Impact of SARS-CoV-2 on the cerebrovasculature as a risk factor for VCID: Role of Wnt/beta-catenin
- Funded by National Institutes of Health (NIH)
- Total publications:0 publications
Grant number: 1R56NS138437-01
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Key facts
Disease
COVID-19Start & end year
20242025Known Financial Commitments (USD)
$561,155Funder
National Institutes of Health (NIH)Principal Investigator
ASSISTANT PROFESSOR Sarah LutzResearch Location
United States of AmericaLead Research Institution
UNIVERSITY OF ILLINOIS AT CHICAGOResearch Priority Alignment
N/A
Research Category
Pathogen: natural history, transmission and diagnostics
Research Subcategory
Pathogen genomics, mutations and adaptations
Special Interest Tags
N/A
Study Type
Non-Clinical
Clinical Trial Details
N/A
Broad Policy Alignment
Pending
Age Group
Not Applicable
Vulnerable Population
Not applicable
Occupations of Interest
Not applicable
Abstract
Abstract COVID-19 increases the risk of vascular contributions to cognitive impairment and dementia (VCID). VCID is one of the most prevalent forms of dementia, so the potential public health impact of the COVID-19 pandemic on future VCID is substantial. However, the mechanisms by which COVID-19 modifies VCID are unknown. Identifying mechanisms that regulate how prior COVID-19 influences the brain endothelial cell response to vascular stress is important. Here, we provide preliminary evidence that COVID-19 decreases resistance to VCID by weakening the blood-brain barrier (BBB). This is accompanied by cerebrovascular inflammation. This grant will test the novel mechanism that SARS-CoV-2 infection accelerates VCID by suppressing cerebrovascular Wnt/β-catenin signaling. In Aim 1, we determine how prior SARS-CoV-2 infection influences BBB permeability and cognition upon subsequent vascular insult, by genetic and epigenetic modification. In Aim 2 we use endothelial-targeted genetic interventions to assess the contribution of Wnt/β- cat targets to resistance to post-infectious VCID. In Aim 3, we ask whether established post-infectious VCID can be reversed by increasing cerebrovascular Wnt/β-catenin. These studies could lead to novel approaches to identify individuals at high risk for VCID and novel potential therapeutic strategies to mitigate the impact of prior infection on the development of dementia.