Researchers at the Brain Health Imaging Centre have identified a 16% to 20% reduction in dopamine-releasing neurons in patients with long COVID, according to a study published July 10, 2026, in eBioMedicine. This physical evidence correlates with persistent symptoms like memory loss, fatigue, and motor slowing, suggesting a potential shift toward dopamine-targeted therapies.
Dopamine System Injury as a Biological Marker
For years, individuals living with long COVID have reported debilitating neurological symptoms that often failed to appear on standard clinical tools like structural magnetic resonance imaging (MRI) scans. The absence of visible lesions on conventional scans led some physicians to dismiss these symptoms as psychological. However, new research suggests the root cause may be a measurable disorder of the brain’s dopamine system.

In a study led by the Centre for Addiction and Mental Health (CAMH) in Toronto, researchers used positron emission tomography (PET) imaging to examine 24 adults with long COVID against a control group of 24 healthy individuals. The team focused on a protein called vesicular monoamine transporter 2 (VMAT2), which serves as a marker for the density of dopamine nerve terminals. The findings revealed that patients with long COVID had significantly lower levels of VMAT2, indicating reduced dopamine nerve terminal density in key brain regions compared with the control group.
Mapping Regional Deficits to Clinical Symptoms
The study found that the specific location of dopamine neuron loss closely matched the symptoms reported by patients. Susan Deuville, a lived experience research advisor to senior study author Jeffrey Meyer, caught COVID in 2021 and never fully recovered. She participated in the study, which identified that the pattern of damage varied by region in ways that matched each patient’s specific symptoms. For five years I have been seeking answers on what happened to me after I contracted COVID in 2021,
Deuville said in a press release. It was a crush.
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Long COVID is estimated to affect approximately nine million adults in the United States and about 5% of the global population, including two million Canadians. The condition is characterized by a wide range of persistent symptoms that continue for at least three months following the initial infection. Despite its prevalence, no evidence-based treatments currently exist, largely due to a limited understanding of the underlying brain pathology.
Scientific Context and Future Directions
This new research builds on earlier work from the same team at CAMH that had found inflammation in these same regions. While some researchers have explored the theory that long COVID involves ongoing brain inflammation, a separate study from the University of Turku in Finland reported, We did not observe evidence of widespread brain inflammation in patients with long COVID when compared to healthy controls.
Instead, that study found that patients with more severe symptoms showed increased activity in brain regions linked to emotion, stress, and memory.

The CAMH study published in eBioMedicine provides what is described as the strongest evidence to date that long COVID is associated with injury to dopamine-releasing neurons. These findings suggest that dopamine-targeted treatments could potentially be repurposed to help treat long COVID symptoms. Because the biology of the brain is complex, patients experiencing persistent symptoms are encouraged to consult with qualified medical professionals to discuss these findings and their personal health circumstances. As no evidence-based treatments are currently established for this specific pathology, professional guidance remains the appropriate next step for those seeking to manage symptoms like fatigue, brain fog, or memory decline.