Brain scans reveal dopamine damage may explain long COVID fatigue and brain fog

For five years, Susan Deuville has been trying to understand what happened inside her brain after she caught COVID-19 in 2021. The fatigue that followed was not the kind that sleep fixes. The fog that settled over her thinking did not lift. She lost the life she had been living and, in a way that was hard to explain to people who had not experienced it, lost herself. Now, researchers at a Canadian brain imaging center have found something concrete in the scans: evidence that the virus may have damaged the very neurons responsible for motivation, movement, and memory.

Long COVID is estimated to affect roughly five percent of the world's population—about two million people in Canada alone. The condition persists for at least three months after the initial infection and can involve a bewildering range of symptoms, many of them centered in the brain. Fatigue, brain fog, memory problems, and low mood are among the most common complaints. Yet despite how widespread and disruptive the condition has become, there are no evidence-based treatments. Scientists have not fully understood what is actually happening inside the brain to cause these symptoms.

Using positron emission tomography—a brain imaging technique that measures biological activity—researchers examined a well-established marker of dopamine neuron health in people with long COVID and compared them to healthy controls. What they found was striking: substantially lower levels of this marker across all major regions of the striatum, a group of brain structures that regulate motivation, movement, and cognition. The reduction in these markers suggests that the density of dopamine nerve terminals has declined. More than that, the pattern of loss mapped onto the pattern of symptoms. People with lower marker levels in the ventral striatum experienced greater loss of motivation. Those with reductions in the dorsal putamen moved more slowly. Those with lower levels in the caudate putamen had memory difficulties.

Dr. Jeffrey Meyer, the senior scientist leading the research, describes the findings as compelling evidence that long COVID involves the loss of dopamine-releasing neurons. This type of injury is well known to produce exactly the symptoms long COVID patients report—lack of motivation, slowed movement, and cognitive impairment. The discovery builds on earlier work by the same team showing that people with long COVID have unusually high levels of inflammation in the brain, particularly in regions rich with dopamine neurons. The new study provides direct evidence that dopamine neuron damage occurs in those same inflamed regions, and that the degree of damage correlates with how severely patients experience their symptoms.

The implications for treatment are significant. Most previous research into long COVID has focused on brain inflammation and immune system changes. Very few clinical trials have targeted dopamine neurons directly. Meyer suggests that medications already known to enhance dopamine function—dopamine precursors and inhibitors of dopamine metabolism—could be repurposed to treat long COVID. The approach represents a shift in how researchers think about the condition's biology.

For people living with long COVID, the findings offer something that has been scarce: a biological explanation for symptoms that are often invisible to others and difficult to measure objectively. Deuville, who has been advising the research team based on her own experience, describes the work as bringing hope and validation. Long COVID is real, she says, and the effects are devastating.

The research team is planning to launch a clinical trial within the coming months to test whether modifying dopamine activity can improve memory, motivation, and fatigue in long COVID patients. The trial will be conducted in partnership with University Health Network, part of a broader effort to bridge the gap between mental and physical health care. The results could reshape how long COVID is understood and treated.