The authors found that the former group had reduced cortical thickness, which correlated with cognitive impairment and symptoms such as anxiety and depression.
The authors analyzed brain samples from 26 people who had died of COVID-19 and found that samples taken from five of these individuals had tissue damage.
Further analysis of damaged brain samples revealed that astrocytes, which are brain cells that maintain neuronal metabolism, were particularly likely to be infected by SARS-CoV-2 and that the virus enters these cells via the NRP1 receptor.
Once infected, astrocytes showed altered metabolites used to produce neurons and neurotransmitters, and infected cells secreted neurotoxic molecules. According to the authors, the findings reveal the structural changes observed in the brains of patients with COVID-19.
The significance of the study describes neurological symptoms, which are one of the most common extrapulmonary complications of COVID-19, occurring in more than 30 percent of patients. In this study, we provide evidence that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is found in the human brain, where it infects astrocytes and, to a lesser extent, neurons.
We also show that astrocytes are susceptible to SARS-CoV-2 infection through a non-canonical mechanism involving spike-NRP1 interaction and respond to infection by remodeling energy metabolism, which in turn alters the levels of metabolites used to feed neurons and support neurotransmitter release. synthesis. The altered secretory phenotype of infected astrocytes then impairs neuronal viability. These properties may explain the damage and structural changes observed in the brains of patients with COVID-19.
Although increasing evidence confirms neuropsychiatric manifestations mainly associated with severe COVID-19 infection, long-term neuropsychiatric dysfunction (recently characterized as part of the “long-term COVID-19” syndrome) has been observed frequently after mild infection.
The study shows a spectrum of brain effects of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, ranging from long-term changes in mildly infected individuals (orbitofrontal cortical atrophy, neurocognitive impairment, excessive fatigue and anxiety symptoms) to severe. an acute lesion confirmed in brain tissue samples obtained from the orbitofrontal region (via endonasal transethmoidal access) from individuals who have died of COVID-19.
In an independent cohort of 26 individuals who died of COVID-19, we used histopathological signs of brain damage as a guide to possible SARS-CoV-2 brain infection and found that of the five individuals with these symptoms, all had genetic markers. viral material in the brain.
Brain tissue samples from these five patients also showed foci of SARS-CoV-2 infection and replication, especially in astrocytes. In support of the astrocyte infection hypothesis, neural stem cell-derived human astrocytes in vitro are susceptible to SARS-CoV-2 infection through a non-canonical mechanism involving spike-NRP1 interaction.
SARS-CoV-2-infected astrocytes exhibited changes in energy metabolism and key proteins and metabolites used to fuel neurons, as well as in neurotransmitter biogenesis. In addition, human astrocyte infection induces a secretory phenotype that reduces neuronal viability.
The results of the study show that cognitive impairment and neuropsychiatric symptoms in recovered COVID-19 patients are correlated with altered cortical thickness. Cortical surface-based morphometry analysis (using high-resolution 3T MRI) in 81 patients diagnosed with mild COVID-19 infection (62 self-reported anosmia or dysgeusia) who did not require oxygen support (methodological details and patient demographics are presented on SI -annex).
Analysis was performed within a mean (SD) interval of 57 (26) days after detection of SARS-CoV-2 by qRT-PCR, and subjects were compared to 81 healthy volunteers (without neuropsychiatric comorbidities) scanned during the COVID-19 pandemic. (balanced for his age [P = 0.97] and sex [P = 0.3]). The COVID-19 group showed higher levels of anxiety and depression symptoms, fatigue, and excessive daytime sleepiness ( SI Appendix , Table S1 shows epidemiological and clinical data).
Analysis of cortical thickness (corrected for multiple comparisons using the Holm-Bonferroni method) revealed areas of reduced cortical thickness exclusively in the left hemisphere, including left gyrus rectus (P = 0.01), superior temporal gyrus (P = 0.036), inferior temporal sulcus (P = 0.02) and posterior transverse lateral closure (P = 0.003) (Figure 1A). No increase in cortical thickness was observed.
HT
Source: ANI
Source: The Nordic Page