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Molecular and cellular similarities in the brain of SARS-CoV-2 and Alzheimer's disease individuals
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 Pasinetti.
Afiliação
  • Elizabeth Griggs; Icahn School of Medicine at Mount Sinai
  • Kyle Trageser; Icahn School of Medicine at Mount Sinai
  • Sean Naughton; Icahn School of Medicine at Mount Sinai
  • Eun-Jeong Yang; Icahn School of Medicine at Mount Sinai
  • Brian Mathew; Icahn School of Medicine at Mount Sinai
  • Grace Van Hyfte; Icahn School of Medicine at Mount Sinai
  • Linh Hellmers; Tulane National Primate Research Center
  • Nathalie Jette; Icahn School of Medicine at Mount Sinai
  • Molly Estill; Icahn School of Medicine at Mount Sinai
  • Li Shen; Icahn School of Medicine at Mount Sinai
  • Tracy Fischer; Tulane National Primate Research Center; Department of Microbiology and Immunology
  • Giulio Pasinetti; Icahn School of Medicine at Mount Sinai; James J. Peters Veterans Affairs Medical Center
Preprint em Inglês | bioRxiv | ID: ppbiorxiv-517706
ABSTRACT
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, Alzheimers 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-1 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. TeaserSARS-CoV-2 and Alzheimers disease share similar neuroinflammatory processes, which may help explain neuro-PASC.
Licença
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Texto completo: Disponível Coleções: Preprints Base de dados: bioRxiv Tipo de estudo: Estudo de etiologia / Experimental_studies / Estudo prognóstico Idioma: Inglês Ano de publicação: 2022 Tipo de documento: Preprint
Texto completo: Disponível Coleções: Preprints Base de dados: bioRxiv Tipo de estudo: Estudo de etiologia / Experimental_studies / Estudo prognóstico Idioma: Inglês Ano de publicação: 2022 Tipo de documento: Preprint
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