral white matter with its greatest period of risk when white matter is immature, that is, when oligodendrocyte precursors are proliferating and differentiating, and before myelin sheaths are actively synthesized. Although the pathogenesis of perinatal cerebral white matter damage involves multiple factors, the correlation of the timing of the lesion with dominance of oligodendrocyte precursors in cerebral white matter suggests that intrinsic factors related to oligodendrocyte precursors are critical. Ischemia and infection have both been implicated as causes of perinatal white matter damage. Major mechanisms underlying oligodendrocyte injury in ischemia include glutamate toxicity, free-radical injury, and cytokine damage mediated by macrophages accompanying ischemia-induced inflammation. Factors related to a vulnerability of immature oligodendrocytes to ischemia potentially include a developmental lack of antioxidant enzymes to mediate oxidative stress. Cytokine-mediated injury to oligodendrocytes is also potentially important. A complete understanding of the role of immature white matter in the pathogenesis of periventricular leukomalacia is essential for developing strategies to prevent it.

Original languageEnglish (US)
Pages (from-to)180-189
Number of pages10
JournalSeminars in Pediatric Neurology
Volume5
Issue number3
DOIs
StatePublished - 1998
Externally publishedYes

Fingerprint

Periventricular Leukomalacia
Oligodendroglia
Human Development
Ischemia
Wounds and Injuries
Cytokines
Intrinsic Factor
Myelin Sheath
Premature Infants
Free Radicals
White Matter
Glutamic Acid
Oxidative Stress
Antioxidants
Macrophages
Inflammation
Enzymes
Infection

ASJC Scopus subject areas

  • Clinical Neurology

Cite this

Human oligodendroglial development : Relationship to periventricular leukomalacia. / Kinney, H. C.; Back, Stephen.

In: Seminars in Pediatric Neurology, Vol. 5, No. 3, 1998, p. 180-189.

Research output: Contribution to journalArticle

@article{36688c415965457e8b269052a9e75d10,
title = "Human oligodendroglial development: Relationship to periventricular leukomalacia",
abstract = "Periventricular leukomalacia in the premature infant is a lesion of cerebral white matter with its greatest period of risk when white matter is immature, that is, when oligodendrocyte precursors are proliferating and differentiating, and before myelin sheaths are actively synthesized. Although the pathogenesis of perinatal cerebral white matter damage involves multiple factors, the correlation of the timing of the lesion with dominance of oligodendrocyte precursors in cerebral white matter suggests that intrinsic factors related to oligodendrocyte precursors are critical. Ischemia and infection have both been implicated as causes of perinatal white matter damage. Major mechanisms underlying oligodendrocyte injury in ischemia include glutamate toxicity, free-radical injury, and cytokine damage mediated by macrophages accompanying ischemia-induced inflammation. Factors related to a vulnerability of immature oligodendrocytes to ischemia potentially include a developmental lack of antioxidant enzymes to mediate oxidative stress. Cytokine-mediated injury to oligodendrocytes is also potentially important. A complete understanding of the role of immature white matter in the pathogenesis of periventricular leukomalacia is essential for developing strategies to prevent it.",
author = "Kinney, {H. C.} and Stephen Back",
year = "1998",
doi = "10.1016/S1071-9091(98)80033-8",
language = "English (US)",
volume = "5",
pages = "180--189",
journal = "Seminars in Pediatric Neurology",
issn = "1071-9091",
publisher = "W.B. Saunders Ltd",
number = "3",

}

TY - JOUR

T1 - Human oligodendroglial development

T2 - Relationship to periventricular leukomalacia

AU - Kinney, H. C.

AU - Back, Stephen

PY - 1998

Y1 - 1998

N2 - Periventricular leukomalacia in the premature infant is a lesion of cerebral white matter with its greatest period of risk when white matter is immature, that is, when oligodendrocyte precursors are proliferating and differentiating, and before myelin sheaths are actively synthesized. Although the pathogenesis of perinatal cerebral white matter damage involves multiple factors, the correlation of the timing of the lesion with dominance of oligodendrocyte precursors in cerebral white matter suggests that intrinsic factors related to oligodendrocyte precursors are critical. Ischemia and infection have both been implicated as causes of perinatal white matter damage. Major mechanisms underlying oligodendrocyte injury in ischemia include glutamate toxicity, free-radical injury, and cytokine damage mediated by macrophages accompanying ischemia-induced inflammation. Factors related to a vulnerability of immature oligodendrocytes to ischemia potentially include a developmental lack of antioxidant enzymes to mediate oxidative stress. Cytokine-mediated injury to oligodendrocytes is also potentially important. A complete understanding of the role of immature white matter in the pathogenesis of periventricular leukomalacia is essential for developing strategies to prevent it.

AB - Periventricular leukomalacia in the premature infant is a lesion of cerebral white matter with its greatest period of risk when white matter is immature, that is, when oligodendrocyte precursors are proliferating and differentiating, and before myelin sheaths are actively synthesized. Although the pathogenesis of perinatal cerebral white matter damage involves multiple factors, the correlation of the timing of the lesion with dominance of oligodendrocyte precursors in cerebral white matter suggests that intrinsic factors related to oligodendrocyte precursors are critical. Ischemia and infection have both been implicated as causes of perinatal white matter damage. Major mechanisms underlying oligodendrocyte injury in ischemia include glutamate toxicity, free-radical injury, and cytokine damage mediated by macrophages accompanying ischemia-induced inflammation. Factors related to a vulnerability of immature oligodendrocytes to ischemia potentially include a developmental lack of antioxidant enzymes to mediate oxidative stress. Cytokine-mediated injury to oligodendrocytes is also potentially important. A complete understanding of the role of immature white matter in the pathogenesis of periventricular leukomalacia is essential for developing strategies to prevent it.

UR - http://www.scopus.com/inward/record.url?scp=0031664916&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031664916&partnerID=8YFLogxK

U2 - 10.1016/S1071-9091(98)80033-8

DO - 10.1016/S1071-9091(98)80033-8

M3 - Article

VL - 5

SP - 180

EP - 189

JO - Seminars in Pediatric Neurology

JF - Seminars in Pediatric Neurology

SN - 1071-9091

IS - 3

ER -