A new long COVID dopamine study suggests some patients have lost dopamine-releasing nerve endings in the brain. PET scans of 24 people with long COVID in Canada showed reduced levels of a dopamine marker in the striatum compared with healthy controls, researchers reported in eBioMedicine, as ScienceAlert reported Oct. 4, 2026.
What the long COVID dopamine scans found
The team used positron emission tomography with a radioactive tracer that binds a protein on dopamine nerve endings. None of the 24 participants had an active infection, but all had persistent symptoms after COVID-19. As a group, they reported a lack of motivation and scored worse on memory and movement-speed tests.
Compared with healthy people of similar age, the patients showed lower density of dopamine nerve endings in several regions of the striatum, a brain area tied to motivation, movement and memory. Lower signal tracked with more apathy, poorer memory and slower performance on movement and reading tests. ScienceAlert reported that about 25% of the variation in those symptoms was associated with the dopamine marker.
Why dopamine could be vulnerable
“Our findings provide compelling evidence that long COVID involves the loss of dopamine-releasing neurons,” psychiatrist Jeffrey Meyer of the Brain Health Imaging Center in Canada said, as quoted by ScienceAlert. Researchers have proposed two possible routes: immune cells that prune synapses, which are elevated in some long COVID patients, and direct infection of dopamine neurons by SARS-CoV-2, since those cells carry receptors the virus could use.
Limits and possible treatments
The study is small and preliminary. The scans measure a protein on nerve endings rather than counting neurons directly, and long COVID symptoms vary widely, so the findings may apply only to patients with motivation, memory or movement problems. The authors call for larger, well-controlled studies, and ScienceAlert noted that Meyer has a pending patent application for a dopamine-based long COVID treatment.
If the link holds, the authors argue, therapies that boost dopamine release, similar in approach to Parkinson’s drugs such as L-dopa, could be worth testing. They note that no current trials focus on that strategy. Such drugs carry real side effects, so patients should not self-treat.
What comes next for patients
For people with long COVID, the work adds biological evidence to symptoms that are often hard to measure. Research on new treatment platforms keeps moving, from Novartis’ Abogen mRNA deal to AI tools such as Microsoft’s Quine biology AI that aim to speed lab discovery. Funding for that kind of science is also a live issue locally, as our report on Harvard’s $150 million research push shows.
Sources: Liu et al., eBioMedicine (2026); ScienceAlert.