Covid may trigger Parkinson’s, Alzheimer’s

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Australian researchers found that covid can activate the same inflammatory response as some neurodegenerative diseases.


Covid-19’s notorious spike protein has yet another trick up its sleeve, with University of Queensland researchers finding that it can trigger a similar neurological response to Parkinson’s and Alzheimer’s proteins.

The research team studied the effect of the virus on lab-grown human microglia cells, which form part of the brain’s immune defence and play a role in the progression of degenerative brain conditions.

Writing in Nature: Molecular Psychiatry, the authors found the spike protein could prime or activate the microglia via the ACE2 enzyme, which then promoted NLRP3 inflammasome activation (NOD-, LRR- and pyrin domain-containing protein 3), with that inflammation leading to the neurological symptoms seen in some covid survivors.

“Further, this process may be enhanced in the presence of neurodegenerative disease triggers such as ?-synuclein aggregates, supporting a possible role for covid-19 in triggering brain diseases such as Parkinson’s Disease.”

In other words, covid’s spike protein can anger the brain’s immune cells, switching on the same inflammasome pathway that Parkinson’s and Alzheimer’s proteins activate, and effectively triggering the onset of neurodegenerative diseases.

“So if someone is already predisposed to Parkinson’s, having covid-19 could be like pouring more fuel on that ‘fire’ in the brain,” lead author and neuroinflammation researcher Professor Trent Woodruff said.

“The same would apply for a predisposition for Alzheimer’s and other dementias that have been linked to inflammasomes.”

The good news, though, is that research has already started on treatments to inhibit NLRP3 inflammasome activation for use in Parkinson’s patients, which the study authors believe could also be used in covid-driven neurological manifestations.

Experimental NLRP3 inhibitors developed at UQ successfully blocked the inflammatory pathway activated by covid, and reduced inflammation in the lab-grown microglia cells.

“Further research is needed, but this is potentially a new approach to treating a virus that could otherwise have untold long-term health ramifications,” Professor Woodruff said.

Molecular Psychiatry 2022, online 1 November

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