Infection with the etiological agent of COVID-19, SARS-CoV-2, appears capable of impacting cognition, which some patients with Post-acute Sequelae of SARS-CoV-2 (PASC). To evaluate neuro-pathophysiological consequences of SARS-CoV-2 infection, we examine transcriptional and cellular signatures in the Broadman area 9 (BA9) of the frontal cortex and the hippocampal formation (HF) in SARS-CoV-2, Alzheimer’s disease (AD) and SARS-CoV-2 infected AD individuals, compared to age- and gender-matched neurological cases. Here we show similar alterations of neuroinflammation and blood-brain barrier integrity in SARS-CoV-2, AD, and SARS-CoV-2 infected AD individuals. Distribution of microglial changes reflected by the increase of Iba-1 reveal nodular morphological alterations in SARS-CoV-2 infected AD individuals. Similarly, HIF-1α is significantly upregulated in the context of SARS-CoV-2 infection in the same brain regions regardless of AD status. The finding may help to inform decision-making regarding therapeutic treatments in patients with neuro-PASC, especially those at increased risk of developing AD.
Teaser SARS-CoV-2 and Alzheimer’s disease share similar neuroinflammatory processes, which may help explain neuro-PASC.
### Competing Interest Statement
NJ receives grant funding paid to her institution from NINDS (NIH U24NS107201, NIH IU54NS100064, 3R01CA202911-05S1, R21NS122389, R01HL161847). Some of these grants are COVID-19 related but focus on the neuroimaging findings. The other authors declare that they have no conflict of interest with the contents of this article.
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