Inflammation at the crossroads of COVID-19, cognitive deficits and depression.

Autor: Lyra E Silva NM; Centre for Neuroscience Studies, Department of Biomedical and Molecular Sciences, Queen's University, Kingston, ON, Canada; Department of Psychiatry, Queen's University, Kingston, ON, Canada. Electronic address: ndml@queensu.ca., Barros-Aragão FGQ; D'OR Institute for Research & Education, RJ, Brazil; Institute of Medical Biochemistry Leopoldo de Meis, Federal University of Rio de Janeiro, RJ, Brazil. Electronic address: fernanda.aragao@idor.org., De Felice FG; Centre for Neuroscience Studies, Department of Biomedical and Molecular Sciences, Queen's University, Kingston, ON, Canada; Department of Psychiatry, Queen's University, Kingston, ON, Canada; D'OR Institute for Research & Education, RJ, Brazil; Institute of Medical Biochemistry Leopoldo de Meis, Federal University of Rio de Janeiro, RJ, Brazil., Ferreira ST; D'OR Institute for Research & Education, RJ, Brazil; Institute of Medical Biochemistry Leopoldo de Meis, Federal University of Rio de Janeiro, RJ, Brazil; Institute of Biophysics Carlos Chagas Filho, Federal University of Rio de Janeiro, RJ, Brazil.
Jazyk: angličtina
Zdroj: Neuropharmacology [Neuropharmacology] 2022 May 15; Vol. 209, pp. 109023. Date of Electronic Publication: 2022 Mar 04.
DOI: 10.1016/j.neuropharm.2022.109023
Abstrakt: Acute neurological alterations have been associated with SARS-CoV-2 infection. Additionally, it is becoming clear that coronavirus disease 2019 (COVID-19) survivors may experience long-term neurological abnormalities, including cognitive deficits and mood alterations. The mechanisms underlying acute and long-term impacts of COVID-19 in the brain are being actively investigated. Due to the heterogeneous manifestations of neurological outcomes, it is possible that different mechanisms operate following SARS-CoV-2 infection, which may include direct brain infection by SARS-CoV-2, mechanisms resulting from hyperinflammatory systemic disease, or a combination of both. Inflammation is a core feature of COVID-19, and both central and systemic inflammation are known to lead to acute and persistent neurological alterations in other diseases. Here, we review evidence indicating that COVID-19 is associated with neuroinflammation, along with blood-brain barrier dysfunction. Similar neuroinflammatory signatures have been associated with Alzheimer's disease and major depressive disorder. Current evidence demonstrates that patients with pre-existing cognitive and neuropsychiatric deficits show worse outcomes upon infection by SARS-CoV-2 and, conversely, COVID-19 survivors may be at increased risk of developing dementia and mood disorders. Considering the high prevalence of COVID-19 patients that recovered from infection in the world and the alarming projections for the prevalence of dementia and depression, investigation of possible molecular similarities between those diseases may shed light on mechanisms leading to long-term neurological abnormalities in COVID-19 survivors.
(Copyright © 2022 Elsevier Ltd. All rights reserved.)
Databáze: MEDLINE
Externí odkaz: