Editorial: The Pathogenesis of Long-Term Neuropsychiatric COVID-19 and the Role of Microglia, Mitochondria, and Persistent Neuroinflammation: A Hypothesis.
Med Sci Monit
; 27: e933015, 2021 May 10.
Article
in English
| MEDLINE | ID: covidwho-1239178
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.
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Central Nervous System
/
Microglia
/
Cognitive Dysfunction
/
COVID-19
/
Inflammation
/
Mitochondria
Topics:
Long Covid
Limits:
Humans
Language:
English
Journal:
Med Sci Monit
Journal subject:
Medicine
Year:
2021
Document Type:
Article
Affiliation country:
MSM.933015
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