Developmental neuropathology in bronchopulmonary dysplasia: alteration of glial fibrillary acidic protein and myelination.
Developmental changes of glial fibrillary acidic protein (GFAP) and myelination were examined in the brains of 25 children with bronchopulmonary dysplasia (BPD). Widespread GFAP-positive, bouquet-shaped glia occurred in the cerebral white matter and medulla oblongata of most cases and increased during the perinatal period, independent of the presence of luekomalacia. Acceleration of myelination was suggested in five of 10 cases during the period of 40 to 48 weeks postconceptional age, just before myelin sheaths normally appear. However, in two of four cases seen during late infancy myelination was delayed. The increase of GFAP-positive glia may be related to the induction of myelination. On the other hand, increased astroglial processes may occur secondary to chronic hypoxia and may interfere with myelination, accounting for the poor myelination seen in late infancy.
D001997:Bronchopulmonary Dysplasia / Q000473:pathology*; D002543:Cerebral Hemorrhage / Q000473:pathology*; D002657:Child Development; D004678:Encephalomalacia / Q000473:pathology*; D005625:Frontal Lobe / Q000473:pathology; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism*; D006801:Humans; D007124:Immunoenzyme Techniques; D007223:Infant; D007231:Infant, Newborn; D008526:Medulla Oblongata / Q000473:pathology; D009186:Myelin Sheath / Q000648:ultrastructure*; D009457:Neuroglia / Q000648:ultrastructure
D005904:Glial Fibrillary Acidic Protein