A brain-imaging study from Toronto's Centre for Addiction and Mental Health has found direct evidence that long COVID is associated with damage to dopamine-releasing neurons, a finding researchers say could help explain the persistent fatigue, apathy and memory problems that define the condition for millions of patients.
The team used positron emission tomography to scan the brains of 24 adults with long COVID and 24 age-matched healthy controls, measuring a protein called VMAT2 that marks the density of functioning dopamine nerve terminals. Across all three major regions of the striatum — the brain area that governs motivation, movement and cognition — VMAT2 levels were 16 to 20 percent lower in long COVID patients than in controls.
Symptom patterns line up with brain regions
The location of the loss tracked with specific symptoms: lower VMAT2 in the ventral striatum correlated with greater apathy and loss of motivation, reductions in the dorsal putamen were tied to slower movement, and losses in the caudate were linked to worse memory performance. The results were published in the journal eBioMedicine.
"Our findings provide compelling evidence that long COVID involves the loss of dopamine-releasing neurons. This kind of injury is well known to produce symptoms like lack of motivation and motor slowing, and may contribute to memory difficulties."
— Dr. Jeffrey Meyer, CAMH Brain Health Imaging Centre, lead author
Long COVID is estimated to have affected roughly 8.3 percent of U.S. adults at some point, according to federal survey data, and fatigue and cognitive symptoms — often described as brain fog — remain among its most disabling and least understood features. Until now, no imaging study had identified a specific neurotransmitter system injured by the condition, leaving clinicians with few biological targets for treatment.
Meyer's group, described in a CAMH release distributed via EurekAlert, says the small case-control study needs to be replicated in a larger cohort, but the consistency between symptom severity and the location of neuronal loss strengthens the case for a real biological mechanism rather than a secondary effect of fatigue itself. The team is now preparing a clinical trial with Toronto's University Health Network to test whether drugs that boost dopamine signaling can ease fatigue, restore motivation and improve memory in long COVID patients — a trial that, if successful, would offer one of the first treatments aimed at a specific mechanism behind the condition rather than its symptoms alone.