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COVID-19: Cellular and Molecular Mechanisms of Brain Damage

Authors
  • Gomazkov, O. A.
Type
Published Article
Journal
Biology Bulletin Reviews
Publisher
Pleiades Publishing
Publication Date
Apr 06, 2022
Volume
12
Issue
2
Pages
131–139
Identifiers
DOI: 10.1134/S2079086422020037
PMCID: PMC8985060
Source
PubMed Central
Keywords
Disciplines
  • Article
License
Unknown

Abstract

The most common clinical manifestation of COVID-19 is bilateral pneumonia, a diffuse, alveolar injury with severe microangiopathy. Systemic infection is accompanied by an increase in circulating chemokines and interleukins in the blood, which penetrate the blood–brain barrier (BBB) and enter the brain. Clinical materials indicate lesions of the brain and peripheral nervous system, as well as neurodegenerative and mental disorders. Due to violations of the cerebral endothelium system and changes in the balance of ACE2-coupled cytochemical processes, coagulopathy develops, leading to microthrombosis and vascular occlusion. The concept of SARS-CoV-2 “neurotropism” is discussed as a rationale for the penetration by the virus into the brain. Infection can occur as axonal transport through the bulbar zone and the olfactory area of the cerebral cortex. Even more common is the “hematogenous pathway” of viral transfection, which includes damage to the vascular endothelium and a violation of the protective role of the BBB. Another concept that explains the mechanism of brain damage relates to the phenomenon of neuroinflammation. Astrocytes and microglia are considered potential targets of the SARS-CoV-2 coronavirus. The dissonance of the biochemical processes of the axis ACE2/ACE and changes in the functions of angiotensin peptides leads to the activation of astroglia with the development of neurodestructive processes in COVID-19.

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