Researchers have shown in detail how COVID-19 affects the central nervous system


COVID-19 patients commonly report having headaches, confusion and other neurological symptoms, but doctors don’t fully understand how the disease targets the brain during infection.

Now, researchers at Tulane University have shown in detail how COVID-19 affects the central nervous system, according to a new study published in Nature Communications.

The findings are the first comprehensive assessment of neuropathology associated with SARS-CoV-2 infection in a nonhuman primate model.

The team of researchers found severe brain inflammation and injury consistent with reduced blood flow or oxygen to the brain, including neuron damage and death. They also found small bleeds in the brain.

Surprisingly, these findings were present in subjects that did not experience severe respiratory disease from the virus.

Tracy Fischer, Ph.D., lead investigator and associate professor of microbiology and immunology at the Tulane National Primate Research Center, has been studying brains for decades. Soon after the primate center launched its COVID-19 pilot program in the spring of 2020, she began studying the brain tissue of several subjects that had been infected.

Fischer’s initial findings documenting the extent of damage seen in the brain due to SARS-CoV-2 infection were so striking that she spent the next year further refining the study controls to ensure that the results were clearly attributable to the infection.

“Because the subjects didn’t experience significant respiratory symptoms, no one expected them to have the severity of disease that we found in the brain,” Fischer said. “But the findings were distinct and profound, and undeniably a result of the infection.”

The findings are also consistent with autopsy studies of people who have died of COVID-19, suggesting that nonhuman primates may serve as an appropriate model, or proxy, for how humans experience the disease.

Neurological complications are often among the first symptoms of SARS-CoV-2 infection and can be the most severe and persistent. They also affect people indiscriminately – all ages, with and without comorbidities, and with varying degrees of disease severity.

Fischer hopes that this and future studies that investigate how SARS-CoV-2 affects the brain will contribute to the understanding and treatment of patients suffering from the neurological consequences of COVID-19 and long COVID.

Putative neuropathogenic effects of SARS-CoV-2

Putative neuropathogenic effects of SARS-CoV-2
Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can lead to neuropsychiatric effects during acute COVID-19, including confusion, stroke, and neuromuscular disorders. These may arise from neuroinflammation, coagulopathy, neuronal injury, and possibly viral infection in the central nervous system. Causes of Long Covid symptoms affecting the nervous system may result from the emergence and persistence of these mechanisms.

Hypothalamus-pituitary-adrenal axis and hypoxia: Decisive factors of immunological state
The immunological state of a COVID patient is also crucial for the psychological well-being of individuals. With increasing age, immunosenescence causes dysregulation of the immune system and maintains a low-grade chronic inflammatory condition, a predisposing factor to SARS-CoV-2 severity (Grolli et al. 2020). The incidence of cytokine storm can eventually amplify this predisposing factor (Grolli et al. 2020). Moreover, the decisive factors of the severe inflammatory condition include the hypothalamus–pituitary–adrenal (HPA) axis (Waszkiewicz 2020). The HPA axis functions in a negative feedback mechanism and holds homeostasis between the beneficial and harmful effects of pro-inflammatory cytokines. Following activation of the HPA axis, the hypothalamic hormone stimulates the release of adrenocorticotrophic hormone from the pituitary, which subsequently stimulates the adrenal glands to release corticosteroids (Chen et al. 2017). In a normal situation, the corticosteroid triggers negative feedback after reaching the brain and balances the stimulation of the pituitary and adrenal gland, and releases the corticosteroid itself (Chen et al. 2017). However, during the hyper-inflammation of COVID-19, the prolonged activation of the HPA axis by increased pro-inflammatory cytokines leads to the excessive release of corticosteroids (Steenblock et al. 2020). This excess amount of corticosteroids not only contributes to immune dysfunction but also influence to maintain an elevated viral load (Deek 2020; Waszkiewicz 2020).

On the other hand, hypoxia associated with COVID-19 is a significant risk factor for venous thromboembolism (Algahtani et al. 2020). Also, prolonged hypoxia following SARS-CoV-2 infection may worsen the immunothrombosis initiated by the virus (Thachil 2020). Some hospitalized COVID patients suffer from acute hypoxia, which may indirectly cause further nervous system injury (Guo et al. 2020). Jaunmuktane et al. demonstrated that SARS-CoV-2 related neurological complications resulted from the thromboembolism or thrombus formation within the brain (Jaunmuktane et al. 2020). Also, the immune response to the virus leading to damage in the brain’s blood vessel wall has been shown clearly by Jaunmuktane et al. (2020). Moreover, a few autopsy reports confirmed the neuropathological manifestations due to hypoxia and subsequent thromboembolism in COVID patients’ brains (Kantonen et al. 2020).

Altogether, these findings have proven interplay between several factors, including HPA axis, hypoxia, and immunological responses leading to a severe neuropathological condition in COVID patients.

reference link :,2020).

More information: Neuropathology and virus in brain of SARS-CoV-2 infected non-human primates, Nature Communications (2022). DOI: 10.1038/s41467-022-29440-z


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