Long COVID Disrupts Brain Dopamine
PET scans revealed reduced dopamine neuron markers in patients with long COVID.
What if the root of long COVID's most frustrating neurological symptoms comes down to a single chemical messenger?
A study, published in eBioMedicine, from the Centre for Addiction and Mental Health (CAMH), suggests that the condition is a physical disorder of the brain's dopamine system.
Using specialized positron emission tomography (PET) scans, researchers found that patients with long COVID have a reduction in dopamine nerve terminals, explaining their struggles with memory, movement, and motivation.
The physical link between long COVID and dopamine
Millions of people worldwide live with the effects of long COVID, struggling daily with brain fog, fatigue, and memory loss. However, standard tools such as structural magnetic resonance imaging (MRI) scans usually show no brain damage. Since conventional scans showed nothing, many physicians dismissed these symptoms as simply psychological.
But the absence of a visible lesion on a standard MRI does not mean the brain is healthy; it may mean doctors are just using the wrong tools. To help patients, objective biological markers that shift the approach from describing symptoms to treating their physical causes are needed.
Previous research in this area has focused on inflammation and changes in brain metabolism. Earlier work by CAMH showed that long COVID patients have high levels of inflammation in brain regions rich in dopamine. However, researchers still lacked direct evidence of pathway injury in patients.
The new study aimed to see if long COVID symptoms are directly linked with injury to dopamine-releasing neurons. Using advanced molecular imaging, the team sought to find out whether the persistent symptoms represented a measurable brain network disorder.
Mapping dopamine system deficits to patient symptoms
The researchers compared 24 adults with long COVID against healthy individuals, using PET scans to measure a protein called VMAT2. All patients in the study had experienced mild or moderate initial COVID-19 infections, including the healthy controls.
VMAT2
VMAT2 is a transporter protein that acts as a marker at the terminals of dopamine-releasing nerves, indicating how healthy and dense the connections are.
Patients with long COVID had lower levels of this marker across all main regions of the striatum—the brain's hub for motivation, movement, and thinking. The team found a 20% reduction in the ventral striatum, a 16% reduction in the dorsal putamen, and a 17% reduction in the dorsal caudate.
The regional deficits mapped directly to patient symptoms. Lower markers in the ventral striatum correlated with severe apathy, reductions in the dorsal putamen were tied to slower movement, and marker loss in the caudate matched up with poorer memory.
The scale of the dopamine marker loss in the long COVID patients was comparable to what doctors typically observe in mild-to-moderate Parkinson's disease.
“We know that inflammation can injure dopamine neurons,” said corresponding author Dr. Jeffrey Meyer, a senior scientist at the Brain Health Imaging Centre. “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.”
Repurposing dopamine medications to treat long COVID
These findings provide concrete physical evidence of brain-level changes, which allows researchers to categorize patients biologically rather than relying on subjective symptoms.
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“Our findings provide compelling evidence that long COVID involves the loss of dopamine-releasing neurons,” said Meyer. “This kind of injury is well known to produce symptoms like lack of motivation and motor slowing, and may contribute to memory difficulties in other neurological conditions. Our results suggest a similar process is occurring in long COVID.”
For patients, this physical validation is an important turning point: “For five years I have been seeking answers on what happened to me after I contracted COVID in 2021,” said Susan Deuville, lived experience research advisor to Meyer. “It was a crushing loss of the life I had and the person I was before. The research of Meyer brings hope. It also validates what long COVID sufferers have always known—long COVID is real, and the effects are devastating.”
However, a lower PET signal does not necessarily prove permanent cell death. It could reflect temporary, adaptive changes in how nerves store dopamine. Confirming whether this damage is reversible requires longer studies and control groups with other psychiatric illnesses.
“These results indicate that long COVID is, at least in part, a disorder of the brain’s dopamine system,” said Meyer. “This suggests that repurposing medications that augment the function of dopamine-releasing neurons, including dopamine precursors and inhibitors of dopamine metabolism, could be a promising approach”.
To test this, the CAMH team is partnering with the University Health Network to launch clinical trials utilizing repurposed dopamine-boosting drugs.
Reference: Liu YK, Persaud D, Vieira EL, et al. Loss of vesicular monoamine transporter 2 in striatum of long COVID and relationship to neuropsychiatric symptoms. eBioMedicine. 2026:106339. doi: 10.1016/j.ebiom.2026.106339
This article is a rework of a press release issued by the Centre for Addiction and Mental Health. Material has been edited for length and content.
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