Researchers have uncovered a clear alteration in the brains of people with long COVID indicating that neurons releasing dopamine may suffer burnout or damage, which could account for some of the condition’s most severe symptoms. A preliminary Canadian study of 24 people with long COVID identified clear differences in specific brain regions when compared with healthy participants of the same age, pointing to a biological root for severe memory decline, slow physical movements, and a lack of motivation.
Brain Scans Reveal Reduced Dopamine Nerve Endings in Patients
Using positron emission tomography (PET) scans with a radioactive tracer, researchers at the Centre for Addiction and Mental Health (CAMH) in Canada measured a marker of dopamine nerve endings among the 24 participants. None of these individuals had an active infection, yet all grappled with debilitating symptoms since first falling ill with COVID-19. Their brains exhibited fewer dopamine nerve terminals across multiple parts of the striatum—a brain zone critical for memory, movement pacing, and drive—when contrasted with healthy control subjects. The study noted that roughly 25 percent of the variance in these symptoms among patients was associated with this loss of dopaminergic neurons.
Our findings provide compelling evidence that long COVID involves the loss of dopamine-releasing neurons,
said Dr. Jeffrey Meyer, Senior Scientist at the Brain Health Imaging Centre, Canada Research Chair, and senior author of the study. This kind of injury is well known to produce symptoms like lack of motivation and motor slowing, and may contribute to memory difficulties in other neurological conditions. Our results suggest a similar process is occurring in long COVID.
Connecting Persistent Brain Inflammation to Dopamine System Damage
While previous investigations among people with long COVID mainly focused on general brain inflammation and immune changes, this work directly examined whether the brain’s dopamine-producing neurons were affected. The new findings build on previous work by the same research team showing that long COVID patients have unusually high levels of inflammation in the brain, particularly in regions containing large numbers of dopamine-releasing neurons. We know that inflammation can injure dopamine neurons. While our earlier research showed high levels of inflammation in those regions, this study provides direct evidence that the dopamine neuron marker is reduced in the same regions — and that this loss correlates with patients’ symptoms,
Dr. Meyer explained. Beyond inflammation, individuals with long COVID also show elevated markers for cells that prune back synapses, which may damage these neurons, alongside the theoretical possibility that SARS-CoV-2 can directly infect and injure dopamine-releasing cells from within.
Parkinson's Drugs Could Treat Long COVID Dopamine Deficits
The research indicates that long COVID is, at least in part, a disorder of the brain’s dopamine system, suggesting a shift from current therapeutic development since no active clinical trials focus on augmenting dopamine-releasing neuron functions. The study noted that if these preliminary findings are verified, drugs like L-dopa used for Parkinson’s disease could theoretically be repurposed to treat patients. These interventions would enhance tonic dopamine release broadly, and phasic release in intact synapses, thereby reducing impact of lost synapses,
the study authors theorize. However, these medications carry significant side effects and may only assist patients whose specific symptoms involve dopamine disruption. Susan Deuville, a patient with long COVID and a lived-experience research advisor to Dr. Meyer, shared the personal impact of the findings: For five years I have been seeking answers on what happened to me after I contracted COVID in 2021. It was a crushing loss of the life I had and the person I was before. The research of Dr Meyer brings hope. It also validates what long COVID sufferers have always known – long COVID is real, and the effects are devastating.
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