WHAT YOU NEED TO KNOW
  • Brain scans found substantially lower levels of a dopamine neuron marker across major striatal regions in people with long COVID.
  • Different patterns of marker loss were associated with reduced motivation, slower movement, and memory difficulties.
  • Earlier research found elevated inflammation in brain regions containing many dopamine-releasing neurons.
  • Researchers plan a clinical trial testing whether modifying dopamine activity can improve memory, motivation, and fatigue.

A brain imaging study led by scientists at the Centre for Addiction and Mental Health has produced what researchers describe as the strongest evidence yet that long COVID is associated with damage to dopamine-releasing neurons. The findings were published in eBioMedicine.

The results may help explain persistent symptoms including fatigue related loss of motivation, slower movement, memory difficulties, and brain fog. Researchers say the discovery could also open new paths for treating a condition that currently has no evidence based therapies.

Long COVID is estimated to affect about 5% of the global population, including approximately two million people in Canada. Its wide range of symptoms continues for at least three months after the initial COVID-19 infection.

Brain related symptoms commonly include fatigue, memory problems, low mood, and brain fog. Although the condition is widespread and disruptive, scientists still do not fully understand the biological changes occurring in the brain.

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For the study, researchers used positron emission tomography, known as PET, to measure biological activity in the brain. They examined a widely used marker associated with the health and integrity of dopamine neurons in people with long COVID.

The research team then compared those scans with results from healthy participants. People with long COVID had substantially lower levels of the marker across all major areas of the striatum, a collection of brain regions involved in motivation, movement, and thinking.

Lower levels of the marker suggest that people with long COVID may have a reduced density of dopamine nerve terminals. The patterns of marker loss also differed according to the symptoms participants experienced.

Lower marker levels in the ventral striatum were associated with a greater loss of motivation. Reductions in the dorsal putamen were connected with slower movement, while lower levels in the caudate putamen were associated with memory difficulties.

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“Our findings provide compelling evidence that long COVID involves the loss of dopamine-releasing neurons,” said Dr. Jeffrey Meyer, Senior Scientist at the Brain Health Imaging Centre, Canada Research Chair, and senior author of the study.

Meyer said this type of injury is known to cause symptoms such as reduced motivation and motor slowing. It may also contribute to memory difficulties in other neurological conditions, suggesting that a similar biological process may be occurring in long COVID.

The findings build on earlier work by the same research team, which found unusually high levels of brain inflammation in people with long COVID. That inflammation appeared particularly pronounced in regions containing large numbers of dopamine-releasing neurons.

“We know that inflammation can injure dopamine 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 explained.

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Taken together, the studies suggest a possible connection between persistent brain inflammation and damage involving the dopamine system. The new results also shift attention toward dopamine-releasing neurons, which have been the direct focus of very few clinical trials compared with inflammation and immune activity.

“These results indicate that long COVID is, at least in part, a disorder of the brain's dopamine system,” Meyer said. He added that medications designed to augment dopamine neuron function, including dopamine precursors and inhibitors of dopamine metabolism, could offer a promising research direction.

The findings may also provide biological validation for patients whose symptoms can be difficult for others to measure. Susan Deuville, a lived experience research advisor to Meyer, said she had spent five years seeking answers about what happened after she contracted COVID in 2021.

“It was a crushing loss of the life I had and the person I was before. The research of Dr. Meyer brings hope,” Deuville said. She added, “It also validates what long COVID sufferers have always known -- long COVID is real and the effects are devastating.”

Researchers plan to begin a clinical trial within the upcoming couple of months that will target dopamine function in people with long COVID. The trial will examine whether modifying dopamine activity can improve memory, motivation, and fatigue.

The trial will be conducted with University Health Network as part of a partnership between the hospitals intended to bridge mental and physical health care. The study was supported by the Canadian Institutes of Health Research.