NeuroRepair Department, Mossakowski Medical Research Centre, Polish Academy of Sciences, 5 Pawinskiego str., 02-106, Warsaw, Poland.
Mol Neurobiol. 2018 May;55(5):4388-4402. doi: 10.1007/s12035-017-0647-7. Epub 2017 Jun 28.
Perinatal asphyxia results from the action of different risk factors like complications during pregnancy, preterm delivery, or long and difficult labor. Nowadays, it is still the leading cause of neonatal brain injury known as hypoxic-ischemic encephalopathy (HIE) and resulting neurological disorders. A temporal limitation of oxygen, glucose, and trophic factors supply results in alteration of neural cell differentiation and functioning and/or leads to their death. Among the affected cells are oligodendrocytes, responsible for myelinating the central nervous system (CNS) and formation of white matter. Therefore, one of the major consequences of the experienced HIE is leukodystrophic diseases resulting from oligodendrocyte deficiency or malfunctioning. The therapeutic strategies applied after perinatal asphyxia are aimed at reducing brain damage and promoting the endogenous neuroreparative mechanisms. In this review, we focus on the biology of oligodendrocytes and discuss present clinical treatments in the context of their efficiency in preserving white matter structure and preventing cognitive and behavioral deficits after perinatal asphyxia.
围产期窒息是由多种风险因素引起的,如妊娠并发症、早产或产程延长和困难。如今,它仍然是新生儿脑损伤的主要原因,即缺氧缺血性脑病(HIE)和由此导致的神经功能障碍。氧、葡萄糖和营养因子供应的时间限制会导致神经细胞分化和功能的改变,或者导致它们的死亡。受影响的细胞包括少突胶质细胞,其负责中枢神经系统(CNS)的髓鞘形成和白质的形成。因此,经历 HIE 的主要后果之一是少突胶质细胞缺乏或功能障碍导致的白质营养不良疾病。围产期窒息后应用的治疗策略旨在减少脑损伤并促进内源性神经修复机制。在这篇综述中,我们重点介绍少突胶质细胞的生物学,并讨论目前的临床治疗方法在保护白质结构和预防围产期窒息后认知和行为缺陷方面的效果。