Blood-brain barrier dysfunction, TGFβ signaling, and astrocyte dysfunction in epilepsy.

Blood-brain barrier dysfunction, TGFβ signaling, and astrocyte dysfunction in epilepsy.
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DOI:
10.1002/glia.22311
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发表时间:
2012-08
期刊:
影响因子:
6.2
通讯作者:
Friedman, Alon
Friedman, Alon
中科院分区:
医学1区
文献类型:
--
作者:
Heinemann, Uwe;Kaufer, Daniela;Friedman, Alon

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脑损伤,包括外伤性和缺血性损伤,常常伴随着急性发作和癫痫的延迟发展。血脑屏障(BBB)功能障碍是脑损伤的标志,通常围绕核心病变。最近几个实验室的研究证实,血管病理参与癫痫的发展,并证明星形胶质细胞在这一过程中起关键作用。在这篇综述中,我们将重点关注与血管病理,特别是血脑屏障功能障碍有关的神经胶质相关机制与癫痫发作和癫痫的关系。我们总结了分子和生理实验数据,证明星形胶质细胞的功能由于直接暴露于血清白蛋白而改变,由转化生长因子β信号介导。我们讨论了报道的变化及其在观察到的高兴奋性中的潜在作用,以及这些发现对未来发展新的诊断方式和治疗的潜在影响,以便为癫痫患者的利益充分实施所获得的知识。
Brain insults, including traumatic and ischemic injuries, are frequently followed by acute seizures and delayed development of epilepsy. Dysfunction of the blood-brain barrier (BBB) is a hallmark of brain insults and is usually surrounding the core lesion. Recent studies from several laboratories confirmed that vascular pathology is involved in the development of epilepsy and demonstrate a key role for astroglia in this process. In this review, we focus on glia-related mechanisms linking vascular pathology, and specifically BBB dysfunction, to seizures and epilepsy. We summarize molecular and physiological experimental data demonstrating that the function of astrocytes is altered due to direct exposure to serum albumin, mediated by transforming growth factor beta signaling. We discuss the reported changes and their potential role in the observed hyperexcitability as well as potential implications of these findings for the future development of new diagnostic modalities and treatments to allow a full implementation of the gained knowledge for the benefit of patients with epilepsy.
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