Pathogenesis of neuropsychic complications of new coronavirus infection

Infection caused by the SARS-CoV-2 coronavirus is characterized by neurological and mental complications in a significant number of patients, which are based on disruption of the permeability of the blood-brain barrier, penetration of pro-inflammatory cytokines into the brain, neuroinflammation and coagulopathy. Studies of the brains of patients who died during an acute period of the disease showed a presence of foci of perivascular inflammation containing macrophages and, in a small number, CD8+ T cells. Microglial cells, mast cells, macrophages, and endothelial cells are involved in the development of neuroinflammation. Microglial nodules were observed in brain tissue samples, indicating neurophagia and neuronal loss. Some SARS-CoV-2 proteins, in particular the S protein, have pathogenic properties towards neurons. Biochemical markers in the cerebrospinal fluid of COVID-19 patients — NfL (neurofilament light chain) and GFAp (glial fibrillary acidic protein) indicate axonal destruction and astrocyte damage. Many patients with COVID-19, develop autoantibodies to self-antigens, including some CNS receptors, and encephalitis due to immune dysfunction and molecular mimicry. In patients with Alzheimer’s disease and Parkinson’s disease, coronavirus infection increases the symptoms of these diseases. The purpose of the review is summarizing the literary data for the analysis of immunopathogenesis of neuropsychic complications of acute coronavirus infection (COVID-19) and post-COVID syndrome.