Long COVID brain fog is a common but hard-to-explain complaint, since routine brain scans usually look normal. A new imaging study offers a concrete biological reason instead of a vague label.
Scientists at Toronto’s Centre for Addiction and Mental Health scanned 24 long COVID patients and found their dopamine-releasing nerve endings were measurably reduced, in a paper published September 21, 2026.[1]
Long COVID Brain Fog, What the Brain Scans Show
The study compared 24 adults with long COVID to 24 healthy, age-matched volunteers using PET imaging, a scan that tracks a small radioactive marker to show how active certain tissue is.[1]
The marker used, VMAT2, sits inside dopamine nerve endings. Across three brain regions in the striatum, VMAT2 levels were 16 to 20 percent lower in the long COVID group than in healthy volunteers.[1]
That gap shows long COVID brain fog has a specific biological marker attached to it, rather than being a symptom with no physical trace at all.[1]
Most earlier brain fog research relied on symptom questionnaires alone, without measuring what had actually changed inside the brain.[3]
Long COVID Brain Fog and Dopamine, Why the Connection Matters
Dopamine is best known for reward and movement, but it also drives motivation and working memory. Losing nerve endings that release it can touch several everyday functions at once.[2]
The researchers linked each region to a specific symptom: lower signal in the ventral striatum tracked with apathy, in the dorsal putamen with slowed movement, and in the caudate with weaker memory.[1]
A related mouse study on restoring one aging-related brain protein showed a single damaged pathway can disrupt several functions at once — a pattern that echoes these dopamine findings.[2]
If this holds up, it gives doctors something concrete to tell patients who are stuck hearing that their brain fog “looks normal” on standard scans.[2]
Inside the Study, How Researchers Measured Nerve Damage
The research team, led by senior scientist Dr. Jeffrey Meyer with graduate student Yuhan Liu, used PET scans because they can detect small chemical changes that standard MRI cannot pick up.[1]
The work was funded by the Canadian Institutes of Health Research. Dr. Meyer has filed patents on rasagiline and tyramine-based approaches that support dopamine function, a financial interest disclosed alongside the findings.[2]
Dr. Meyer described the results as “compelling evidence” that long COVID involves a real loss of dopamine-releasing nerve cells, rather than a symptom with no physical trace.[2]
How Common Is Brain Fog After COVID-19
Brain fog is only one of many long COVID complaints, and its reported frequency varies widely depending on how studies define and measure it.[3]
A large 2026 meta-analysis pooling over 2 million confirmed COVID-19 cases across 429 studies estimated overall long COVID prevalence at 36 percent, with brain fog reported as an isolated symptom in about 4 percent of cases and memory problems in about 11 percent.[3]
Fatigue and brain fog also overlap with other treatable causes, including vitamin B12 deficiency, so ruling out common causes remains a sensible first step for patients.[3]
| Aspect | Finding |
|---|---|
| Study design | 24 long COVID patients vs. 24 age-matched healthy controls, single site |
| Dopamine marker change | VMAT2 down 16–20% across three striatal regions |
| Global long COVID rate | 36% of confirmed COVID-19 cases, from a 2-million-person meta-analysis |
| Brain fog as isolated symptom | About 4% of long COVID cases across 27 pooled studies |
| Planned next step | Clinical trial of a dopamine-boosting treatment, expected within months |
What This Could Mean for Treatment
Because the injury pattern resembles other dopamine-related conditions, the team plans a clinical trial testing a treatment that boosts dopamine function, in partnership with the University Health Network.[2]
“Repurposing medications that augment the function of dopamine-releasing neurons could be a promising approach,” Dr. Meyer said, though any such treatment still needs to be tested directly in long COVID patients.[2]
Limitations and What Comes Next
The study is small and was conducted at a single site, so the findings need to be confirmed in larger, more diverse groups before they can guide treatment decisions.[1]
The design also cannot show whether dopamine changes caused the symptoms, followed them, or reflect a temporary drop in storage rather than permanent loss of nerve endings.[1]
The study also did not separately analyze factors such as the COVID-19 variant involved, vaccination status, or number of reinfections, so how much these might have influenced the results is unknown.[1]
It is also unclear whether these changes persist over time or fade as patients recover, since the scans captured only a single point after infection. Until larger trials are done, long COVID brain fog cannot yet be diagnosed this way in the clinic.[1]
Long COVID Brain Fog in Context, How the Numbers Compare
Dopamine neuron loss is not a new idea in neuroscience. In Parkinson’s disease, motor symptoms typically appear only after striatal dopamine terminals have already dropped by about 70 to 80 percent.[4]
Measured against that threshold, the 16 to 20 percent reduction found here is far smaller, suggesting a milder, partial injury rather than a Parkinson’s-like process.
Long COVID brain fog also echoes a pattern researchers have puzzled over for decades. Post-viral fatigue and cognitive complaints have long followed illnesses such as mononucleosis.
Studies of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) have searched for a shared brain mechanism for years without a single confirmed cause.
Seen against that history, this study stands out less for the size of the change and more for pinpointing one specific, measurable circuit — something earlier post-viral fatigue research rarely achieved.
What This Study Leaves for Future Work
Using PET to directly measure dopamine neurons is an established method in Parkinson’s research, but applying it to long COVID patients this way is close to a first.[1]
What makes this finding notable is that it does not try to explain all of long COVID brain fog at once; it narrows in on one measurable circuit, which also means treatment can be tested against that circuit specifically.
That kind of result could feed into future biomarker research for long COVID brain fog. Diagnosis today relies entirely on what patients report, but a repeatable brain-imaging signal could eventually change how it is diagnosed and treated.[2]
The findings drew considerable attention from the field right after publication, and whether other research teams can reproduce them is now the next open question.[2]
Reproducibility matters here because a single site’s results cannot show whether this pattern applies broadly to long COVID patients or is specific to these 24 people.
That kind of verification takes time and resources, but it is what would decide whether this becomes a tool clinics can actually use.[1]
References
- Liu Y, Meyer JH, et al. “Dopamine-releasing neuron injury in long COVID.” eBioMedicine, Vol. 130, Article 106339 (September 21, 2026).
- Centre for Addiction and Mental Health (CAMH). “New Study Provides First Evidence of Dopamine System Injury in the Brain of Long COVID Patients” (September 2026).
- “Global Prevalence of Long COVID, Its Subtypes, and Risk Factors: An Updated Systematic Review and Meta-analysis.” Open Forum Infectious Diseases (2026).
- Cheng HC, et al. “Imaging of Dopamine in PD and Implications for Motor and Neuropsychiatric Manifestations of PD.” Frontiers in Neurology (2013).
