Why Can Nerve Cells In The Brain Die During COVID-19?

  • How can corona infection affect the brain?
  • US scientists investigated this issue.
  • Here we explain why testing them is important and what the result could also mean for the treatment and prevention of long COVID.

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American scientists from the National Institute of Neurological Disorders and Stroke use material from an autopsy on a corona to show what consequences SARS-CoV-2 infection can have on the nervous tissue. Accordingly, the virus itself appears to be less responsible for the death of nerve cells and the formation of tiny blood clots in the brain’s microvessels than an inappropriate immune response.

Why is research important

Soon after the pandemic started, it became clear: COVID-19 is not just a respiratory disease. In addition to the lungs, corona infection can also damage other organs – such as the heart, blood vessels, kidneys, brain, and liver. The virus itself can destroy tissues by reproducing itself in cells. But the immune system is also involved in damage when it attacks cells infected with the virus.

Some patients with corona infection develop neurological complications. This can happen in the acute phase of the disease or later. Many complain of difficulty concentrating, sleep disturbances, headaches, fatigue, sensory problems, and even a stroke near a corona infection. COVID-19 may possibly increase the risk of Alzheimer’s dementia or speed up the course of the disease.

It is not yet clear how the virus damages nerve cells and what exactly causes the neurological symptoms. Better understanding of disease processes is absolutely necessary to develop treatment or prevention strategies.

What the researchers did

Avindra Nath is a neuroimmunologist who has been studying the neurological consequences of viral infections, especially HIV / AIDS and the flu for decades. Nath and his team at the National Institute of Neurological Disorders and Stroke in Bethesda, USA, published their first observations of patients who died from COVID-19 during the first corona wave a year and a half ago. Scientists examined the brain of the deceased using magnetic resonance imaging. In some of them, they found visible damage to the tissues scattered around the examined areas of the brain.

In the present investigation, the Americans tried to find out how the damage might have happened. To this end, they prepared tissue scraps from different areas of the brain. Using special staining methods and other detection methods, they examined the tissue for the presence of immune cells, signaling substances, tiny blood clots, and SARS-CoV-2.

Autopsy material was obtained from two women and seven men aged 24 to 73 who died from COVID-19 between March and July 2020. Five of them died very suddenly, only one was treated in the intensive care unit for severe the course of the disease.

What the results of the study look like

Although the deceased was a carrier of the virus at the time of death, SARS-CoV-2 was not detected in any of the brain samples tested. However, Avindra Nath’s team found clear signs of the destruction of the protective blood-brain barrier in damaged areas of the brain in all of the dead. Protein fibrinogen, normally found in blood serum, has leaked into brain tissue.

Wall cells lining the brain’s microvasculature were activated, immune complexes of antibodies and components of the complement cascade (the defense system that assisted the elimination of pathogens) built up, inflammatory cells migrated, some of the tiny vessels blocked by blood clots. Nerve cells died in the vicinity of these inflammatory lesions. The American team found most of the damage in the so-called hindbrain, which also includes the cerebellum and the brainstem.

Scientists suspect that anti-virus or autoimmune antibodies triggered the immune cascade and caused the damage.

What are the weaknesses of the study?

Despite various technical efforts, scientists have been unable to detect the coronavirus in brain tissue. This does not necessarily mean that the virus was not present in the brain at that point in time, which the study does not record. The negative result could be due to very little virus below the detection limit or to methodological errors. As most of those affected were found dead, there was not enough data on their medical history or the course of COVID-19 disease.

The probability that the virus and the immune response induced are responsible for the damage is extremely high. Nevertheless, it cannot be completely excluded that damage to the blood-brain barrier (with clot formation and inflammation) is also not due to events other than corona infection, and Avindra Nath and his colleagues are limiting their results.

What does the result mean

In fact, due to damage to brain tissue, he expected the coronavirus to be detected immediately, says Avindra Nath. Some other previous studies also found no or very little viral material in the central nervous system. These, if any, only small amounts of the virus were in no way sufficient to explain the observed effects on the brain and neurological consequences, the neuroimmunologist told Science.

It could have been an immune reaction to the infection which (in part) resulted in the death of those affected. If patients survived, the running processes could lead to a long COVID, Avindra Nath speculates. It is possible that this immune response persists to some extent in patients with long-term COVID and causes nerve damage and neurological symptoms, says Nath. Therapies that alleviate these adverse events have the potential to help those affected. The build-up of immune complexes in the blood vessels, which has led to turbulence, must be prevented.

In fact, a study led by Avindra Nath begins in the US in the coming weeks to see if immune suppression drugs can help those affected by long-term COVID. Scientists are testing the drug methylprednisolone, which inhibits inflammation, as well as high-dose immunoglobulin preparations, which are used, among others, in some autoimmune diseases.

It is not yet known exactly why they can mitigate an attack on the body’s own tissue, such as in multiple sclerosis. Presumably highly concentrated antibody preparations inhibit the production of autoantibodies and reduce the release of inflammatory substances.

About which the investigation does not make any statements

It is still unknown which antigen triggers the erroneous immune response. Also, why some people have neurological complications and others don’t. Immune complexes of antibodies and viral spike proteins may have formed. They accumulated at the ACE-2 receptor on the vessel wall and thus triggered inflammatory processes.

Or, during the immune response, autoimmune antibodies have developed that bind not to the coronavirus’s spike protein, but to its “opposite” protein, the ACE2 protein on the cells of the vessel wall. Based on the results of these studies, one can only speculate whether similar mechanisms actually form the basis of Long COVID.

Sources used:

  • Oxford University Press: Neurovascular injury with complement activation and inflammation in COVID-19
  • Alzheimer’s Association: Alzheimer’s-like signaling in the brains of COVID-19 patients
  • National Library of Medicine: Microvascular Injury in COVID-19 Patients Brains
  • Science.org: Here’s what we know about the effects of COVID-19 on the brain
  • ClinicalTrials.gov: Neurological immunotherapy after the acute sequelae of SARS-CoV-2
  • Medical journal: Autoimmune diseases: wider use of immunoglobulins
This post is from the RiffReporter journalism portal. On riffreporter.de, around 100 independent journalists report together on current affairs and general information. RiffReporter received the Grimme Online Award for its offer.

Long COVID is a disease clearly defined by the World Health Organization. It usually occurs three months after a corona infection. One of the most common symptoms is: “brain fog”, also known as brain fog.

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