Neuroinflammation in post-acute sequelae of COVID-19 (PASC) as assessed by [11C]PBR28 PET correlates with vascular disease measures

Journal article


VanElzakker, M.B., Bues, H. F., Brusaferri, L., Kim, M., Saadi, D., Ratai, E.M., Dougherty, D.D. and Loggia, M.L. (2024). Neuroinflammation in post-acute sequelae of COVID-19 (PASC) as assessed by [11C]PBR28 PET correlates with vascular disease measures. Brain, Behavior and Immunity. 119, pp. 713-723. https://doi.org/10.1016/j.bbi.2024.04.015
AuthorsVanElzakker, M.B., Bues, H. F., Brusaferri, L., Kim, M., Saadi, D., Ratai, E.M., Dougherty, D.D. and Loggia, M.L.
Abstract

The COVID-19 pandemic caused by SARS-CoV-2 has triggered a consequential public health crisis of post-acute
sequelae of COVID-19 (PASC), sometimes referred to as long COVID. The mechanisms of the heterogeneous
persistent symptoms and signs that comprise PASC are under investigation, and several studies have pointed to
the central nervous and vascular systems as being potential sites of dysfunction. In the current study, we
recruited individuals with PASC with diverse symptoms, and examined the relationship between neuroinflammation and circulating markers of vascular dysfunction. We used [
11C]PBR28 PET neuroimaging, a marker
of neuroinflammation, to compare 12 PASC individuals versus 43 normative healthy controls. We found
significantly increased neuroinflammation in PASC versus controls across a wide swath of brain regions including
midcingulate and anterior cingulate cortex, corpus callosum, thalamus, basal ganglia, and at the boundaries of
ventricles. We also collected and analyzed peripheral blood plasma from the PASC individuals and found significant positive correlations between neuroinflammation and several circulating analytes related to vascular
dysfunction. These results suggest that an interaction between neuroinflammation and vascular health may
contribute to common symptoms of PASC.

KeywordsCOVID-19; Long COVID pathogenesis; Neuroimaging; Positron emission tomography; Fibrinogen; Cardiovascular; Glia; Microglia; Brain inflammation
Year2024
JournalBrain, Behavior and Immunity
Journal citation119, pp. 713-723
PublisherElsevier
ISSN1090-2139
Digital Object Identifier (DOI)https://doi.org/10.1016/j.bbi.2024.04.015
Web address (URL)https://www.sciencedirect.com/science/article/pii/S0889159124003593?via%3Dihub
Publication dates
Print18 Apr 2024
Publication process dates
Accepted16 Apr 2024
Deposited02 May 2024
Publisher's version
License
File Access Level
Open
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