Researchers at the Centre for Addiction and Mental Health in Toronto found that a selected group of people with long COVID had lower levels of a marker of dopamine nerve endings in three areas of the brain. These changes were statistically associated with apathy, slowed movements and poorer performance on memory tests. The study was published on 10 July 2026 in the journal eBioMedicine.
Briefly about the main points
- The VMAT2 marker was lower in three brain regions by 16–201 TP3T.
- Lower scores in certain areas were associated with apathy, motor function and memory.
- All patients had previously had mild or moderate COVID.
- PET does not prove neuronal death or the direct cause of the symptoms.
- The researchers plan to investigate approaches to enhancing dopamine transmission.
PET assessed the nerve ending marker
The researchers used positron emission tomography to measure the binding of the type 2 vesicular monoamine transporter — VMAT2. This protein serves as a marker of the state of nerve endings that release dopamine. Dopamine itself plays a role in regulating motivation, learning, movement and other brain functions.
Statistically significant differences were observed in the ventral striatum, the dorsal part of the putamen and the dorsal caudate nucleus. In these structures, the index was lower by 20%, 16% and 17%, respectively. The ventral striatum is involved in motivational processes, the putamen in motor control, and the caudate nucleus in cognitive processes and memory.
The localisation of the differences was compared with individual symptoms
Participants with lower VMAT2 scores in the ventral striatum exhibited more pronounced apathy. Changes in other regions were associated with slower movements, whilst a lower score in the caudate nucleus correlated with poorer memory test results.
Senior author of the study, researcher at CAMH Jeffrey Meyer, stated that the results provide strong grounds for suspecting a disruption of the dopamine system during prolonged COVID. The authors consider it to be one of the possible mechanisms underlying post-COVID symptoms and draw attention to a possible link with previously identified signs of neuroinflammation.
The participants experienced symptoms following a mild course of the infection
The baseline comparison involved 24 people with long COVID and 24 healthy volunteers of a similar age. All patients had previously experienced a mild or moderate infection. The average age of this group was around 32 years, and between two and 56 months had elapsed between the acute phase of the illness and the examination.
The control group was subsequently expanded to 43 healthy individuals, and the key findings remained statistically significant. However, the sample size was small, and patients were selected on the basis of having pronounced symptoms. Therefore, these findings cannot automatically be generalised to everyone who has had coronavirus.
The study does not establish the cause of the changes nor does it suggest a treatment
PET scans do not allow for a direct count of lost neurons. Consequently, a lower level of the marker is not conclusive evidence of the physical destruction of dopaminergic neurons. The study also does not determine whether these changes are irreversible, nor does it imply that all cases of fatigue or apathy share the same underlying mechanism.
Researchers plan to investigate whether approaches aimed at enhancing dopamine transmission can improve patients’ motivation, memory and well-being. The effectiveness of such treatment has not yet been proven, so the results do not justify self-medicating with drugs that affect the dopamine system. Larger-scale studies are needed to assess the causes, duration of changes and treatment options.
