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Molecular targets in cerebral malaria for developing novel therapeutic strategies.
Brain Research Bulletin ( IF 3.5 ) Pub Date : 2020-01-30 , DOI: 10.1016/j.brainresbull.2020.01.020
Ravisankar Vanka 1 , Venkata Prasuja Nakka 2 , Simhadri Praveen Kumar 3 , Uday Krishna Baruah 4 , Phanithi Prakash Babu 5
Affiliation  

Cerebral malaria (CM) is the severe neurological complication associated with Plasmodium falciparum infection. In clinical settings CM is predominantly characterized by fever, epileptic seizures, and asexual forms of parasite on blood smears, coma and even death. Cognitive impairment in the children and adults even after survival is one of the striking consequences of CM. Poor diagnosis often leads to inappropriate malaria therapy which in turn progress into a severe form of disease. Activation of multiple cell death pathways such as Inflammation, oxidative stress, apoptosis and disruption of blood brain barrier (BBB) plays critical role in the pathogenesis of CM and secondary brain damage. Thus, understanding such mechanisms of neuronal cell death might help to identify potential molecular targets for CM. Mitigation strategies for mortality rate and long-term cognitive deficits caused by existing anti-malarial drugs still remains a valid research question to ask. In this review, we discuss in detail about critical neuronal cell death mechanisms and the overall significance of adjunctive therapy with recent trends, which provides better insight towards establishing newer therapeutic strategies for CM.

中文翻译:

用于开发新型治疗策略的脑型疟疾的分子靶点。

脑型疟疾 (CM) 是与恶性疟原虫感染相关的严重神经系统并发症。在临床环境中,CM 的主要特征是发烧、癫痫发作和血涂片上的无性寄生虫、昏迷甚至死亡。儿童和成人即使在存活后的认知障碍也是 CM 的显着后果之一。诊断不当通常会导致不适当的疟疾治疗,进而发展为严重的疾病。炎症、氧化应激、细胞凋亡和血脑屏障 (BBB) 破坏等多种细胞死亡途径的激活在 CM 和继发性脑损伤的发病机制中起着关键作用。因此,了解神经元细胞死亡的这种机制可能有助于确定 CM 的潜在分子靶点。现有抗疟疾药物引起的死亡率和长期认知缺陷的缓解策略仍然是一个有效的研究问题。在这篇综述中,我们详细讨论了关键的神经元细胞死亡机制和辅助治疗的整体意义以及最近的趋势,这为建立新的 CM 治疗策略提供了更好的见解。
更新日期:2020-01-31
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