Recapitulation of pathophysiological features of AD in SARS-CoV-2-infected subjects

Elizabeth Griggs, Kyle Trageser, Sean Naughton, Eun Jeong Yang, Brian Mathew, Grace Van Hyfte, Linh Hellmers, Nathalie Jette, Molly Estill, Li Shen, Tracy Fischer, Giulio Maria Pasinetti

Research output: Contribution to journalArticlepeer-review

2 Scopus citations


Infection with the etiological agent of COVID-19, SARS-CoV-2, appears capable of impacting cognition in some patients with post-acute sequelae of SARS-CoV-2 (PASC). To eval-uate neuropathophysiological consequences of SARS-CoV-2 infection, we examine transcriptional and cellular signatures in the Brodmann 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 in Iba-1 reveals 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 in informing decision-making regarding therapeutic treatments in patients with neuro-PASC, especially those at increased risk of developing AD.

Original languageEnglish
Article numbere86333
StatePublished - 2023


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