Australian research has shown that COVID-19 activates the same neuroinflammatory response as Parkinson’s disease.
The discovery identifies a potential future risk for neurodegenerative conditions in people who’ve had COVID-19, but also a possible treatment, according to a Queensland University team led by Professor Trent Woodruff.
The team studied the effect of the virus on human microglia by infecting lab-grown cells, finding that SARS-CoV-2 isolates could bind and enter human microglia in the absence of viral replication.
SARS-CoV-2 was also shown to promote microglial NLRP3 inflammasome activation, a major driver of neurodegeneration.
Co-investigator Dr Eduardo Albornoz Balmaceda said triggering the inflammasome pathway sparked a long term neurodegenerative process in the brain.
“It’s kind of a silent killer, because you don’t see any outward symptoms for many years,” he said.
“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 also found the purified SARS-CoV-2 spike glycoprotein was able to activate the inflammasome pathway in microglia and this was further exacerbated when there were already in LPS-primed proteins in the brain linked to Parkinson’s.
“Spike protein also could prime the inflammasome in microglia through NF-κB signalling, allowing for activation through either ATP, nigericin or α-synuclein,” their paper (link here) in Nature Molecular Psychiatry noted.
“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,” said Professor Woodruff.