Coronavirus: Abnormal proteins which cause Alzheimer's could be responsible for COVID-19 neurological symptoms, blood clots; study says

The cause of the many mysterious and lingering symptoms brought on by COVID-19 has remained a difficult puzzle for scientists and health professionals. Researchers have been looking into various systems in the body to find the cause behind various short-term and long-term symptoms caused by SARS-CoV-2, the virus that causes COVID-19.

A recent study, published in the Journal of American Chemical Society, has provided a suggested mechanism to explain why some people develop complicated COVID-19 symptoms after infection. One such symptom has been micro clots in people with long COVID.

Researchers of the new study found that amyloids, the abnormal proteins that are also known to cause Alzheimer’s, could be formed during SARS-CoV-2 infection, which could explain some of the symptoms experienced. The research suggests that the immune system’s interaction with SARS-CoV-2 may be resulting in blood clots and neurological symptoms, due to the production of these misfolded spike proteins.

Amyloids are fibrous, abnormal protein structures that can build up in the body. These amyloids are present in a variety of disorders, such as Alzheimer’s disease, a condition that affects thinking and memory. Certain amyloids are also associated with several other health problems, such as – cardiac arrhythmias (Improper beating of the heart when electrical impulses in the heart don't work properly), atherosclerosis (buildup of fats, cholesterol and other substances in and on artery walls), type 2 diabetes mellitus (a chronic disease characterized by high levels of sugar in the blood) and rheumatoid arthritis (an autoimmune and inflammatory disease wherein the immune system attacks healthy cells in the body by mistake).

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In the present study, researchers sought to examine if the spike protein in SARS-CoV-2 could be converted to amyloids in the body. The spike protein or S-protein plays a major role in the virus’ transmission and evolution. The researchers found that several components of the S-protein could potentially produce amyloids.

When the study authors combined the S-protein in vitro with neutrophil elastase—a proteolytic enzyme (protease) that is produced in the human body by a type of white blood cell released early in SARS-CoV-2 infection called neutrophils—the researchers found that the S-protein broke up into sections that could lead to amyloid production. They also found that combining the S-protein with protease neutrophil elastase formed amyloid-like fibrils. Further research in this study looked at the relationship between the S-protein and blood clot formation.

Study author Sofie Nystrom explained that under normal circumstances, when we get an injury, fibrinogen (that we have in our bloodstream) is transformed into fibrin to form clots. To prevent ‘overclotting,’ there is another blood component, plasmin, that will dissolve the fibrin clots when there are enough and ultimately get rid of all fibrin when it is not needed anymore. “Our experiment shows that if fibrin is formed in the presence of spike amyloid, the plasmin can not totally remove the fibrin clots.”

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Dr. Arturo Casadevall, an infectious disease expert at John Hopkins University in Baltimore, who was not involved in the study, has expressed skepticism about amyloid production being the cause of the neurological side effects seen in people with COVID-19. “To infer that these amyloid structures are responsible for the neurological effects is too speculative at this time simply because there is no evidence that such structures are produced during human infection.” The findings of the study don’t infer that COVID-19 infection increases a person’s risk of developing dementia.