Long COVID symptoms linked to measurable damage in the brain's dopamine system

PsyPost

Mental Health

Social Psychology

Cognitive Science

Neuroscience

About

No Result

View All Result

Join

My Account

PsyPost

No Result

View All Result

Home

Exclusive

COVID-19

Long COVID symptoms linked to measurable damage in the brain’s dopamine system

by<br>Eric W. Dolan

July 30, 2026

Reading Time: 8 mins read

[Adobe Stock]

Share on TwitterShare on Facebook

A recent study published in eBioMedicine provides evidence that individuals suffering from long COVID show a measurable reduction in the brain’s dopamine-releasing neurons. These physical brain changes tend to be associated with common persistent symptoms such as apathy, memory problems, and a slowing of physical movements. The findings suggest that treatments aimed at boosting dopamine function could offer a new therapeutic direction for people experiencing the neuropsychiatric effects of long COVID.

Long COVID is a condition where individuals experience ongoing physical and mental symptoms long after their initial infection with the COVID-19 virus has resolved. Many people report persistent brain-related symptoms, including a profound lack of motivation, difficulty experiencing pleasure, memory lapses, and general cognitive sluggishness. The biological mechanisms responsible for these lingering issues remain poorly understood by the medical community.

Past medical research primarily focused on how immune system overreactions and persistent brain inflammation might drive these symptoms. Jeffrey Meyer, a Canada Research Chair, senior research scientist, and professor in the department of psychiatry at the University of Toronto, authored the new study. His prior work focused extensively on similar inflammatory processes.

“We had top international level expertise in measuring brain inflammation in psychiatric illnesses,” Meyer said. “When COVID came, I decided to use the same imaging tools to study long COVID.”

During that earlier research, Meyer found a distinct pattern linking inflammation and specific brain networks. He noted that the most intense areas of inflammation overlapped with the brain’s dopamine pathways.

Free daily newsletter

“When I discovered evidence for brain inflammation in long COVID, I noticed that the greatest elevations in the inflammation marker were in regions where there are nerve terminals that release dopamine,” Meyer said.

These brain regions also control basic physical movements. Dopamine is a chemical messenger in the brain that regulates motivation, learning, and physical movement, and its neurons are highly concentrated in a deep brain structure called the striatum.

“Also, the inflammation marker correlated with a measure of movement speed that can be affected by injury to dopamine releasing nerves so I speculated that injury to dopamine releasing nerves could account for the symptom of slowed movement speed, and be related to inflammation in the same region,” Meyer said. “Sometimes inflammation can damage dopamine releasing nerves.”

Google News Preferences

Add PsyPost to your preferred sources

Scientists had additional reasons to look at the dopamine system in relation to COVID-19. The specific cells that produce dopamine contain high levels of the receptor proteins that the COVID-19 virus uses to enter and infect human cells.

“Also, the key binding site for the virus to enter cells is higher density on nerves that release dopamine which is another reason to see if their terminals are lost,” Meyer added.

To measure the health of dopamine neurons, the researchers looked at a protein called vesicular monoamine transporter 2. This protein acts like a microscopic pump, packaging dopamine into tiny cellular sacs so that it can be released to communicate with neighboring cells. Because this protein is almost exclusively found within dopamine-releasing neurons in the striatum, measuring its presence provides a highly accurate estimate of how many intact dopamine nerve terminals exist.

The researchers conducted a case-control study involving 24 adults diagnosed with long COVID and 24 healthy adults matched closely for age. The healthy control group was later expanded to 43 participants for additional exploratory comparisons. Participants in the long COVID group had experienced only mild to moderate illness during their initial infection. However, they all developed significant neuropsychiatric symptoms within three months of their acute illness, and these symptoms had persisted for at least three months.

The scientists established strict exclusion criteria for all participants to ensure the accuracy of their measurements. Anyone with a history of neurological illness prior to their COVID-19 infection was excluded from the study. The team also excluded individuals with a history of moderate or severe substance abuse, as well as anyone who had smoked cigarettes or used recreational drugs within the past two...