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-19
  • Start & end year

    2024
    2025
  • Known Financial Commitments (USD)

    $561,155
  • Funder

    National Institutes of Health (NIH)
  • Principal Investigator

    ASSISTANT PROFESSOR Sarah Lutz
  • Research Location

    United States of America
  • Lead Research Institution

    UNIVERSITY OF ILLINOIS AT CHICAGO
  • Research 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.