For millions of people whose energy, focus, and drive never returned after a COVID infection, doctors have struggled to point to anything concrete in the brain. A small Canadian brain imaging study now offers one.
Researchers at the Centre for Addiction and Mental Health (CAMH) in Toronto found significantly fewer dopamine nerve terminals in a movement and reward hub of the brain in people with long COVID.
The size of the loss tracked with the symptoms patients describe most often.
The study, published in eBioMedicine in July 2026, used positron emission tomography, a brain scan that measures brain proteins, to count a marker called VMAT2.
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This protein sits on the endings of dopamine-releasing neurons and serves as a stand-in for how many endings are still working.
Compared with 24 healthy adults, 24 long COVID patients had 20 percent less of the marker in the ventral striatum, 17 percent less in the dorsal caudate, and 16 percent less in the dorsal putamen.
All three areas belong to the striatum, a deep brain structure that helps drive movement, motivation, and memory.
What dopamine actually does
Dopamine is often labeled the feel-good chemical. In the striatum, though, its job is quieter.
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It is the signal the brain uses to start a movement, push through a task, and hold information long enough to act on it.
When that signal weakens, the outward result can look a lot like the long COVID description. Sluggish body. Empty motivation. A mind that skips a beat.
The Toronto team saw that same alignment in the data. Less VMAT2 in the ventral striatum, the motivation hub, tracked with greater apathy.
Losses in the dorsal putamen tracked with slower movement. A drop in the dorsal caudate tracked with weaker memory performance, Technology Networks reported.
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Why inflammation is the leading suspect
The same CAMH group had already shown elevated brain inflammation in these regions after COVID. Inflammation is known to injure dopamine neurons.
Senior author Dr. Jeffrey Meyer said the new scans give direct evidence that dopamine neurons in those inflamed regions have been thinned out, and that the drop tracks with patients' symptoms.
The two findings together, he told Technology Networks, tie long COVID biologically to the dopamine system.
Notably, Fortune reported that patients and controls had only mild or moderate acute COVID infections, so the dopamine drop cannot simply be written off as a scar of severe illness.
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How solid the finding is
The evidence is early. Twenty-four patients cannot settle whether every long COVID case involves dopamine loss, or whether the deficit reverses over time.
The scans also do not tell us whether the same pattern appears in people whose main long COVID trouble is not brain fog but the heart and kidney risks that other studies have flagged.
Because dopamine is one of the most studied systems in medicine, treatment testing can move quickly.
Meyer's team plans a clinical trial with the University Health Network in Toronto.
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It will test whether existing drugs that boost dopamine, such as dopamine precursors and drugs that block dopamine breakdown, can ease fatigue and improve motivation and memory in long COVID.
What to do if this sounds like you
Long COVID is common. In 2023, 6.4 percent of US adults reported having it, and nearly one in five of those said the symptoms limit their daily activities.
Anyone with fatigue, brain fog, or persistent motivation problems months after a COVID infection should raise it with their doctor.
A doctor can rule out other causes and point patients toward long COVID trials as the dopamine research moves into treatment testing.
This article is made and published by Mie Hermansen, who may have used AI in the preparation.