Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 22, Issue 5, Pages -Publisher
MDPI
DOI: 10.3390/ijms22052681
Keywords
blood-brain barrier; SARS-CoV-2; COVID-19; brain; inflammation; thrombosis; hypoxia; APOE
Funding
- Veterans Administration
- National Institutes of Health-National Institute on Aging [1RF1AG059088-01]
- Biological Mechanisms of Healthy Aging Training Program [NIH T32AG066574]
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This review discusses the mechanisms by which SARS-CoV-2 interactions with the blood-brain barrier (BBB) may lead to neurological dysfunction associated with COVID-19. It considers peripheral diseases such as hypoxia and systemic inflammatory response syndrome, as well as CNS infection and viral entry into the brain. Additionally, it explores the contribution of risk factors for severe COVID-19 to BBB dysfunction.
Emerging data indicate that neurological complications occur as a consequence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. The blood-brain barrier (BBB) is a critical interface that regulates entry of circulating molecules into the CNS, and is regulated by signals that arise from the brain and blood compartments. In this review, we discuss mechanisms by which SARS-CoV-2 interactions with the BBB may contribute to neurological dysfunction associated with coronavirus disease of 2019 (COVID-19), which is caused by SARS-CoV-2. We consider aspects of peripheral disease, such as hypoxia and systemic inflammatory response syndrome/cytokine storm, as well as CNS infection and mechanisms of viral entry into the brain. We also discuss the contribution of risk factors for developing severe COVID-19 to BBB dysfunction that could increase viral entry or otherwise damage the brain.
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