COVID-19 immune response could be causing brain damage, study finds

NIH researchers said the body’s own defenses, triggered by the virus, are attacking cells within the brain’s blood vessels. The insight could have implications for treating patients.

Some of those who have been infected with COVID-19 can develop neurological problems, and researchers say they have gained new insight on what is happening in those patients.

In a study published in Brain, researchers with the National Institutes of Health said they found the body’s own defenses actually damaged blood vessels in the brain. NIH researchers examined nine patients who died after they were infected with the coronavirus.

The study found the virus didn’t appear to be infecting the brain, but it was the immune system’s antibodies that attacked and damaged cells within the brain’s blood vessels.

It’s an admittedly small study, but it could provide valuable insight into neurological problems tied to COVID-19, and present new opportunities to develop different treatments and therapies, researchers said.

Researchers at the National Institute of Neurological Disorders and Stroke, a division of the NIH, performed the study.

Avindra Nath, M.D., clinical director at NINDS and the senior author of the study, said she thinks the research has shed light into what’s happening in COVID-19 patients with neurological symptoms.

“Patients often develop neurological complications with COVID-19, but the underlying pathophysiological process is not well understood,” Nath said in an NIH news release. “We had previously shown blood vessel damage and inflammation in patients’ brains at autopsy, but we didn’t understand the cause of the damage. I think in this paper we’ve gained important insight into the cascade of events.”

Each of the patients died between March and July 2020, during the first wave of the pandemic. The patients, who ranged in age from 24 to 73, were examined because they showed signs of blood vessel damage in the brain, the NIH said.

The patients studied did not have serious damage to their lungs. The researchers speculated the patients would have likely developed long-COVID, if they had survived.

“Since several of the patients in our series died suddenly with very minor lung involvement, we believe that had these patients survived they would probably have progressed to develop long-COVID. Hence the pathological findings here are relevant to this population as well,” the authors wrote.

Some of the neurological symptoms after COVID infection include “brain fog,” fatigue, headaches, and loss of taste and smell.

In the NIH news release accompanying the study, Nath said understanding the immune response and its role in neurological damage could present opportunities to help patients.

“It is quite possible that this same immune response persists in Long COVID patients resulting in neuronal injury,” Nath said in a statement. “There could be a small indolent immune response that is continuing, which means that immune-modulating therapies might help these patients. So these findings have very important therapeutic implications.”

The authors found that immune complexes damaged minute blood vessels, resulting in the breakdown of the blood-brain barrier, which protects the brain from viruses, bacteria or parasites.

“We postulate that these events are central to the development of the neurological manifestations seen in acute COVID-19 and possibly in long-COVID,” the authors wrote. “Importantly, these studies suggest that therapeutic approaches targeted against the development of immune complexes should be considered.”

Patient advocates and some lawmakers have grown impatient with the pace of the NIH’s research, particularly into long COVID.

U.S. Sens. Sheldon Whitehouse, D-R.I., and Ed Markey, D-Mass., wrote a letter to the NIH in May to express their disappointment about progress in studies of long COVID. The lawmakers said they understand basic research is necessary but also said the agency must focus on therapies for those currently struggling with long COVID.