Your browser doesn't support javascript.
Blood-brain barrier penetration of non-replicating SARS-CoV-2 and S1 variants of concern induce neuroinflammation which is accentuated in a mouse model of Alzheimer's disease.
Erickson, Michelle A; Logsdon, Aric F; Rhea, Elizabeth M; Hansen, Kim M; Holden, Sarah J; Banks, William A; Smith, Jessica L; German, Cody; Farr, Susan A; Morley, John E; Weaver, Riley R; Hirsch, Alec J; Kovac, Andrej; Kontsekova, Eva; Baumann, Kristen K; Omer, Mohamed A; Raber, Jacob.
  • Erickson MA; Geriatrics Research Educational and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA, USA; Division of Gerontology and Geriatric Medicine, Department of Medicine, School of Medicine, University of Washington, Seattle, WA, USA.
  • Logsdon AF; Geriatrics Research Educational and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA, USA; Division of Gerontology and Geriatric Medicine, Department of Medicine, School of Medicine, University of Washington, Seattle, WA, USA.
  • Rhea EM; Geriatrics Research Educational and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA, USA; Division of Gerontology and Geriatric Medicine, Department of Medicine, School of Medicine, University of Washington, Seattle, WA, USA.
  • Hansen KM; Geriatrics Research Educational and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA, USA.
  • Holden SJ; Department of Behavioral Neurosciences, Oregon Health and Science University, Portland, OR, USA.
  • Banks WA; Geriatrics Research Educational and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA, USA; Division of Gerontology and Geriatric Medicine, Department of Medicine, School of Medicine, University of Washington, Seattle, WA, USA. Electronic address: wabanks1@uw.edu.
  • Smith JL; The Vaccine and Gene Therapy Institute, Oregon Health and Sciences University, Beaverton, OR, USA; Division of Pathobiology and Immunology Oregon National Primate Research Center, Oregon Health and Sciences University, Beaverton, OR, USA.
  • German C; The Vaccine and Gene Therapy Institute, Oregon Health and Sciences University, Beaverton, OR, USA; Division of Pathobiology and Immunology Oregon National Primate Research Center, Oregon Health and Sciences University, Beaverton, OR, USA.
  • Farr SA; Saint Louis Veterans Affairs Medical Center, Research Service, St. Louis, MO, USA; Division of Geriatric Medicine, Saint Louis University School of Medicine, St. Louis, MO, USA.
  • Morley JE; Division of Geriatric Medicine, Saint Louis University School of Medicine, St. Louis, MO, USA.
  • Weaver RR; Geriatrics Research Educational and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA, USA.
  • Hirsch AJ; The Vaccine and Gene Therapy Institute, Oregon Health and Sciences University, Beaverton, OR, USA; Division of Pathobiology and Immunology Oregon National Primate Research Center, Oregon Health and Sciences University, Beaverton, OR, USA.
  • Kovac A; Institute of Neuroimmunology, Slovak Academy of Sciences, Bratislava, Slovak Republic.
  • Kontsekova E; Institute of Neuroimmunology, Slovak Academy of Sciences, Bratislava, Slovak Republic.
  • Baumann KK; Geriatrics Research Educational and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA, USA.
  • Omer MA; Geriatrics Research Educational and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA, USA.
  • Raber J; Department of Behavioral Neurosciences, Oregon Health and Science University, Portland, OR, USA; Department of Neurology, Psychiatry, and Radiation Medicine, Division of Neuroscience, Departments of Neurology and Radiation Medicine, Oregon National Primate Research Center, Oregon Health Sciences Uni
Brain Behav Immun ; 109: 251-268, 2023 03.
Article in English | MEDLINE | ID: covidwho-2258334
ABSTRACT
COVID-19 and especially Long COVID are associated with severe CNS symptoms and may place persons at risk to develop long-term cognitive impairments. Here, we show that two non-infective models of SARS-CoV-2 can cross the blood-brain barrier (BBB) and induce neuroinflammation, a major mechanism underpinning CNS and cognitive impairments, even in the absence of productive infection. The viral models cross the BBB by the mechanism of adsorptive transcytosis with the sugar N-acetylglucosamine being key. The delta and omicron variants cross the BB B faster than the other variants of concern, with peripheral tissue uptake rates also differing for the variants. Neuroinflammation induced by icv injection of S1 protein was greatly enhanced in young and especially in aged SAMP8 mice, a model of Alzheimer's disease, whereas sex and obesity had little effect.
Subject(s)
Keywords
Fulltext
Print
XML
PubMed Links
Search on Google

Full text: Available Collection: International databases Database: MEDLINE Main subject: Alzheimer Disease / COVID-19 Type of study: Prognostic study / Randomized controlled trials Topics: Long Covid / Variants Limits: Animals / Humans Language: English Journal: Brain Behav Immun Journal subject: Allergy and Immunology / Brain / Psychophysiology Year: 2023 Document Type: Article Affiliation country: J.bbi.2023.01.010

Similar

MEDLINE
LILACS
LIS
Fulltext
Print
XML
PubMed Links
Search on Google

Full text: Available Collection: International databases Database: MEDLINE Main subject: Alzheimer Disease / COVID-19 Type of study: Prognostic study / Randomized controlled trials Topics: Long Covid / Variants Limits: Animals / Humans Language: English Journal: Brain Behav Immun Journal subject: Allergy and Immunology / Brain / Psychophysiology Year: 2023 Document Type: Article Affiliation country: J.bbi.2023.01.010