Matrix Metalloproteinase in Blood-Brain Barrier Breakdown in Dementia

被引:82
|
作者
Weekman, Erica M. [1 ]
Wilcock, Donna M. [1 ]
机构
[1] Univ Kentucky, Sanders Brown Ctr Aging, Dept Physiol, Lexington, KY 40536 USA
关键词
Alzheimer's disease; cerebral amyloid angiopathy; hemorrhagic transformation; matrix metalloproteinases; stroke; vascular cognitive impairment; TISSUE-PLASMINOGEN ACTIVATOR; CEREBRAL-AMYLOID-ANGIOPATHY; SMOOTH-MUSCLE-CELLS; BASE-LINE FREQUENCY; NERVE GROWTH-FACTOR; HEMORRHAGIC TRANSFORMATION; ISCHEMIC-STROKE; COGNITIVE IMPAIRMENT; EDEMA FORMATION; GENE-EXPRESSION;
D O I
10.3233/JAD-150759
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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.
引用
收藏
页码:893 / 903
页数:11
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