PET scans tie long COVID brain fog to damaged dopamine neurons

Eighteen percent. That is the average shortfall in dopamine nerve terminals that Jeffrey Meyer, a senior scientist at Toronto’s Brain Health Imaging Centre, reported in people with long COVID who also had neuropsychiatric symptoms. The estimate comes from positron emission tomography scans of 24 patients set beside healthy volunteers.

The work was done at the Centre for Addiction and Mental Health in Toronto. Meyer’s group words its conclusion with care: long COVID is associated with injury to dopamine-releasing neurons.

VMAT2 Binding in the Striatum

The scans did not photograph dopamine itself, and that distinction runs through everything else in the study. The team injected a radioactive tracer, (+)[11C]DTBZ, that latches onto vesicular monoamine transporter 2, or VMAT2, a protein found almost exclusively in the terminals of dopamine-releasing neurons, as Radiology Business reported. Less tracer binding means fewer of those terminals, or terminals holding less of the transporter. The striatum, a deep cluster of structures that receives dopamine from the midbrain, was the focus because it governs reward, movement and aspects of learning, which is why a loss there could plausibly show up as flat motivation, slowed hands and a weaker memory for recent events.

Across three parts of the striatum, the long COVID group showed 16 to 20 percent lower binding than controls, with a significance level below P < .0001, according to Pharmacy Times. That study ran from August 2022 to April 2025 and compared 24 adults with long COVID against 24 age-matched controls; the control pool was widened to 43 for exploratory analyses.

Each region lined up with a different complaint. Lower binding in the ventral striatum went with greater loss of motivation, lower binding in the dorsal putamen with slower movement on a finger-tapping task, and lower binding in the caudate with poorer memory recall, as summarized in the ScienceDaily release built on the CAMH announcement. Memory is the link to brain fog; the other two regions account for the apathy and physical slowing that often travel with it.

Correlation, Cross-Section and the Word Damaged

Meyer told reporters that “this kind of injury is well known to produce symptoms like lack of motivation and motor slowing, and may contribute to memory difficulties in other neurological conditions.” The injury comparison borrows from Parkinson’s disease and related disorders, where loss of dopamine terminals is established. In long COVID the same marker was found lowered in the same regions, which is the core of the CAMH argument.

The design limits how far that argument can travel. PsyPost noted the study was cross-sectional, measuring everyone once, so it cannot say whether lowered dopamine markers caused the symptoms or came from something else. Blood biomarkers in the same patients did not correlate with the imaging results, which leaves the trigger unexplained.

A second caution comes from the case-control write-up in Pharmacy Times: reduced VMAT2 binding may reflect altered storage capacity in surviving terminals rather than irreversible loss of neurons. The sample was modest, and it covered only patients with significant neuropsychiatric symptoms, so the 18 percent figure describes that group and not every person with long COVID. The paper appeared in eBioMedicine (2026; volume 130, article 106339), where it was accompanied by independent commentary from researchers at Aix Marseille University and Helmholtz Munich.

Coverage from CIDRAP put the enrolled group at 24 long COVID patients with neuropsychiatric symptoms and gave the same 16 to 20 percent range, adding that the findings show association only. In plain terms, the scans show a measurable difference in a dopamine marker that varies alongside symptoms from person to person, which is stronger than a self-reported complaint and weaker than proof of a mechanism.

Inflammation as the Proposed Route

Meyer’s proposed mechanism runs through inflammation. “Inflammation can injure dopamine neurons,” he said, and the scans give what he calls direct evidence that a dopamine neuron marker is lowered in the regions tied to symptoms. CAMH’s account is that the immune response to infection, if it persists, could wear down these terminals over months.

That reasoning shapes the treatment idea. The team points to repurposing drugs that raise dopamine signaling, including dopamine precursors and monoamine oxidase B inhibitors, which slow the breakdown of the chemical. Meyer has said this should be tested in trials instead of tried off-label, and a pilot clinical trial aimed at dopamine function is planned within two to three years.

Patient advocates have already welcomed the result. Susan Deuville, a lived-experience research advisor on the project, said the work “validates what long COVID sufferers have always known” and called the effects devastating. Whether treatments aimed at dopamine will shift cognitive symptoms in a controlled trial is the claim that the 24-patient scan study leaves unproven, and the planned pilot is the first scheduled test of it.

This article was produced with the assistance of AI and reviewed by Morning Overview editors prior to publication.

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