Long COVID Study Finds Fewer Dopamine Signals in the Brain

COVID-19 can leave brain injuries that remain detectable on scans years later in people experiencing neurological symptoms linked to long COVID.

Previous research has associated cognitive problems in long COVID with disruption of the blood–brain barrier, an enlarged hippocampus, raised markers of brain injury, and lower brain volume seen on MRI scans.

Researchers in Canada have now found that people who developed ongoing apathy and depression for the first time in their lives several months after COVID-19 infection had around 18 percent fewer dopamine nerve endings in the brain than healthy people.

Dopamine is a neurotransmitter involved in regulating movement and motivation. Losing nerve endings that communicate through dopamine can impair cognitive function and may contribute to the development of neurodegenerative diseases.

Long COVID and dopamine nerve endings

For the study, published in eBioMedicine, the researchers examined positron emission tomography (PET) brain scans from 24 adults with long COVID and 24 healthy adults of comparable age.

Their analysis assessed dopamine nerve-ending loss in the striatum, a central brain region involved in movement and motivation.

Participants received an injection containing a radiotracer that attaches to a protein found on dopamine-signalling nerves: vesicular monoamine transporter 2 (VMAT2).

VMAT2 is an established biomarker in neurodegenerative disorders, including Parkinson's disease.

PET imaging indicated that dopamine nerve-ending loss in the ventral striatum was associated with reduced motivation.

Within the dorsal striatum, a loss of dopamine nerve endings in the putamen was linked to slower movement and more time needed to finish tasks. Losses in the caudate nucleus, meanwhile, were associated with worsening memory and difficulty recalling words.

The damage to dopamine nerve endings was observed in people who had lived with long COVID for as long as 4.6 years.

Although the study involved a relatively small number of patients, the result is especially striking because the changes could be identified on brain scans. Put simply, they can be seen.

"What cannot be seen is too often considered uncertain," nuclear medicine researcher Eric Guedja and neuroscientist Danielle Beckman write in a commentary on the research.

"Liu and colleagues report a PET study that translates a clinically elusive neuropsychiatric phenotype of long COVID into a measurable dopaminergic signal."

People with long COVID had lower levels of a tracer that binds to dopamine nerve endings than healthy people. Healthy people who had been infected with COVID-19 had fewer dopamine nerve endings than healthy people who had not been infected with the virus. (Lui et al., eBioMedicine, 2026)

Potential tests and treatments for long COVID

Jeffrey Meyer, a neurochemist at the University of Toronto, told ScienceAlert that the nerve-damage marker used in the research could potentially serve as a diagnostic test for long COVID.

According to Meyer, some people with long COVID may respond to "treatments which either increase the density of dopamine nerve terminals or improve the release of dopamine by the remaining dopamine nerve terminals".

Meyer and his team will test whether a repurposed medicine that affects dopamine can ease long COVID symptoms in an upcoming clinical trial. The work is patented by the hospital carrying out the research, the Centre for Addiction and Mental Health, and Meyer is the inventor named on that patent.

Validated, evidence-based long COVID treatments and tests are urgently needed, as none currently exist. The condition is managed either by treating symptoms or through trial and error using repurposed medicines.

Many people receive no treatment, either because specialist care is inaccessible or because they are offered ineffective, outdated, and sometimes harmful approaches, such as graded exercise therapy or cognitive behavioural therapy, which do not address the underlying pathologies.

It remains unclear precisely how many people develop long COVID following acute COVID-19 infection, as estimates differ. They range from 2 percent to 10 percent of those infected.

At least 65 million people around the world have long COVID, including 10–20 percent of children who have previously had COVID-19.

Related: Strange Structures Found Lurking in The Blood of People With Long COVID

The disabling condition affects multiple organ systems and is linked to more than 200 symptoms, including fatigue, memory problems, sleep disorders, impaired concentration, dizziness, orthostatic intolerance, sensory overload, post-exertional malaise, headaches, anxiety, depression, and gastrointestinal problems.

It can also result in potentially lifelong conditions, including dysautonomia, cardiovascular disease, myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), postural orthostatic tachycardia syndrome (POTS), diabetes, and mast cell activation syndrome (MCAS).

"We need to find biological changes in long COVID that plausibly account for symptoms, and then develop treatments to address the biological changes in people with long COVID who have these symptoms," said Meyer.

This paper was published in eBioMedicine.

This article was fact-checked by Clare Watson and edited by Rebecca Dyer. While we pride ourselves on our process, we are only human. If you spot a mistake, please let us know.