There’s new insight into so-called ‘zombie’ cells that can age the brains of Covid-19 patients, contributing to brain fog and memory loss.
Scientists have uncovered how to reverse the ageing effects of ‘zombie’ cells in Covid-19 patients, sparking fresh hope the findings could be used in Alzheimer’s research.
Senescent cells, also known as zombie cells, occur naturally as people age and can contribute to brain fog or memory loss as tissue is inflamed or degenerates.
University of Queensland scientists have confirmed Covid-19 accelerates the presence of those cells, after studying synthetic brains created from human stem cells.
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They then tested drugs on the synthetic brains to see if they could undo the damage, with the results published in peer-reviewed journal Nature Ageing.
Four drugs were found to be effective – navitoclax, ABT-737, fisetin, and a combination of dasatinib plus quercetin.
Lead researcher Dr Julio Aguado said they were found to rejuvenate the brain and reduce the effect of developing symptoms.
“More research is needed to fully understand the mechanisms at play, but this study marks a significant step forward in our knowledge of the intricate relationship between viral infections, ageing and neurological wellbeing,” Aguado said.
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He expects in the future the drugs will also be used to treat serious infections triggered by viruses other than Covid.
The study involved research from scientists in Australia, the UK, the US, Chile, Germany and Russia.
The findings are also significant due to the use of synthetic human brain models.
The study shows how they could be used for research that would otherwise be ethically fraught or difficult on humans, according to Professor Ernst Wolvetang.
“Our study beautifully demonstrates how human brain models can accelerate the pre-clinical screening of therapeutics, while also moving towards animal-free testing, with potentially global impacts,” Wolvetang said.
“This same method of drug screening could also help Alzheimer’s research and a whole host of neurodegenerative diseases where senescence is a driver.”