A small new study released Tuesday by scientists at the US National Institutes of Health suggests the immune response triggered by coronavirus infections damages the brain’s blood vessels and could be responsible for long-lasting Covid symptoms.
The paper, published in Brain magazine, was based on brain autopsies of nine people who died suddenly after contracting the virus.
Instead of finding evidence of Covid in the brain, the team found that it was people’s own antibodies that attacked the cells lining the brain’s blood vessels, causing inflammation and damage.
This discovery could explain why some people experience lingering effects from infections, including headaches, fatigue, loss of taste and smell, and trouble sleeping, as well as “brain fog” – and could also help develop new treatments for long Covid.
NIH scientist Avindra Nath, the paper’s senior author, said in a statement, “Patients often develop neurological complications with COVID-19, but the underlying pathophysiological process is not well understood.”
“We had previously shown blood vessel damage and inflammation in the brains of patients at autopsy, but we did not understand the cause of the damage. I think that in this paper we have gained important insights into the cascade of events.”
The nine people, aged 24 to 73, were chosen from the team’s previous study because scans showed evidence of blood vessel damage in their brain.
Their brains were compared to those of 10 controls, with the team examining neuroinflammation and immune responses using a technique called immunohistochemistry.
The scientists discovered that antibodies produced against Covid-19 wrongly targeted cells that make up the “blood-brain barrier” – a structure designed to keep harmful invaders out of the brain while allowing necessary substances to pass through.
Damage to these cells can lead to protein leakage, bleeding, and blood clots, all of which increase the risk of stroke.
The leaks also trigger immune cells called macrophages to rush to the site to repair damage, leading to inflammation.
The team found that normal cellular processes in the areas affected by the attack were severely disrupted, impacting things like their ability to detoxify and regulate metabolism.
The findings offer clues to the biology at play in patients with long-term neurological symptoms and may inform new treatments — for example, a drug that targets antibodies building up at the blood-brain barrier.
“It’s entirely possible that the same immune response persists in long-COVID patients, resulting in neuronal injury,” Nath said.
This would mean that a drug that weakens this immune response could help these patients, he added. “So these results have very important therapeutic implications.”
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