脑淀粉样血管病发病机制的研究进展

The Research Progress of the Pathogenesis of Cerebral Amyloid Angiopathy

脑淀粉样血管病的发病机制在近年来已成为研究热点,其所造成的脑出血,短暂性脑缺血发作,认知功能障碍等表现在临床上十分常见。研究发现,β淀粉样蛋白在脑血管壁上过量沉积,进而引发氧化应激反应,再结合相关生化分子和遗传因素,共同构成了脑淀粉样血管病的发病机制。随着对发病机制的深入研究,其相关疾病的诊断、治疗和预防得到了长足发展,因此定期将国内外关于脑淀粉样血管病的研究进展做出总结,对进行相关疾病诊疗工作的人员来说是很有必要的。本文就近期脑淀粉样血管病发病机制的研究进展进行论述。

The research of the pathogenesis of cerebral amyloid angiopathy has become a hot topic in recent years. The hematencephalon, transient cerebral ischemia, and cognitive disorder et al. caused by cerebral amyloid angiopathy are clinically common. It has been found that amyloid protein-13 could deposit on the cerebral vascular wall excessively, thus results in oxidative stress injury. Combined with the clearing of related biochemical molecule and heredity, the main pathogenic mechanism of cerebral amyloid angiopathy has gradually becoming elucidated. The diagnosis, therapy and prevention have achieved great progress with further research of the pathogenesis recently. Therefore it is necessary for scientists to summarize the domestic and overseas research progress of the pathogenesis regarding cerebral amyloid angiopathy regularly. In this article, we will summarize the recent research progress of the pathogenesis regarding cerebral amyloid angiopathy.