Study explains how COVID-19 damages the brain

According to research How SARS-COV-2 infects brain cells called astrocytes and causes structural changes in the brain. SARS-CoV-2 infection can lead to brain alterations and neurocognitive dysfunction, especially in the long-lasting COVID-19 syndrome, but the underlying mechanisms are elusive.

Daniel Martin de Souza and colleagues used MRI to compare the brain structures of 81 study participants and 81 healthy individuals who had recovered from mild COVID-19 infection.

The authors found that the former group exhibited reduced cortical thickness, which correlated with cognitive impairment and symptoms such as anxiety and depression.

The authors analyzed brain samples from 26 people who died of COVID-19 and found that samples from 5 of these individuals showed tissue damage.

Further analysis of the injured brain samples showed that astrocytes, brain cells that maintain neuronal metabolism, were particularly likely to be infected with SARS-CoV-2 and that the virus entered these cells via the NRP1 receptor. became clear to do.

Upon infection, astrocytes exhibited altered levels of metabolites used to fuel neuron and neurotransmitter production, and infected cells secreted neurotoxin molecules. According to the authors, the findings reveal structural changes observed in the brains of COVID-19 patients.

The significance of this study is that it represents the most common neurological manifestation among the extrapulmonary complications of COVID-19, affecting more than 30% of patients. This study provides evidence that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is found in the human brain and infects astrocytes and, to a lesser extent, neurons.

Astrocytes are also susceptible to SARS-CoV-2 infection through non-canonical mechanisms involving spike and NRP1 interactions, and respond to infection by remodeling their energy metabolism to fuel neurons. It has also been shown to alter levels of metabolites used to supply and support neurotransmitters. synthetic. The altered secretory phenotype of infected astrocytes impairs neuronal viability. These features may explain the damage and structural changes observed in the brains of COVID-19 patients.

Although there is increasing evidence confirming neuropsychiatric symptoms primarily associated with severe COVID-19 infection, long-term neuropsychiatric dysfunction (most recently as part of the “long-term COVID-19” syndrome) has been reported after mild infection. part) are frequently observed.

This study demonstrates the spectrum of brain effects of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, with long-term changes (orbitofrontal cortex atrophy, neurocognitive impairment) in mildly infected individuals. acute injury identified in brain tissue samples extracted (via intranasal transethmoid access) from the orbitofrontal region of individuals who died of severe COVID-19 from severe fatigue and anxiety symptoms).

Using histopathologic signs of brain injury as a guide for possible SARS-CoV-2 brain infection in an independent cohort of 26 people who died of COVID-19, all five patients who exhibited those signs found to have heritable 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. Supporting the hypothesis of astrocyte infection, in vitro neural stem cell-derived human astrocytes are susceptible to SARS-CoV-2 infection through non-canonical mechanisms involving spike and NRP1 interactions.

Astrocytes infected with SARS-CoV-2 showed alterations in energy metabolism, key proteins and metabolites used to fuel neurons, and neurotransmitter biosynthesis. Furthermore, human astrocyte infection induces a secretory phenotype that reduces neuronal viability.

The results of this study correlate cognitive deficits and neuropsychiatric symptoms in convalescent COVID-19 patients with changes in cerebral cortical thickness. Cortical surface-based morphometric analysis (using high-resolution 3T MRI) on her 81 subjects (62 self-reported anosmia or dysgeusia) diagnosed with mild her COVID-19 infection. SI Appendix).

Analyzes were performed within a mean (SD) interval of 57 (26) d after SARS-CoV-2 detection by qRT-PCR, and subjects were 81 healthy volunteers (neuropathy) scanned during the COVID-19 pandemic. compared with those without psychiatric comorbidities). (age-balanced [P = 0.97] sex with [P = 0.3]). The COVID-19 group showed higher levels of anxiety and depressive symptoms, fatigue, and excessive daytime sleepiness (SI Appendix, Table S1 presents epidemiological and clinical data).

Analysis of cortical thickness (adjusted for multiple comparisons using the Holm-Bonferroni method) revealed the left hemisphere, including the left rectus gyrus (P = 0.01), superior temporal gyrus (P = 0.036), and inferior temporal gyrus. only revealed areas of reduced cortical thickness. temporal sulcus (P = 0.02), and posterior lateral minor sulcus (P = 0.003) (Figure 1A). No increase in cortical thickness was observed.


Source: Ani Study explains how COVID-19 damages the brain

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