COVID-19 activates the same inflammatory response in the brain as Parkinson’s disease, new research in human cells and mice suggests.
The paper identifies a potential future risk for neurodegenerative conditions in people who’ve had COVID-19, but also a possible treatment.
“We studied the effect of the virus on the brain’s immune cells, ‘microglia’ which are the key cells involved in the progression of brain diseases like Parkinson’s and Alzheimer’s,” says study author Trent Woodruff, professor at the University of Queensland’s School of Biomedical Sciences.
“Our team grew human microglia in the laboratory and infected the cells with SARS-CoV-2, the virus that causes COVID-19. We found the cells effectively became ‘angry’, activating the same pathway that Parkinson’s and Alzheimer’s proteins can activate in disease, the inflammasomes.”
Study author and professor Eduardo Albornoz Balmaceda says triggering the inflammasome pathway sparked a ‘fire’ in the brain, which begins a chronic and sustained process of killing off neurons.
“It’s kind of a silent killer, because you don’t see any outward symptoms for many years,” Albornoz Balmaceda says. “It may explain why some people who’ve had COVID-19 are more vulnerable to developing neurological symptoms similar to Parkinson’s disease.”
The researchers found the spike protein of the virus was enough to start the process and was further exacerbated when there were already proteins in the brain linked to Parkinson’s.
“So if someone is already pre-disposed to Parkinson’s, having COVID-19 could be like pouring more fuel on that ‘fire’ in the brain,” Woodruff says. “The same would apply for a predisposition for Alzheimer’s and other dementias that have been linked to inflammasomes.”
But the study also indicates a potential treatment.
The researchers administered a class of inhibitory drugs which are currently in clinical trials with Parkinson’s patients.
“We found it successfully blocked the inflammatory pathway activated by COVID-19, essentially putting out the fire,” Albornoz Balmaceda says. “The drug reduced inflammation in both COVID-19-infected mice and the microglia cells from humans, suggesting a possible treatment approach to prevent neurodegeneration in the future.”
Woodruff says that while the similarity between how COVID-19 and dementia diseases affect the brain was concerning, it also meant a possible treatment was already in existence.
“Further research is needed, but this is potentially a new approach to treating a virus that could otherwise have untold long-term health ramifications.”
The study appears in the journal Molecular Psychiatry.
Source: University of Queensland
