Department of Pathophysiology, College of Basic Medical Sciences, Dalian Medical University, Dalian 116044, China.
Center for Energy Metabolism and Reproduction, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518055, China.
Int J Mol Sci. 2024 Oct 15;25(20):11062. doi: 10.3390/ijms252011062.
Preeclampsia, a hypertensive disorder during pregnancy, frequently correlates with adverse neurological outcomes in offspring, including cognitive impairments, autism spectrum disorder, depressive disorder, attention deficit hyperactivity disorder, and cerebral palsy. Despite these known consequences, the understanding of neuronal damage in the offspring of preeclamptic mothers remains insufficient. Here, we review the neuronal abnormalities resulting from maternal preeclampsia exposure, which include disrupted neurogenesis, loss of neuronal cell integrity, accumulation of cellular debris, decreased synaptogenesis and myelination, and increased neurite growth stimulated by maternal preeclampsia serum. The underlying mechanisms potentially driving these effects involve microglial activation, inflammatory responses, and reduced angiogenesis. Intervention strategies aimed at improving fetal neuronal outcomes are also discussed, encompassing pharmacological treatments such as pravastatin, tadalafil, and melatonin, as well as non-pharmacological approaches like dietary modifications, maternal exercise, and standard care for children. These interventions hold promise for clinical application, offering avenues to address early neuronal abnormalities and prevent the onset of long-term neurological disorders.
子痫前期是一种妊娠高血压疾病，常与后代的不良神经结局相关，包括认知障碍、自闭症谱系障碍、抑郁障碍、注意缺陷多动障碍和脑瘫。尽管有这些已知的后果，但对子痫前期母亲后代神经元损伤的理解仍然不足。在这里，我们综述了母体子痫前期暴露导致的神经元异常，包括神经发生障碍、神经元细胞完整性丧失、细胞碎片堆积、突触生成和髓鞘形成减少，以及母体子痫前期血清刺激的神经突生长增加。潜在的机制可能涉及小胶质细胞激活、炎症反应和血管生成减少。还讨论了旨在改善胎儿神经元结局的干预策略，包括药物治疗，如普伐他汀、他达拉非和褪黑素，以及非药物治疗，如饮食改变、母体运动和儿童标准护理。这些干预措施具有临床应用的潜力，为解决早期神经元异常和预防长期神经障碍的发生提供了途径。
