COVID-19 activates a similar inflammatory response in the brain to Parkinson's disease, a University of Queensland-led study suggests.
Lead researcher Trent Woodruff, from the university's neuro-inflammation laboratory, said the findings illustrated a potential future risk for neurodegenerative conditions in people who had been infected with SARS-CoV-2, the virus that causes COVID-19.
But he said it was too early for the study to cause alarm, with much more work needed into how the virus may affect the human brain.
"It may explain some of the symptoms that are occurring in patients with long COVID and brain fog," Professor Woodruff said.
"It's certainly something that we should be looking at and monitoring.
"But I want to emphasise, we're not saying from this work that everyone who's had COVID is going to end up getting Parkinson's disease."
UQ researchers studied the effect of SARS-CoV-2 on the brain's immune cells, known as microglia, which are key cells involved in the progression of brain diseases, such as Parkinson's and Alzheimer's disease.
They grew microglia from the donor blood of healthy volunteers and infected the cells with the virus.
"We identified that the cells became highly inflammatory, we like to think of them as angry microglia, and they turned on a pathway called the inflammasome, which we have previously shown is linked to certain brain diseases, like Parkinson's and Alzheimer's," Professor Woodruff said.
"It didn't matter whose blood it was or whose cells we looked at, all the cells reacted quite strongly to this virus."
The researchers also compared mice infected with SARS-CoV-2 and those which had not been infected with the virus.
They found inflammasome activation in the brains of the mice infected with SARS-CoV-2.
Possible treatment also identified
But the researchers, including Professor Woodruff's UQ colleague Eduardo Albornoz Balmaceda, also identified a potential treatment.
They gave the infected mice a UQ-developed drug, which is in human trials of Parkinson's disease patients.
The drug blocked the inflammatory pathway in the mouse brain that had been activated by COVID-19.
Dr Albornoz Balmaceda likened the effect of the drug to dousing "a fire" in the brain.
"The drug reduced inflammation in both virus-infected COVID-19 mice and the microglia cells from humans, suggesting a possible treatment approach to prevent neuro-degeneration in the future," he said.
Professor Woodruff said "dozens" of other drugs, designed to block the inflammasome pathway, were in development worldwide.
"We're hopeful that one of these therapies may make it all the way through to clinical application," he said.
The researchers said it was impossible to know from their study, published in the journal Molecular Psychiatry, whether inflammation in the brains of people infected with SARS-CoV-2 dissipated once the virus was cleared from the body.
"It may be that in most individuals that this is entirely what's happening," he said.
"You get an acute infection and you might get this potential inflammation in the brain but then that resolves and then everything goes back to normal."
But he said in people already pre-disposed to Parkinson's disease, having COVID-19 might be like pouring more fuel on that "fire" in the brain.
"There's a lot more research to be done," Professor Woodruff said.
"Our research is really just the first piece of the puzzle. I think it's important to start looking clinically in some of these individuals that may be susceptible to see if what we're discovering in the lab may also be true out in the population."
Infectious disease specialist Paul Griffin, who was not involved in the study, described the research as “extremely valuable” but was cautious about its findings.
“This is a good platform upon which more research can be based but it’s still very early,” Dr Griffin said.
“A lot of this makes sense with what we understand how the virus causes problems.
“A lot of the manifestations from the heart issues to the lung issues to the brain issues, they’re probably all inflammatory in nature.”
Dr Griffin said the study was another reason why it was important “that we still do what we can to reduce the burden” of the pandemic virus.
