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基质金属蛋白酶与痴呆症中血脑屏障的破坏

Matrix Metalloproteinase in Blood-Brain Barrier Breakdown in Dementia.

作者信息

Weekman Erica M, Wilcock Donna M

出版信息

J Alzheimers Dis. 2016;49(4):893-903. doi: 10.3233/JAD-150759.

DOI:10.3233/JAD-150759
PMID:26599057
Abstract

The neurovascular unit, which consists of astrocytic end-feet, neurons, pericytes, and endothelial cells, plays a key role in maintaining brain homeostasis by forming the blood-brain barrier and carefully controlling local cerebral blood flow. When the blood-brain barrier is disrupted, blood components can leak into the brain, damage the surrounding tissue and lead to cognitive impairment. This disruption in the blood-brain barrier and subsequent impairment in cognition are common after stroke and during cerebral amyloid angiopathy and Alzheimer's disease. Matrix metalloproteinases are proteases that degrade the extracellular matrix as well as tight junctions between endothelial cells and have been implicated in blood-brain barrier breakdown in neurodegenerative diseases. This review will focus on the roles of MMP2 and MMP9 in dementia, primarily post-stroke events that lead to dementia, cerebral amyloid angiopathy, and Alzheimer's disease.

摘要

神经血管单元由星形胶质细胞终足、神经元、周细胞和内皮细胞组成,通过形成血脑屏障并精确控制局部脑血流,在维持脑内环境稳定方面发挥关键作用。当血脑屏障被破坏时,血液成分会渗入大脑,损伤周围组织并导致认知障碍。血脑屏障的这种破坏以及随后的认知障碍在中风后、脑淀粉样血管病和阿尔茨海默病期间很常见。基质金属蛋白酶是降解细胞外基质以及内皮细胞之间紧密连接的蛋白酶,与神经退行性疾病中的血脑屏障破坏有关。本综述将重点关注MMP2和MMP9在痴呆中的作用,主要是导致痴呆的中风后事件、脑淀粉样血管病和阿尔茨海默病。

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