PET scans show reduced dopamine neuron markers in long COVID patients, linking dopamine loss to fatigue, motivation loss, slowed movement and memory problems.
A PET imaging study led by researchers at the Centre for Addiction and Mental Health (CAMH) reported substantially lower levels of a vesicular monoamine transporter 2 marker—a proxy for dopamine‑releasing neuron density—across all major regions of the striatum in people with long COVID compared with healthy controls. The reductions correlated with specific symptoms: lower ventral striatum levels with loss of motivation, dorsal putamen reductions with slower movement, and caudate putamen decreases with memory difficulties.
The investigators noted that earlier CAMH work had identified heightened brain inflammation in the same regions, and Dr. Jeffrey Meyer explained that inflammation can injure dopamine neurons, suggesting a link between persistent inflammation and the observed dopamine loss. He described the findings as “compelling evidence that long COVID involves the loss of dopamine‑releasing neurons” and suggested that medications enhancing dopamine function could be explored as treatments.
Building on these results, the team plans a clinical trial, in partnership with University Health Network and funded by the Canadian Institutes of Health Research, to test whether targeting dopamine activity improves motivation, fatigue and memory in long COVID patients. The current evidence is limited to imaging biomarkers and symptom associations; the efficacy of dopamine‑focused therapies remains unproven.