It has been just revealed that neuroscientists found a way to reverse brain aging – they can kill zombie cells following COVID and you should definitely read more to find out how!
Neuroscientists can reverse zombie cells following COVID
Scientists have found that COVID-19 infection can accelerate premature aging in the brain. However, there is some good news – it may be possible to reverse this effect.
The University of Queensland in Australia conducted research using lab-grown mini-brains grown from human stem cells to investigate how different variants of SARS-CoV-2 can affect brain tissues.
Each of our cells functions as a tiny molecular factory, carrying out essential processes that our bodies need to survive.
The problem is that these processes produce harmful waste products that can accumulate in our cells over time, causing damage to our DNA and molecular machinery. At a certain point, these cells become inactive and unable to divide. Nevertheless, they remain active.
As we age, some cells in our body become senescent or “zombie” cells.
These cells can produce proteins and molecules that cause inflammation, leading to cognitive impairments like brain fog and memory loss.
When we are young, our immune systems can clear these cells, but as we age, more of them accumulate.
According to a study by Julio Aguado and his team at the Australian Institute for Bioengineering and Nanotechnology, SARS-CoV-2 can accelerate the accumulation of these zombie cells, which can lead to premature aging.
“We found COVID-19 accelerates the presence of ‘zombie’ or senescent cells, which accumulate naturally and gradually in the brain as we get older,” Aguado said.
“We used the brain organoids [aka the mini brains] to screen a range of therapeutics, looking for any capable of removing those senescent cells,” Aguado said.
In their study, published in the journal Nature Aging, the team found four common drugs selectively destroyed these COVID-induced zombie cells: navitoclax, ABT-737, fisetin and a combination of dasatinib and quercetin.
“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, aging and neurological well-being,” Aguado said.
“Long term, we can expect widespread use of these drugs to treat persistent post-acute infection syndromes caused by viral infections like COVID-19.”
