TY - JOUR
T1 - Human oligodendroglial development
T2 - Relationship to periventricular leukomalacia
AU - Kinney, H. C.
AU - Back, S. A.
N1 - Funding Information:
From the Departments of Neurology and Pathology, Children's Hospital and Harvard Medical School Boston, MA. Supported in part by the National Institutes of Health (NS01855 to S.A.B.) and Children's Hospital Mental Retardation Core Grant (P30-HD18655). Stephen A. Back was funded by Grass Foundation Morison Fellowship, Reynolds Rich Smith Fellowship, Charles A. Janeway Child Health Research Center Award Fellowship, and Hearst Foundation Award. Address reprint requests to Hannah C. Kinney, MD, Department of Pathology, Children's Hospital Boston, MA 02115. Copyright 9 1998 by W.B. Saunders Company 1071-9091/98/0503-000458.00/0
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.
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U2 - 10.1016/S1071-9091(98)80033-8
DO - 10.1016/S1071-9091(98)80033-8
M3 - Article
C2 - 9777676
AN - SCOPUS:0031664916
SN - 1071-9091
VL - 5
SP - 180
EP - 189
JO - Seminars in pediatric neurology
JF - Seminars in pediatric neurology
IS - 3
ER -