Brain scans of 24 people with long COVID showed significantly lower levels of a marker tied to dopamine-releasing nerve endings than scans of healthy volunteers, and the pattern of loss tracked with patients' symptoms, researchers at Toronto's Centre for Addiction and Mental Health (CAMH) reported. The study appeared in eBioMedicine, and CAMH publicized the findings on Sept. 21 along with plans for a clinical trial testing whether boosting dopamine function helps.
For the many people living with fatigue, brain fog, and low motivation after COVID-19, the study offers something they have sought for years: a measurable biological signal behind symptoms that standard tests often miss. It does not prove that dopamine damage causes long COVID, and it does not change treatment today.
That distinction matters because patients may be tempted to act on it. No dopamine-targeting drug has been shown to treat long COVID.
A Dopamine Marker Tracks Motivation, Movement, and Memory
The team used PET imaging to measure vesicular monoamine transporter 2, or VMAT2, a protein that helps package dopamine and serves as a marker of dopamine nerve terminal density. According to the eBioMedicine paper, the case-control study ran from August 2022 to April 2025 and compared 24 adults with long COVID with 24 age-matched healthy controls.
VMAT2 levels were lower across all three major regions of the striatum, a brain area involved in motivation, movement, and thinking. Reductions ranged from 16% to 20% depending on the region, and participants averaged 32 years old, AuntMinnie reported.
Lower levels in the ventral striatum were linked to greater apathy. Reductions in the dorsal putamen were tied to slower movement, and lower levels in the dorsal caudate to worse memory performance.
"Our findings provide compelling evidence that long COVID involves the loss of dopamine-releasing neurons," said Dr. Jeffrey Meyer, the study's senior author and a senior scientist at CAMH's Brain Health Imaging Centre, in the CAMH release.
Earlier Scan Studies Point in Different Directions
The CAMH group previously reported elevated brain inflammation in long COVID, especially in dopamine-rich regions. Meyer said the new work provides direct evidence that the dopamine marker is reduced in those same regions.
Not every imaging study agrees on inflammation. MedicalDaily reported in June on a University of Turku study of 14 long COVID patients that found no widespread brain inflammation compared with healthy controls. The two studies measured different things, used small groups, and are not directly comparable. Together, they show how unsettled the brain biology of long COVID remains.
Small Sample, Early Evidence, and a Disclosed Patent Interest
This was a small, single-site study that captured one point in time. It cannot show whether the dopamine changes came before symptoms, whether they persist, or whether they improve. Lower VMAT2 binding may reflect changes in how nerve endings store dopamine rather than permanent loss of neurons, Pharmacy Times noted in its coverage.
Readers should also know about a financial interest. Meyer has applied for patents on the use of rasagiline and a tyramine-based dopamine approach for long COVID, according to Medscape's report and the study's disclosures. The study was funded by the Canadian Institutes of Health Research.
Long COVID remains common in the U.S. A JAMA Network Open analysis of federal survey data found that 8.3% of adults, an estimated 21.3 million people, reported ever having long COVID in 2024. Nearly 6 in 10 of them reported recovery.
The Planned Trial and What Patients Can Do Now
CAMH plans to begin a clinical trial within the next couple of months with University Health Network in Toronto. It will test whether modifying dopamine activity improves memory, motivation, and fatigue. Meyer has suggested repurposing drugs such as dopamine precursors and inhibitors of dopamine breakdown, which are already used for other conditions.
Those medications have side effects and drug interactions, and none is approved for long COVID. Patients should not take dopamine-related drugs or supplements on their own. People with persistent fatigue, brain fog, or low mood can ask a clinician for a structured evaluation to rule out other causes, such as thyroid problems, anemia, sleep disorders, or depression. Some academic health systems run post-COVID clinics.
New chest pain, sudden weakness, confusion, trouble speaking, or thoughts of self-harm require urgent care.
The finding is promising, but it is a starting point. The CAMH trial and larger studies that follow patients over time will determine whether this signal leads to real treatment.
Key Questions Answered
What did the study find? People with long COVID had 16% to 20% lower levels of a dopamine nerve terminal marker in the striatum than healthy controls, and the losses tracked with symptoms.
How many people were studied? 24 adults with long COVID and 24 age-matched healthy controls in Toronto.
Does this prove dopamine damage causes long COVID? No. The study shows an association at one point in time and cannot establish cause.
Is there a dopamine treatment for long COVID? Not yet. CAMH plans a clinical trial, and no dopamine drug is approved for long COVID.
Should I try dopamine supplements? No. Talk with a clinician before taking any medication or supplement for long COVID symptoms.
How common is long COVID in the U.S.? About 8.3% of U.S. adults reported ever having it in 2024, according to a JAMA Network Open analysis.
