Brain scans reveal a possible cause of long COVID fatigue and brain fog

A recent study conducted by researchers at the Centre for Addiction and Mental Health (CAMH) has provided evidence suggesting that long COVID may be linked to damage in dopamine-releasing neurons within the brain. The findings, published in eBioMedicine, could help explain lingering issues such as fatigue, slower movement, and memory problems associated with the condition.

Long COVID affects around five percent of the global population, or approximately two million people in Canada. Symptoms include fatigue, brain fog, memory issues, and low mood. However, there are currently no proven treatments, as scientists lack a full understanding of the physiological changes occurring in the brain. To investigate, researchers used positron emission tomography (PET) to measure biological activity in the brain.

They compared the results of individuals with long COVID to those of healthy participants, focusing on a well-established marker associated with dopamine neuron health. The study revealed significantly lower levels of this marker in people with long COVID across major areas of the striatum, a group of brain regions that play a role in motivation, movement, and cognitive function.

Different patterns of marker loss were associated with specific symptoms. Lower marker levels in the ventral striatum were linked to reduced motivation, while reductions in the dorsal putamen were connected to slower movement. Lower levels in the caudate putamen were associated with memory difficulties. The lead author, Dr. Jeffrey Meyer, a Senior Scientist at the Brain Health Imaging Centre, stated that these findings provide compelling evidence that long COVID involves the loss of dopamine-releasing neurons.

This type of injury is known to cause symptoms like lack of motivation and motor slowing, and may contribute to memory issues in other neurological conditions. The researchers believe these results suggest a possible connection between persistent brain inflammation and damage involving the dopamine system. The findings could change the approach to understanding the biology and treatment of long COVID, as previous research has primarily focused on inflammation and immune activity in the brain.

Dr. Meyer added that repurposing medications that enhance dopamine-releasing neuron function, such as dopamine precursors and inhibitors of dopamine metabolism, could be a promising approach. The study's findings might also offer a biological explanation for the symptoms experienced by long COVID sufferers, providing validation for the real and devastating effects of the condition.