A new COVID study has found that its effect on the brain is similar to that of dementia.
Experts say that while the brain’s inflammatory response to COVID is a ‘silent killer’, a treatment for Parkinson’s disease could potentially ‘put out the fire’.
Research led by the University of Queensland and published Monday in the journal Nature Molecular Psychiatry tested the virus on lab-grown human immune cells called microglia.
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These cells are “involved in the progression of brain diseases like Parkinson’s disease and Alzheimer’s disease”, said Professor Trent Woodruff of UQ.
“We found that the cells did indeed become ‘angry,’ activating the same pathway that Parkinson’s and Alzheimer’s proteins can activate in the disease, the inflammasomes,” Woodruff said.
A “fire” in the brain is ignited once this inflammasome pathway is triggered, which destroys neurons in the brain through a sustained process, said UQ postdoctoral researcher Dr. Eduardo Albornoz Balmaceda.
“It’s kind of a silent killer, because you don’t see any outward symptoms for many years,” Balmaceda said.
“This may explain why some people who have had COVID are more vulnerable to developing neurological symptoms similar to Parkinson’s disease.”
The report states: “It has become clear that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can affect multiple organs and tissues, including the brain.
“Neuroinflammation is a hallmark of neurodegenerative diseases.”
Fuel for the fire
For people predisposed to dementia diseases such as Parkinson’s disease or Alzheimer’s disease, with the proteins of the disease already in their brain, the process of neurodegeneration is exacerbated by COVID.
“If someone is already predisposed to Parkinson’s disease, having COVID could be like pouring more fuel on that ‘fire’ in the brain,” Woodruff said.
He said while the finding was concerning, the link could lead researchers to finding a treatment for the inflammatory response.
The study administered drugs developed by the university that are currently in clinical trials with patients with Parkinson’s disease, which Balmaceda says have had positive results.
“We found that it successfully blocked the COVID-activated inflammatory pathway, essentially putting out the fire,” Balmaceda said.
“The drug reduced inflammation in both COVID-infected mice and in microglia cells from humans, suggesting a possible therapeutic approach to prevent neurodegeneration in the future.”
More research is needed, but Woodruff said the discovery offers a better understanding of COVID and a potential new approach to addressing the long-term health implications of the virus.
