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eISSN: 1643-3750

Editorial: The Pathogenesis of Long-Term Neuropsychiatric COVID-19 and the Role of Microglia, Mitochondria, and Persistent Neuroinflammation: A Hypothesis

George B. Stefano, Pascal Büttiker, Simon Weissenberger, Anders Martin, Radek Ptacek, Richard M. Kream

Center for Cognitive and Molecular Neuroscience, First Faculty of Medicine, Charles University in Prague, Prague, Czech Republic

Med Sci Monit 2021; 27:e933015

DOI: 10.12659/MSM.933015

Available online: 2021-05-09

Published: 2021-05-10


#933015

ABSTRACT: Persistent comorbidities occur in patients who initially recover from acute coronavirus disease 2019 (COVID-19) due to infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). ‘Long COVID' involves the central nervous system (CNS), resulting in neuropsychiatric symptoms and signs, including cognitive impairment or ‘brain fog' and chronic fatigue syndrome. There are similarities in these persistent complications between SARS-CoV-2 and the Ebola, Zika, and influenza A viruses. Normal CNS neuronal mitochondrial function requires high oxygen levels for oxidative phosphorylation and ATP production. Recent studies have shown that the SARS-CoV-2 virus can hijack mitochondrial function. Persistent changes in cognitive functioning have also been reported with other viral infections. SARS-CoV-2 infection may result in long-term effects on immune processes within the CNS by causing microglial dysfunction. This short opinion aims to discuss the hypothesis that the pathogenesis of long-term neuropsychiatric COVID-19 involves microglia, mitochondria, and persistent neuroinflammation.

Keywords: Editorial, Central Nervous System, Inflammation Mediators, Neuropsychiatry, Mitochondria, Microglia, COVID-19, cognitive dysfunction, severe acute respiratory syndrome coronavirus 2



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