Brain fog, a variety of cognitive symptoms that affect memory, concentration, sleep and speech, is a common symptom in long-term COVID-19 patients. Scientists have been using stem cell research to model the virus' potential impact on the brain. One of the key roles of the brain's immune cells is to clear inactive synapses, or "old connections."

But excess amounts have been eliminated in models infected with COVID-19, which could explain why some people develop post covid brain symptoms. The next step is to study how different drugs suppress the changes seen in infected models, hopefully paving the way for effective treatments. For some people with COVID, symptoms persist for months or even years after the initial infection. This is often referred to as long covid brain fog.

Some people with long-term COVID complain of brain fog, which includes various cognitive symptoms that affect memory, concentration, sleep and speech. There is also growing concern over the finding that people with COVID are at increased risk of developing brain diseases such as dementia.

Scientists are trying to understand exactly how COVID infection affects the human brain. But it's hard to study because we can't do experiments on the post covid brain fog of living people. One way to address this problem is to create organoids, which are miniature organs grown from stem cells.

In a recent study, we created brain organoids slightly larger than a pinhead and infected them with SARS-CoV-2, the virus that causes COVID-19. In these organoids, we found that too many synapses were eliminated, more than you would expect to see in a normal brain.

Synapses are important because they allow neurons to communicate with each other. Still, eliminating a certain number of inactive synapses is part of normal brain function. When no longer needed, the brain essentially sheds old connections and makes way for new ones, allowing for more efficient function. One of the key functions of the brain's immune cells, or microglia, is to prune these inactive synapses.

The excessive elimination of synapses that we saw in our model of COVID infection could explain why some people develop cognitive symptoms during prolonged COVID.

similar to neurodegenerative diseases

Interestingly, this pruning process is thought to go awry in several diseases that affect the brain. In particular, excessive elimination of synapses has recently been linked to neurodevelopmental disorders such as schizophrenia and neurodegenerative diseases such as Alzheimer's and Parkinson's diseases.

By sequencing the RNA of individual cells, we can study how different cell types in organoids respond to the virus. We found that in our COVID-infected organoids, the pattern of genes that are turned on and off by microglia mimics changes seen in neurodegenerative diseases. This may go some way to explaining the link between COVID and the risk of certain neurological diseases.

possible therapeutic target

A limitation of our study is that our organoid models closely resemble fetal or early brains rather than adult brains. So we can't be sure that the changes we noticed in our study are necessarily reflected in the adult brain.

However, several post-mortem and imaging studies have reported neuronal death and reduced gray matter thickness in COVID patients, suggesting a similar scenario for infection-induced synapse loss in adults. If this proves to be a fruitful investigation, we believe our findings may point to a mechanism responsible for the persistence of cognitive symptoms following COVID and other viral infections that affect the brain. Part of the article is from How Long Will Symptoms Of Brain Fog Last After Being Infected With Covid-19? If you want to know more, please go to to continue reading.