Health
covid: Long-lasting Covid infections may be the result of disconnections between nerve cells in the brain, study reveals
Some people who have been infected with the new coronavirus for a long time complain of “brain fog,” which includes various cognitive symptoms that affect memory, concentration, sleep, and speech. Concerns have also been raised about findings that people infected with Covid are at increased risk of developing brain disorders such as dementia.
Scientists work to understand exactly how Covid infection affects human brainHowever, this is difficult to study because it is not possible to experiment with living human brains. One way he gets around this is by creating organoids, small organs grown from stem cells.
A recent study created brain organoids slightly larger than pinheads and infected them with SARS-CoV-2, the virus that causes Covid-19.
They found that an excessive number of synapses (connections between brain cells) had been removed in these organoids. This is a higher number than you would expect to see in a normal brain.
Synapses are important for allowing neurons to communicate with each other. Still, removing a certain amount of inactive synapses is part of normal brain function. The brain basically gets rid of old connections that are no longer needed to make way for new ones, allowing it to function more efficiently.
One of the key functions of brain immune cells, or microglia, is to prune these inactive synapses.
The exaggerated removal of synapses seen in the Covid infection model could explain why some people have cognitive symptoms as part of long Covid.
Similarities to neurodegenerative diseases
Interestingly, this pruning process is thought to go awry in several disorders that affect the brain. It has been associated with neurodegenerative disorders such as Parkinson’s disease.
By sequencing the RNA of single cells, we were able to examine how different cell types in the organoids responded to the virus. We found that the pattern of genes turned on/off by microglia in Covid-infected organoids mimics changes seen in neurodegenerative diseases.
This may help explain some of the links between Covid and the risk of developing certain neurological disorders.
Potential therapeutic targets
One of the limitations of our study is that our organoid model closely resembles the fetal or early brain rather than the adult brain. Therefore, it is not certain whether the changes pointed out in our study are necessarily reflected in the adult brain.
However, several postmortem and imaging studies have reported neuronal cell death and decreased gray matter thickness in Covid patients, suggesting similar examples of synaptic loss caused by infection in adults.
If this proves to be a fruitful series of investigations, our findings may point to a mechanism that contributes to the persistence of cognitive symptoms after Covid and other viral infections that affect the brain. I believe there is.
SARS-CoV-2 is an RNA virus and similar processes are seen in mice infected with other RNA viruses, which can cause residual cognitive symptoms such as: west nile virus.
From here, we hope to study how different drugs can inhibit the changes seen in models of infection, paving the way for effective treatments. However, we observed that microglia can reduce the extent to which synapses are cleaved in the dish. increase.
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Sources 2/ https://economictimes.indiatimes.com/magazines/panache/long-covid-how-lost-connections-between-nerve-cells-in-the-brain-may-explain-cognitive-symptom/articleshow/95146148.cms The mention sources can contact us to remove/changing this article |
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