期刊
CELLS
卷 12, 期 2, 页码 -出版社
MDPI
DOI: 10.3390/cells12020244
关键词
adult human neurogenesis; SARS-CoV-2; COVID-19
类别
Infection with SARS-CoV-2 leads to neurological and psychiatric symptoms due to inflammation and hypoxia in key brain regions. The mechanisms behind these symptoms are largely unknown. A study comparing COVID-19 patients with a control group found a decrease in neuronal progenitor cells and newborn neurons in the infected group. The COVID-19 patients also showed increased microglial activation. The inflammatory response caused by COVID-19 negatively affects adult neurogenesis through increased cytokine concentration.
Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is associated with the onset of neurological and psychiatric symptoms during and after the acute phase of illness. Inflammation and hypoxia induced by SARS-CoV-2 affect brain regions essential for fine motor function, learning, memory, and emotional responses. The mechanisms of these central nervous system symptoms remain largely unknown. While looking for the causes of neurological deficits, we conducted a study on how SARS-CoV-2 affects neurogenesis. In this study, we compared a control group with a group of patients diagnosed with COVID-19. Analysis of the expression of neurogenesis markers showed a decrease in the density of neuronal progenitor cells and newborn neurons in the SARS-CoV-2 group. Analysis of COVID-19 patients revealed increased microglial activation compared with the control group. The unfavorable effect of the inflammatory process in the brain associated with COVID-19 disease increases the concentration of cytokines that negatively affect adult human neurogenesis.
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