Canadian research has found that people with long COVID and symptoms of apathy have 18 percent fewer dopamine nerve endings in the brain, paving the way for new diagnostics and therapies.
New Canadian research has provided concrete evidence that COVID-19 can cause lasting brain damage that remains clearly visible on scans more than four years after the initial infection. The scientific team analyzed the brains of people with long COVID and found significant loss in the dopamine system, which is crucial for motivation and motor control.
The study, published in the journal eBioMedicine, compared brain scans of 24 adults with long COVID and 24 healthy individuals of similar age. Using positron emission tomography (PET), the researchers measured the density of dopamine nerve terminals in the striatum, a region in the center of the brain. Participants were injected with a radiotracer that binds to the protein VMAT2, a well-known biomarker also used in the diagnosis of Parkinson's disease.
The results showed that individuals who developed long-lasting apathy and depression after infection had approximately 18 percent fewer dopamine nerve endings compared to healthy individuals. These damages were present in people who have been living with long COVID for four and a half years.
The significance of the findings lies in the fact that brain changes have become measurable. Nuclear medicine expert Eric Guedj and neuroscientist Danielle Beckman, in a commentary on the study, highlighted the importance of this discovery. "Liu and colleagues have presented a PET study that transforms the clinically ambiguous neuropsychiatric phenotype of long COVID into a measurable dopaminergic signal," they wrote.
The PET scans revealed associations between the loss of dopamine terminals in different brain regions and specific symptoms. Loss in the ventral striatum was linked to reduced motivation, while loss in the dorsal striatum, in a part called the putamen, was associated with slower movement. Damage to the caudate nucleus was linked to memory decline and difficulty finding words. Notably, even individuals without the disease who had been through COVID had a reduced number of dopamine terminals compared to those who had never encountered the virus.
Jeffrey Meyer, a neurochemist at the University of Toronto, told ScienceAlert that the nerve damage marker used in the study could be applied to diagnose long COVID. "Some long COVID patients might respond to treatments that either increase the density of dopamine terminals or improve the release of dopamine from those that remain," Meyer said.
In an upcoming clinical trial, Meyer and his team will test a medication that acts on dopamine, aiming to determine its effectiveness for long COVID symptoms. The invention is protected by a patent owned by the institution where the research is taking place, the Centre for Addiction and Mental Health, with Meyer listed as the patent creator.
Although estimates vary, it is believed that between 2 and 10 percent of the infected population develops long COVID. This means that at least 65 million people worldwide are living with this condition, including 10 to 20 percent of children who have had the virus. It is a debilitating condition that affects multiple organ systems and is associated with more than 200 symptoms, including fatigue, memory problems, sleep disturbances, dizziness, and anxiety.
Meyer emphasizes the urgency of further research. "We need to find biological changes in long COVID that convincingly explain the symptoms. Then we need to develop treatments targeting those changes in patients who have such symptoms," he concluded.
