Long COVID involves a distinct loss of dopamine-releasing neurons in the brain, according to a preliminary study published in the journal eBioMedicine and covered by sciencealert.com. Researchers in Canada using positron emission tomography (PET) scans discovered that patients suffering from persistent cognitive and physical symptoms showed reduced dopamine nerve endings compared to healthy individuals.
Dopamine Nerve Loss Linked to Long COVID Symptoms
The preliminary study examined 24 participants in Canada who experienced long COVID symptoms after their initial SARS-CoV-2 infections. None of the participants had active infections at the time of scanning, but all reported ongoing memory decline, slow physical movements, and a lack of motivation. When researchers analyzed their brain scans, they found a lower density of dopamine nerve endings within several regions of the striatum, an area of the brain responsible for motivation, movement speed, and memory. Approximately 25 percent of the variance in patient symptoms correlated directly with this reduction in dopaminergic neurons, sciencealert.com reported.
Our findings provide compelling evidence that long COVID involves the loss of dopamine-releasing neurons,
said psychiatrist Jeffrey Meyer from the Brain Health Imaging Center in Canada. Meyer explained that this specific type of neural injury typically produces motor slowing and a lack of motivation in other neurological conditions.
Shifting Focus From Brain Inflammation to Dopamine Disruption
Previous research into neurological long COVID primarily concentrated on general brain inflammation and immune system changes. The new imaging data redirects attention toward the brain’s dopamine system. Dopamine functions as a primary chemical messenger tied to the brain’s reward system and physical movement. Scientists suspect two potential mechanisms for this neural damage: elevated markers for cells that prune back synapses could be actively destroying dopamine-releasing neurons, or SARS-CoV-2 could directly infect and injure these cells from within due to a high density of susceptible receptors.
These results indicate that long COVID is, at least in part, a disorder of the brain’s dopamine system,
Meyer stated.
Potential Treatment Pathways Through Drug Repurposing
The findings open a theoretical pathway for treating long COVID symptoms by targeting dopamine-releasing neurons. Currently, no clinical trials focus on augmenting dopamine functions in post-viral patients. However, researchers suggest that if the findings are verified, existing medications like L-dopa, which is commonly prescribed for Parkinson’s disease, could potentially be repurposed. These interventions would theoretically enhance tonic dopamine release to compensate for lost synapses.
Researchers caution that drugs like L-dopa carry significant side effects and may only benefit patients who exhibit specific dopamine-related symptoms. Because long COVID manifests diverse symptoms across different individuals, not every patient reports the physical slowing or motivation deficits tied to dopamine loss.
Frequently Asked Questions
How many participants were included in the Canadian study?
The preliminary imaging study analyzed 24 participants suffering from persistent long COVID symptoms, comparing them against healthy control subjects of the same age.
What imaging technology did researchers use to measure brain changes?
Researchers used positron emission tomography (PET) scans alongside a radioactive tracer to measure a specific protein marker found on dopamine nerve endings in the striatum.
Could Parkinson’s disease medications treat long COVID?
Scientists theorize that drugs like L-dopa could theoretically be repurposed to enhance dopamine release if future studies verify that long COVID damages dopamine neurons in ways similar to Parkinson’s disease.
What specific symptoms correlated with dopamine neuron loss?
Patients with lower dopamine marker signals on their PET scans reported higher levels of apathy, poorer memory, and slower performance on physical movement and reading tests.