Long COVID May Leave Visible Dopamine Damage in the Brain

Long COVID and visible brain injury

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

Earlier research has connected cognitive dysfunction in long COVID with disruption of the blood-brain barrier, an enlarged hippocampus, raised markers of brain injury, and reduced brain volume on MRI scans.

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

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

PET scans reveal long COVID dopamine nerve-ending loss

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

They assessed dopamine nerve-ending loss in the striatum, a region at the centre of the brain involved in movement and motivation.

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

VMAT2 is an established biomarker used 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, loss of dopamine nerve endings in the putamen was linked to slower movement and longer task-completion times. Loss in the caudate nucleus, meanwhile, was associated with worsening memory and difficulty recalling words.

Damage to dopamine nerve endings was found in people who had lived with long COVID for as long as 4.6 years.

Although the study involved a small number of patients, the finding is particularly striking because these alterations could be identified on brain scans. Put simply, they are visible.

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

"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)*

Jeffrey Meyer, a neurochemist at the University of Toronto, told ScienceAlert that the nerve-damage marker used in the study could potentially help diagnose long COVID.

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

In an upcoming clinical trial, Meyer and his team will repurpose a medicine that affects dopamine to determine whether it improves long COVID symptoms. The Centre for Addiction and Mental Health, the hospital running the research, holds a patent for this work, and Meyer is the patent's inventor.

The need for long COVID tests and treatments

There is a dire need for validated, evidence-based tests and treatments for long COVID, as neither currently exists. The condition is managed by treating individual symptoms or by trial and error using repurposed medicines.

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

The precise number of people who develop long COVID following an acute COVID-19 infection is unknown because estimates differ, ranging from 2 percent to 10 percent of infected people.

At least 65 million people around the world are living with long COVID, including 10–20 percent of children with a history of COVID-19.

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

The debilitating condition affects several 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 often 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.