摘要:

AbstractThere is clinical and experimental evidence that the response to hypoxic and hypoxic‐ischemic brain injury is age dependent. The effects of perinatal hypoxia, especially its epileptogenic effects, are different in the neonatal brain compared with that of the adult. Experimental models show increased susceptibility of the immature brain to the epileptogenic and toxic effects of hypoxia and hypoxia‐ischemia. This article reviews several maturational factors that are likely to contribute to the enhanced vulnerability of the immature brain. Some of the factors known to be involved in the pathophysiology of hypoxic‐ischemic encephalopathy are also known to be critical for normal brain development. These issues are discussed in the context of defining age‐specific therapies to prevent hypoxic‐ischemic neuronal injury in the immature brain. MRDD Research Reviews 3:85–95, 1997. © 1997 Wil

ISSN:1080-4013    

DOI:10.1002/(SICI)1098-2779(1997)3:1<85::AID-MRDD11>3.0.CO;2-N

出版商:John Wiley&Sons, Inc.    

年代:1997

数据来源: WILEY

摘要:

AbstractPeriventricular white matter injury has a high incidence, particularly in the premature infant. A prominent feature of the pathogenesis of this injury, which ultimately results in disrupted myelination of periventricular white matter tracts, is a loss of oligodendrocytes (OLs). The timing of injury corresponds to the period in white matter development when OL precursors predominate. This article focuses on current understanding of the cellular and molecular basis for the developmental vulnerability of OL precursors that may predispose to their loss in periventricular leukomalacia (PVL). Recent advances in the cellular neurobiology of OL development have permitted study of the processes that regulate survival of developing OLs. Several potentially complementary etiologies for the developmental vulnerability of OL precursors are reviewed: (1) free‐radical–mediated toxicity in the setting of oxidative stress, (2) cytotoxic cytokines, and (3) a critical dependence on selected trophic factors during certain periods in OL development. Recent work indicates that these causes of cell death are mediated by a common mechanism involving apoptosis. Potential therapeutic interventions for interruption of the pathways mediating OL death are examined. MRDD Research Reviews 3:96–107, 1997. © 1997 Wiley‐L

ISSN:1080-4013    

DOI:10.1002/(SICI)1098-2779(1997)3:1<96::AID-MRDD12>3.0.CO;2-M

出版商:John Wiley&Sons, Inc.    

年代:1997

数据来源: WILEY