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Hippocampal network dysfunction as a mechanism of early-onset dementia after preeclampsia and eclampsia
Progress in Neurobiology ( IF 6.7 ) Pub Date : 2020-10-29 , DOI: 10.1016/j.pneurobio.2020.101938
Abbie C Johnson 1 , Zhaojin Li 1 , James E Orfila 2 , Paco S Herson 3 , Marilyn J Cipolla 4
Affiliation  

Preeclampsia is a hypertensive disorder of pregnancy that can involve dangerous neurological symptoms such as spontaneous seizures (eclampsia). Despite being diseases specific to the pregnant state, preeclampsia and eclampsia have long-lasting neurological consequences later in life, including changes in brain structure and cognitive decline at relatively young ages. However, the effects of preeclampsia on brain regions central to memory and cognition, such as the hippocampus, are unclear. Here, we present a case reporting the progressive and permanent cognitive decline in a woman that had eclamptic seizures in the absence of evidence of brain injury on MRI. We then use rat models of normal pregnancy and preeclampsia to investigate mechanisms by which eclampsia-like seizures may disrupt hippocampal function. We show that experimental preeclampsia causes delayed memory decline in rats and disruption of hippocampal neuroplasticity. Further, seizures in pregnancy and preeclampsia caused acute memory dysfunction and impaired neuroplasticity but did not cause acute neuronal cell death. Importantly, hippocampal dysfunction persisted 5 weeks postpartum, suggesting seizure-induced injury is long lasting and may be permanent. Our data provide the first evidence of a model of preeclampsia that may mimic the cognitive decline of formerly preeclamptic women, and that preeclampsia and eclampsia affect hippocampal network plasticity and impair memory.



中文翻译:

海马网络功能障碍作为先兆子痫和子痫后早发性痴呆的机制

先兆子痫是一种妊娠期高血压疾病,可能涉及危险的神经系统症状,例如自发性癫痫发作(子痫)。尽管是妊娠期特有的疾病,但先兆子痫和子痫在以后的生活中会产生长期的神经系统后果,包括大脑结构的变化和相对年轻时的认知能力下降。然而,先兆子痫对记忆和认知中心的大脑区域(例如海马体)的影响尚不清楚。在这里,我们介绍了一个案例,该案例报告了一名患有子痫发作的女性在 MRI 上没有脑损伤证据的情况下出现进行性和永久性认知能力下降。然后,我们使用正常妊娠和先兆子痫的大鼠模型来研究子痫样癫痫发作可能破坏海马功能的机制。我们表明,实验性先兆子痫会导致大鼠记忆力下降延迟和海马神经可塑性破坏。此外,妊娠期癫痫发作和先兆子痫会导致急性记忆功能障碍和神经可塑性受损,但不会导致急性神经元细胞死亡。重要的是,海马功能障碍在产后 5 周持续存在,这表明癫痫引起的损伤是持久的并且可能是永久性的。我们的数据提供了先兆子痫模型的第一个证据,该模型可能模仿以前患有先兆子痫的女性的认知能力下降,并且先兆子痫和子痫会影响海马网络的可塑性并损害记忆力。妊娠期癫痫发作和先兆子痫会导致急性记忆功能障碍和神经可塑性受损,但不会导致急性神经元细胞死亡。重要的是,海马功能障碍在产后 5 周持续存在,这表明癫痫引起的损伤是持久的并且可能是永久性的。我们的数据提供了先兆子痫模型的第一个证据,该模型可能模仿以前患有先兆子痫的女性的认知能力下降,并且先兆子痫和子痫会影响海马网络的可塑性并损害记忆力。妊娠期癫痫发作和先兆子痫会导致急性记忆功能障碍和神经可塑性受损,但不会导致急性神经元细胞死亡。重要的是,海马功能障碍在产后 5 周持续存在,这表明癫痫引起的损伤是持久的并且可能是永久性的。我们的数据提供了先兆子痫模型的第一个证据,该模型可能模仿以前患有先兆子痫的女性的认知能力下降,并且先兆子痫和子痫会影响海马网络的可塑性并损害记忆力。

更新日期:2020-10-29
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