Published: Tue. July 6, 2022 at 9:41 AM
Last updated: Tue. July 6, 2022 at 9:52 AM
A small new study published Tuesday by scientists at the U. S. National Institutes of HealthThe U. S. Food and Drug Administration suggests that the immune reaction brought on by coronavirus infections damages blood vessels in the brain and could be to blame for prolonged covid symptoms.
The paper, published in the journal Brain, was based on brain autopsies of nine other people who died suddenly after contracting the virus.
Instead of stumbling upon 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 localization may also explain why some other people have lingering effects of the infection, such as headaches, fatigue, loss of taste and smell, inability to sleep, and “brain fog,” and possibly also help design new remedies for the long covid.
NIH scientist Avindra Nath, lead author of the paper, said in a statement, “Patients increase neurological headaches with COVID-19, but the underlying pathophysiological procedure is not well understood. “
“In the past, we had shown blood vessel damage and inflammation at the autopsy of the patients’ brains, but we did not perceive the cause of the damage. I think in this article we have obtained vital data on the cascade of events. “
The nine people, aged 24 to 73, were chosen in the team’s previous examination because they showed symptoms of damage to the brain’s blood vessels on the scans.
Their brains were compared to those of 10 controls, and the team examined neuroinflammation and immune responses using a strategy called immunohistochemistry.
The scientists found that antibodies produced against COVID-19 mistakenly targeted the cells that shape the “blood-brain barrier,” a design designed to prevent destructive invaders from entering the brain while allowing ingredients through.
Damage to those cells can lead to protein leakage, bleeding, and clots, increasing the risk of stroke.
The leaks also cause immune cells called macrophages to rush to repair the damage, causing inflammation.
The team found that the overall cellular processes in the spaces targeted by the attack were severely disrupted, which had implications for things like their ability to detoxify and metabolism.
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The findings offer clues about the biology at play in patients with long-term neurological symptoms and could indicate new remedies, for example, a drug that targets the accumulation of antibodies in the blood-brain barrier.
“It’s quite conceivable that this same immune reaction will persist in Long Covid patients and lead to neuronal injury,” Nath said.
This would mean that a drug that reduces this immune reaction could be only for those patients, he added. “So those findings have very important healing implications. “