Blood-Brain Barrier Breakdown in Acute and Chronic Cerebrovascular Disease
By Yi Yang, Gary A. Rosenberg. Stroke, 2011
723 citations recorded by the source corpus.
Disruption of the blood-brain barrier (BBB) and edema formation play a key role in the development of neurological dysfunction in acute and chronic cerebral ischemia. Animal studies have revealed the molecular cascades that are initiated with hypoxia/ischemia in the cells forming the neurovascular unit (NVU) and that contribute to cell death. Matrix metalloproteinases (MMPs) cause reversible degradation of tight junction proteins (TJPs) early after the onset of ischemia and a delayed secondary opening during a neuroinflammatory response occurring from 24 to 72 hrs. Cyclooxgyenases (COX) are important in the delayed opening as the neuroinflammatory response progresses. An early opening of the BBB within the three-hour therapeutic window for tissue plasminogen activator (tPA) can allow it to enter the brain and increase the risk of hemorrhage. Chronic hypoxic hypoperfusion opens the BBB, which contributes to the cognitive changes seen with lacunar strokes and white matter injury in subcortical ischemic vascular disease (SIVD). This review will describe the molecular and cellular events associated with BBB disruption and potential therapies directed toward restoring the integrity of the NVU.
Subfields: Epidemiology, Neurology
View Paper: https://www.semanticscholar.org/paper/04f92acce05fce75b7bdf3c1b3360e1c51658ef9
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Citations in the corpus
- Functional morphology of the blood-brain barrier in health and disease (2018, positive): “Biphasic opening in relation to ischaemia–reperfusion injury has been frequently described [142], while there are also (MRI) reports of continuous BBB leakage from acute to subacute or chronic stages after (transient) cerebral ischaemia in rodents and human patients (for review see [80]).”
- Immune responses to stroke: mechanisms, modulation, and therapeutic potential. (2020, background): “The second opening occurs 24 to 48 hours later and is characterized by proteolytic degradation of tight junctions and basement membranes, and loss of vascular cells, including endothelial cells, pericytes, and astrocytic end-feet (94).”
- Nanoparticle-mediated brain drug delivery: Overcoming blood-brain barrier to treat neurodegenerative diseases. (2016, background): “namely type IV collagen, further increasing BBB permeability [84].”
- The pathobiology of vascular dementia (2013, positive): “Reflecting another aspect of endothelial dysfunction, alterations in BBB permeability are also associated with leukoaraiosis and lacunar stroke (Wardlaw et al., 2013b; Yang and Rosenberg, 2011).”