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Article type: Research Article
Authors: Weekman, Erica M. | Wilcock, Donna M.*
Affiliations: University of Kentucky, Sanders-Brown Center on Aging, Department of Physiology, Lexington KY, USA
Correspondence: [*] Correspondence to: *Donna M. Wilcock, PhD, University of Kentucky, Room 424 Sanders-Brown Center on Aging, 800S Limestone St., Lexington, KY 40536, USA. Tel.: +1 859 218 2390; Fax: +1 859 323 2866; E-mail: donna.wilcock@uky.edu
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.
Keywords: Alzheimer’s disease,, cerebral amyloid angiopathy, hemorrhagic transformation, matrix metalloproteinases, stroke, vascular cognitive impairment
DOI: 10.3233/JAD-150759
Journal: Journal of Alzheimer's Disease, vol. 49, no. 4, pp. 893-903, 2016
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