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CLEARING THE FOG: DEFINING THE MECHANISMS AND PHENOTYPES OF NEUROLOGICAL LONG COVID IN A MOUSE MODEL
Elizabeth Kleemanand 4 co-authors
The Florey Institute of Neuroscience and Mental Health
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS02-07PM-412
Presentation
Date TBA
Board: PS02-07PM-412
Event Information
Poster Board
PS02-07PM-412
Poster
View posterAbstract
To date, the cause and pathophysiology of the neurological symptoms seen in Long COVID remain largely unclear. While an increasing number of large clinical Long COVID studies investigate neurological symptoms, they mostly rely on the participants self-diagnosis of Long COVID which provides limited insights into disease mechanisms due to their lack of powerful invasive experimental paradigms. We aim to uncover the mechanistic underpinnings of neurological and psychiatric of Long COVID in a preclinical C57BL/6J mouse model of Long COVID. In this model, young adult wildtype C57BL6/J mice (both males and females) are intranasally infected with a mouse adapted SARS-CoV-2 virus (P21 model) or mock infected with PBS as the control group. From a month after the infection, we ran a broad behavioural battery of tests and collected the brains after this to look at astrocyte and neuron populations in these mice using immunohistochemistry. We found that the Long COVID mice showed significantly decreased novel object exploration time in the novel object recognition task compared to mock control mice. The female Long COVID mice also showed reduced distance travelled overall in this task compared to mock control female mice, suggesting reduced locomotion. Long COVID mice showed significantly increased amygdala volume and significantly reduced striatum volume compared to control mice There were also significantly less neurons and more astrocytes counted in the amygdala of the Long COVID mice compared to control mice. Overall, the Long COVID mice show reduced short-term memory with region-specific changes in neuron and astrocyte populations to accompany this.
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