Is COVID-19 merely a respiratory illness, or is it messing with our brains?
A recent study by the Washington University School of Medicine in St. Louis estimates that more than 40 million people worldwide, or 7 in 100 COVID-infected patients, developed persistent neurological symptoms in the first year after infection. People who contracted the virus were more likely to experience ‘brain fog’ (cognitive and memory problems), develop mental health disorders such as anxiety or depression, and suffer from seizures and strokes. These findings add to a growing body of evidence that suggests COVID-19, in triggering neuroinflammation, alters our nervous system and reshapes our brains even after the initial viral infection.
Early in the pandemic, autopsy findings of patients who died of COVID-19 did not show brain inflammation or other changes attributable to the virus. At the same time, cerebrospinal fluid (the liquid around our brain and spine) of patients with neurological illnesses resulting from COVID-19 showed no trace of the virus, leading medical professionals to mistakenly conclude that the SARS-CoV-2 virus did not harm the brain. However, a British study published earlier this year demonstrated otherwise.
Analyzing brain imaging data from the UK Biobank, the researchers found that even a mild infection can shrink the brain and reduce the thickness of neuron-rich gray matter (brain cells responsible for processing and transmitting information). These brain changes appeared to be more pronounced in the frontal and temporal lobes of the brain (brain regions responsible for memory, cognitive, and motor function), which could help to explain why COVID-19 patients experienced brain impairments.
Using experiments on mice, neuroscientists like Michelle Monje from Stanford University investigated how the SARS-CoV-2 virus harms the brain without directly infecting it. Her research shows that inflammatory molecules released in the lungs travel to the brain via the blood and activate the brain’s immune cells during an infection. These immune cells, known as the microglia and astrocytes, go into overdrive to fight the virus, causing unnecessary pruning of neuronal connections and the loss of insulating coats on neurons, affecting their communication ability.
Apart from immune-system-mediated injury, the SARS-CoV-2 virus may damage blood vessels, which deprives the brain of its much-needed oxygen and fuel supply. The virus may also cause a loss of integrity of the brain’s protective Blood-Brain-Barrier, resulting in swelling and direct injury to the brain.
The bad news is that post-COVID neurological disorders are becoming more common in younger patients (below 50 years old), even those with mild infections. The good news is that the symptoms may not be permanent or progressive. Nevertheless, this mounting burden of neurological illnesses is alarming. Given its debilitating impact, there is an urgent need to understand the cellular changes behind the neurological risk of COVID-19, so we can intervene and offer more effective therapies.