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A new brain imaging study has found evidence that long COVID is associated with damage to dopamine-releasing nerve cells, potentially explaining persistent symptoms such as fatigue, loss of motivation, slower movement and memory problems.
The study, led by researchers at the Centre for Addiction and Mental Health (CAMH), was published in eBioMedicine. Researchers said the findings provide the strongest evidence so far of changes to the brain’s dopamine system in people with long COVID.
Long COVID can cause symptoms that persist for at least three months after an initial COVID-19 infection. Common neurological symptoms include fatigue, brain fog, memory problems and low mood. The condition is estimated to affect about 5 per cent of the global population, including around two million people in Canada.
The researchers used positron emission tomography (PET) scans to examine a marker of dopamine neuron health in people with long COVID and healthy participants.
They found substantially lower levels of the marker in all major areas of the striatum, a group of brain regions involved in motivation, movement and thinking. The findings suggest a reduced density of dopamine nerve terminals.
The researchers also found links between the changes in specific brain regions and particular symptoms. Lower marker levels in the ventral striatum were associated with reduced motivation, while changes in the dorsal putamen were linked to slower movement. Lower levels in the caudate putamen were associated with memory difficulties.
“Our findings provide compelling evidence that long COVID involves the loss of dopamine-releasing neurons,” said Dr Jeffrey Meyer, senior scientist at CAMH’s Brain Health Imaging Centre and senior author of the study.
He said damage to dopamine neurons is known to cause symptoms including reduced motivation and slower movement, and may contribute to memory problems in other neurological conditions.
The findings build on earlier research by the same team showing unusually high levels of inflammation in the brains of people with long COVID. That inflammation was particularly pronounced in areas containing large numbers of dopamine-releasing neurons.
“While our earlier research showed high levels of inflammation in those regions, this study provides direct evidence that the dopamine neuron marker is reduced in the same regions — and that this loss correlates with patients’ symptoms,” Meyer said.
Researchers said the two studies together suggest that persistent brain inflammation may be linked to damage involving the dopamine system.
The findings could also open a new direction for long COVID research and treatment. Meyer said medicines that enhance the function of dopamine-releasing neurons, including dopamine precursors and drugs that inhibit dopamine metabolism, could be investigated as potential treatments.
However, the study does not establish that such drugs are effective for long COVID.
Researchers plan to launch a clinical trial in the coming months to investigate whether modifying dopamine activity can improve symptoms including memory problems, reduced motivation and fatigue.
The planned trial will be conducted in collaboration with University Health Network as part of a partnership aimed at linking mental and physical health care.
The study was supported by the Canadian Institutes of Health Research.