Long COVID is linked to measurable damage in the brain’s dopamine system, according to a peer-reviewed study published in eBioMedicine. Researchers used positron emission tomography (PET) imaging to examine dopamine-releasing neurons, discovering that patients suffering from persistent neuropsychiatric symptoms show a significant reduction in dopamine nerve terminal density compared to healthy individuals.
Brain Scans Reveal Dopamine Damage
The study provides biological evidence that long COVID affects the striatum, a deep brain structure rich in dopamine-producing neurons that regulates motivation, learning, and physical movement. According to the findings, participants with long COVID exhibited lower levels of vesicular monoamine transporter 2, a protein that acts as a microscopic pump to package dopamine into cellular sacs for release. Jeffrey Meyer, a senior research scientist and professor in the department of psychiatry at the University of Toronto who authored the study, utilized imaging tools originally developed to measure brain inflammation in psychiatric illnesses. “When I discovered evidence for brain inflammation in long COVID, I noticed that the greatest elevations in the inflammation marker were in regions where there are nerve terminals that release dopamine,” Meyer stated according to published reports (psypost.org).
Connection Between Dopamine Loss and Clinical Symptoms
The imaging results closely matched the specific clinical symptoms reported by patients. Lower dopamine markers in the ventral striatum correlated with a profound lack of motivation and difficulty experiencing pleasure. Reductions in the dorsal putamen aligned with a slowing of physical movements, while lower marker levels in the caudate were linked to poorer memory performance. These persistent issues affect an estimated nine million adults in the United States and approximately 5% of the global population, according to epidemiological data cited in the research. The condition is clinically defined by symptoms persisting for at least three months after the initial acute SARS-CoV-2 infection.
Implications for Future Treatments
Researchers suggest that identifying physical damage to the dopamine system points toward new therapeutic directions. Because specific cells producing dopamine contain high levels of the receptor proteins that the COVID-19 virus uses to enter human cells, viral entry may directly contribute to terminal loss alongside inflammatory damage. Therapeutics already approved for other neurological conditions that increase dopamine availability or inhibit dopamine metabolism could potentially be repurposed to treat cognitive and motor symptoms in long COVID patients.