Today’s successful young people, who have mocked that they were the cause of Covid-19, should be preparing to develop Parkinson’s disease or Alzheimer’s in a few decades, when they are in their 60s.
Sars-Cov-2 virus can activate the same inflammatory response in the brain as Parkinson’s disease, inducing a potential risk of neurodegenerative disease in the future, according to a new study by scientists from the University of Queensland, Xinhua reports, via Ziare. com.
“We investigated the effect of the virus on the brain’s immune cells, ‘microglia’, which are key cells involved in the progression of brain diseases such as Parkinson’s and Alzheimer’s,” said Trent Woodruff, co-author and professor of pharmacology at the University of Queensland.
Using blood from a human donor, the researchers cultured the microglia in the laboratory and infected the cells with the SARS-CoV-2 virus. They found that the cells “actually got angry, activating the same pathway that Parkinson’s and Alzheimer’s proteins can activate in the disease, the inflammasome,” Woodruff added.
According to the study published in the journal Molecular Psychiatry by the Nature portfolio, the spike protein of the COVID-19 virus was sufficient to activate and trigger the inflammasome, which could initiate a chronic and prolonged process of killing neurons.
“So if someone is already predisposed to Parkinson’s disease, having COVID-19 could be like pouring more fuel on that ‘fire’ in the brain,” Woodruff warned.
Woodruff told Xinhua that the team is interested in continuing to study different variants of the spike protein on microglia because they believe that “some newer variants may have an even stronger response.”
Examining the long-term impact of a previous COVID-19 infection on the brain is also the next goal for the researchers.
“We are interested in infecting mice with the virus, letting them heal, and then monitoring the mice for motor and cognitive symptoms as they age.
Furthermore, we can induce Parkinson’s disease in mice, to see if they have an exacerbated response, after post-infection recovery, “the scientist said.
