Please use this identifier to cite or link to this item: https://doi.org/10.7150/thno.68304
Title: Pathophysiology of blood brain barrier dysfunction during chronic cerebral hypoperfusion in vascular cognitive impairment
Authors: Rajeev, Vismitha 
Fann, David Y 
Quynh, Nhu Dinh
Kim, Hyun Ah
De Silva, T Michael
Lai, Mitchell KP 
Chen, Christopher Li-Hsian 
Drummond, Grant R
Sobey, Christopher G
Arumugam, Thiruma 
Keywords: Science & Technology
Life Sciences & Biomedicine
Medicine, Research & Experimental
Research & Experimental Medicine
TIGHT JUNCTION PROTEINS
NECROSIS-FACTOR-ALPHA
WHITE-MATTER LESIONS
SMALL VESSEL DISEASE
MONOCYTE CHEMOATTRACTANT PROTEIN-1
ENDOTHELIAL ADHERENS JUNCTIONS
ALZHEIMERS-DISEASE
OXIDATIVE STRESS
MATRIX METALLOPROTEINASES
IN-VITRO
Issue Date: 1-Jan-2022
Publisher: IVYSPRING INT PUBL
Citation: Rajeev, Vismitha, Fann, David Y, Quynh, Nhu Dinh, Kim, Hyun Ah, De Silva, T Michael, Lai, Mitchell KP, Chen, Christopher Li-Hsian, Drummond, Grant R, Sobey, Christopher G, Arumugam, Thiruma (2022-01-01). Pathophysiology of blood brain barrier dysfunction during chronic cerebral hypoperfusion in vascular cognitive impairment. THERANOSTICS 12 (4) : 1639-1658. ScholarBank@NUS Repository. https://doi.org/10.7150/thno.68304
Abstract: The prevalence of cerebrovascular disease increases with age, placing the elderly at a greater lifetime risk for dementia. Vascular cognitive impairment (VCI) encompasses a spectrum of cognitive deficits from mild cognitive impairment to dementia. VCI and its most severe form, vascular dementia (VaD), is becoming a major public health concern worldwide. As growing efforts are being taken to understand VCI and VaD in animal models and humans, the pathogenesis of the disease is being actively explored. It is postulated that chronic cerebral hypoperfusion (CCH) is a major cause of VCI. CCH activates a molecular and cellular injury cascade that leads to breakdown of the blood brain barrier (BBB) and neurodegeneration. The BBB tightly regulates the movement of substances between the blood and the brain, thereby regulating the microenvironment within the brain parenchyma. Here we illustrate how BBB damage is causal in the pathogenesis of VCI through the increased activation of pathways related to excitotoxicity, oxidative stress, inflammation and matrix metalloproteinases that lead to downstream perivascular damage, leukocyte infiltration and white matter changes in the brain. Thus, CCH-induced BBB damage may initiate and contribute to a vicious cycle, resulting in progressive neuropathological changes of VCI in the brain. This review outlines the molecular and cellular mechanisms that govern BBB breakdown during CCH and highlights the clinical evidence in identifying at-risk VCI patients.
Source Title: THERANOSTICS
URI: https://scholarbank.nus.edu.sg/handle/10635/218717
ISSN: 1838-7640
DOI: 10.7150/thno.68304
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