A study published in eBioMedicine on July 10, 2026, reveals that long COVID is linked to a 16-20% reduction in dopamine-releasing neurons in key brain regions, correlating with symptoms like apathy, motor slowing, and memory decline, according to research led by the Centre for Addiction and Mental Health (CAMH).
Dopamine System Injury Confirmed in Long COVID Patients
Brain imaging research published in eBioMedicine shows that long COVID is associated with significant injury to dopamine-releasing neurons, with patients experiencing 16-20% lower dopamine nerve terminal density in the striatum compared to healthy controls, according to a study led by Yuhan Karida Liu of the Centre for Addiction and Mental Health (CAMH). The findings, based on PET scans of 24 adults with long COVID and 24 healthy controls, reveal that reduced dopamine markers in specific brain regions correlate with symptoms like apathy, slowed movement, and memory problems.
These findings suggest that long COVID may involve injury to striatal dopaminergic neurons and that treatments to augment function of dopamine releasing neurons should be tested in long COVID, assessing impact on motivation, motor speed and memory decline,
the researchers wrote. The study, which expanded its control group to 43 participants, found that lower VMAT2 binding—indicating reduced dopamine neuron density—was observed in the striatum, according to AuntMinnie.
The research builds on earlier work by the same team, which identified elevated brain inflammation in long COVID patients. “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,” Jeffrey Meyer, MD, said in a CIDRAP statement.
Symptom Correlations and Clinical Implications
The study found that dopamine neuron loss mapped directly to specific symptoms. Lower markers in the ventral striatum were tied to apathy and cognitive complaints, reductions in the dorsal putamen correlated with slower performance on a finger-tapping test of motor speed, and lower binding in the dorsal caudate correlated with worse verbal memory performance, as reported by Drug Discovery from Technology Networks.
The research also highlights potential treatment avenues. 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,
the team suggested. This aligns with Inside Precision Medicine’s reporting that the dopamine system injury could open a potential biological explanation for persistent symptoms
and guide new therapies.
Future Trials and Broader Implications
The study’s authors plan to launch a clinical trial to test dopamine-targeted treatments. The trial, in collaboration with University Health Network, will evaluate whether restoring dopamine function can alleviate symptoms, as outlined in CAMH’s announcement.
Despite the study’s limitations, including its focus on patients with significant neuropsychiatric symptoms, the results offer hope for those with long-COVID-related neuropsychiatric symptoms. Deuville said the research “brings hope” and validates the experiences of long COVID sufferers. The study’s lead author, Yuhan Karida Liu of CAMH, emphasized that the findings provide compelling evidence that long COVID involves the loss of dopamine-releasing neurons,
as detailed in AuntMinnie.
