It is known that the novel coronavirus that has brought the corona pandemic (pandemic) cannot enter the human brain.
However, many of the patients who contract this virus infection (COVID-19) suffer from several types of neurological diseases.
The virus can’t get in, but a strange thing happens that damages brain tissue.
Scientists at the National Institutes of Health (NIH) in the United States have uncovered how this antinomy occurs.
Antibodies produced as an immune response to the novel coronavirus infection have been found to cause inflammation in the blood-brain barrier blood vessels in the brain, which act as a powerful filter.
It means that it is not the virus that damages the blood vessels in the brain, but the antibody made by the immune system to attack the virus.
This discovery is expected to be of great help in treating not only the neurological diseases accompanying COVID-19, but also similar symptoms of the so-called ‘Long COVID’ (Corona Aftermath).
The study was conducted by Dr. Avindra Nass and his team, clinical director at the National Institute of Neurological Disorders and Stroke (NINDS) under the NIH.
The related paper was published in the neurology journal ‘Brain’ on the 5th (local time).
This ‘peer review’ journal published by Oxford University Press in England was founded in 1878.
It has been more than two years since the corona pandemic has swept the globe.
However, it is still unclear how COVID-19 causes brain and nervous system complications.
An autopsy of the brain tissue of the COVID-19 deceased showed damage to blood vessels due to inflammation, but the cause of the inflammation was unknown.
This time, Dr. Nas’s team confirmed for the first time the veiled cerebrovascular damage pathway.
It was discovered that immune complexes were deposited on the surface of blood-brain endothelial cells constituting the blood-brain barrier.
Immune complexes are formed when antibodies and antigens that inform the identity of foreign invaders bind. These immune complexes can cause inflammation and damage tissues.
The blood-brain barrier, formed by the close bonding of vascular endothelial cells, prevents harmful foreign substances from penetrating the brain tissue.
Why do antibodies generated by the immune response of COVID-19 attack the vascular endothelial cells of the blood-brain barrier?
This could be a kind of ‘target misidentification’, scientists say. It is assumed that way, but it is not known for certain.
In any case, damage to the endothelial cells of the blood vessels in the brain causes blood proteins to leak, leading to bleeding and the formation of blood clots.
In fact, some COVID-19 patients are at an increased risk of stroke due to these symptoms.
In a previous study, Dr. Nasu’s team confirmed that the thinned cerebral blood vessels of Corona 19 patients leak and damage the brain tissue.
At that time, it was thought that the body had a natural inflammatory response to the invading virus.
But the exact truth has not been revealed.
Therefore, the brain tissues of 9 patients (ages 24-73) with cerebrovascular damage among the COVID-19 deaths tested at the time were re-examined and compared with 10 healthy controls.
Den ‘immunohistochemistry’ was used to look at neuroinflammation and immune responses. It is to identify a specific protein label in a tissue with an antibody.
Again, signs of leaking blood vessels were found. A biopsy revealed a blood protein that normally does not cross the blood-brain barrier.
In addition, immune complexes found on the surface of cerebrovascular endothelial cells suggested that the endothelial cells were stimulated by some antibody-mediated attack.
Normally, when endothelial cells are activated, proteins called ‘junction molecules’ appear that make platelets stick to each other.
In fact, high levels of junction molecules are released from cerebrovascular endothelial cells of patients who have died from COVID-19.
In the end, activation of cerebrovascular endothelial cells acted as a catalyst.
When that happens, platelets adhere to the inner walls of blood vessels, causing blood clots and a chain reaction that causes blood vessels to leak.
At the same time, the blood-brain barrier also loses its strict ‘filter function’ as the tight bond is loosened.
Once blood vessels started leaking, immune cells such as macrophages flocked to repair them, causing more severe inflammation, which led to more serious nerve cell (neuron) damage.
The research team also confirmed that the expression level of 300 genes was lowered in the vascular endothelial cells of the damaged area.
However, the expression level of 6 genes involved in oxidative stress, DNA damage, and metabolic abnormality regulation was rather increased.
Clearly, this study has provided new insights into the immune response that triggers brain damage.
However, the existence of the novel coronavirus has not yet been confirmed in the brain. Which antigen (foreign substance) stimulates this immune response remains a challenge.
Dr. Nas, the lead author of the paper, emphasized that it is a clue to understanding the neurological disease of ‘Long Covid’.
“It is possible that the same immune response will persist in Long Covid patients who have had nerve damage,” he said.
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