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Matrix Metalloproteinase-Mediated Disruption of Tight Junction Proteins in Cerebral Vessels is Reversed by Synthetic Matrix Metalloproteinase Inhibitor in Focal Ischemia in Rat
The results provide direct evidence that MMPs open the BBB by degrading TJPs and that an MMP inhibitor prevents degradation of the TJPs by M MPs. Expand
Matrix metalloproteinases in neuroinflammation
Understanding their expression in various CNS insults will allow for the use of MMP inhibitors in the treatment of neurological disorders, and hydroxymate‐based compounds have been shown to reduce injury in experimental allergic encephalomyelitis, experimental allergic neuritis, cerebral ischemia, intracerebral hemorrhage, and viral and bacterial infections. Expand
National Institute of Neurological Disorders and Stroke–Canadian Stroke Network Vascular Cognitive Impairment Harmonization Standards
Using the same standards will help identify individuals in the early stages of cognitive impairment, will make studies comparable, and by integrating knowledge, will accelerate the pace of progress. Expand
Matrix metalloproteinases and their multiple roles in neurodegenerative diseases
  • G. Rosenberg
  • Biology, Medicine
  • The Lancet Neurology
  • 1 February 2009
By examining the effects of neuroinflammation, this Review tries to understand the role that MMPs might have in neurodegenerative diseases and Therapeutic strategies that use inhibitors of M MPs could represent potential novel treatments for neurological diseases. Expand
Diverse roles of matrix metalloproteinases and tissue inhibitors of metalloproteinases in neuroinflammation and cerebral ischemia
Regulation of the extracellular matrix by proteases and protease inhibitors is a fundamental biological process for normal growth, development and repair in the CNS. Matrix metalloproteinases (MMPs)Expand
Matrix metalloproteinases and TIMPs are associated with blood-brain barrier opening after reperfusion in rat brain.
Brain sucrose uptake increased after 3 and 48 hours of reperfusion, with maximal opening at 48 hours and return to normal by 14 days, suggesting different mechanisms of injury for the biphasic BBB injury. Expand
Collagenase-induced intracerebral hemorrhage in rats.
Collagenase-induced intracerebral hemorrhage is a reproducible animal model for the study of the effects of the hematoma and brain edema in rats and characterized the lesion by histology, brain water content, and behavior. Expand
Blood-brain barrier breakdown in acute and chronic cerebrovascular disease.
This review will describe the molecular and cellular events associated with BBB disruption and potential therapies directed toward restoring the integrity of the neurovascular unit. Expand
Proteolytic Cascade Enzymes Increase in Focal Cerebral Ischemia in Rat
The time of appearance of gelatinase B suggests a role in secondary tissue damage and vasogenic edema, while gelatinase A may be involved in tissue repair. Expand
Cortical spreading depression activates and upregulates MMP-9.
It is found that CSD alters blood-brain barrier (BBB) permeability by activating brain MMPs via an MMP-9-dependent mechanism, and intense neuronal and glial depolarization initiates a cascade that disrupts the BBB. Expand