Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, United States
Brian Mathew
Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, United States
Grace Van Hyfte
Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, United States
Linh Hellmers
Tulane National Primate Research Center, Covington, United States
Nathalie Jette
Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, United States
Molly Estill
Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, United States
Li Shen
Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, United States
Tracy Fischer
Tulane National Primate Research Center, Covington, United States; Department of Microbiology and Immunology, Tulane University School of Medicine, New Orleans, United States
Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, United States; Geriatric Research, Education and Clinical Center, James J. Peters Veterans Affairs Medical Center, New York, United States
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 evaluate 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.
