Brain Imaging Study Links Long COVID to Dopamine Neuron Injury, Pointing to Repurposed Treatments

A new brain imaging study offers the strongest evidence to date that long COVID is associated with injury to dopamine-releasing neurons, a finding that may explain some of the condition’s most persistent neuropsychiatric symptoms and open new pharmacologic treatment avenues.^1,2

Long COVID affects an estimated 2% of the global population and is marked by a range of debilitating symptoms, including fatigue, brain fog, memory problems, and low mood that persist for at least 3 months after acute infection.¹ Despite its prevalence, no evidence-based treatments currently exist, largely because the underlying brain pathology remains poorly understood.¹ Dopaminergic neurons are known to be vulnerable to inflammatory injury and carry a high density of ACE2 receptors, the entry point for SARS-CoV-2, but their integrity had not previously been studied in long COVID patients.^1-3

Study Design and Findings

Researchers at the Centre for Addiction and Mental Health (CAMH) in Toronto, Ontario, Canada, conducted a case-control study (August 2022-April 2025) involving 24 adults with long COVID and 24 age-matched healthy controls, with the control group extended to 43 participants for exploratory analyses. Using PET with the radiotracer (+)-α-dihydrotetrabenazine C-11, investigators measured vesicular monoamine transporter 2 (VMAT2) binding potential, a well-established marker of dopamine nerve terminal density, across the ventral striatum, dorsal putamen, and dorsal caudate.^1,4

VMAT2 binding was significantly lower across all 3 regions in patients with long COVID vs healthy controls (P < .0001), with reductions ranging from 16% to 20% across regions; results held when the control group was expanded to 43 participants (P = .0006).¹ Regional reductions correlated with specific symptom domains: Lower ventral striatum binding was associated with greater loss of motivation, dorsal putamen reductions with slower motor performance, and caudate-putamen losses with memory difficulties.^1,2,4

Building on Prior Inflammation Findings

These results build on the same research team's earlier work demonstrating elevated brain inflammation in patients with long COVID, particularly in regions rich in dopamine-releasing neurons. "We know that inflammation can injure dopamine neurons," senior author Jeffrey Meyer, MD, PhD, a senior scientist, Canada Research Chair in the Neurochemistry of Major Depression, and head of the Neurochemical Imaging Program in Mood and Anxiety Disorders at the Brain Health Imaging Centre at CAMH, said in a news release.² "This study provides direct evidence that the dopamine neuron marker is reduced in the same regions—and that this loss correlates with patients' symptoms."

An accompanying study in eBioMedicine cautioned that although VMAT2 PET is a robust marker of presynaptic dopaminergic terminal integrity, reduced binding does not necessarily indicate irreversible neuronal loss; it may instead reflect altered vesicular storage capacity or adaptive presynaptic changes that longitudinal studies will need to clarify.³

Clinical and Pharmacologic Implications

For pharmacists, the findings mark a potential shift away from an almost exclusive research focus on anti-inflammatory and immune-modulating approaches to long COVID toward pharmacologic strategies that support dopaminergic function. Meyer noted that repurposing medications that augment dopamine-releasing neuronal activity—including dopamine precursors and inhibitors of dopamine metabolism such as monoamine oxidase B inhibitors—could represent a promising therapeutic avenue.² Notably, disclosures accompanying the study indicate that Meyer has a pending patent application involving rasagiline and a tyramine-based dopamine precursor approach specifically for long COVID, filed in January 2026.^1,5

The CAMH team, in collaboration with University Health Network, plans to launch a clinical trial in the coming months targeting dopamine function to address memory, motivation, and fatigue in patients with long COVID.²

Looking Ahead

Although the study is limited by a modest sample size and its case-control design, it represents one of the first mechanistic links between a specific, measurable neurochemical deficit and the neuropsychiatric symptom burden of long COVID. As pharmacologic trials targeting the dopamine system advance, pharmacists may play an increasing role in counseling patients on emerging off-label or repurposed therapies and in monitoring for drug interactions and adverse effects associated with dopaminergic agents in a medically complex, often treatment-fatigued patient population.^1-3,5

Expert Insights

Pharmacy Times spoke with Jeffrey H. Meyer, MD, PhD, FRCP(C), professor and canada research chair in neurochemistry of major depressive disorder and head of neurochemical imaging in mood disorders at the Toronto PET Centre, to discuss the implications of his team's findings on dopamine neuron injury in long COVID. Meyer outlines the dopamine-targeted treatment approaches under investigation, what pharmacists and prescribers should watch for as this research advances, and the timeline for a pilot clinical trial and subsequent regulatory pathway.

Pharmacy Times: Your team notes that repurposing dopamine-boosting medications — dopamine precursors and dopamine metabolism inhibitors — could be a promising treatment direction. What existing drug classes do you think pharmacists and prescribers should be watching most closely as this research moves toward clinical trials?

Jeffrey H. Meyer, MD, PhD, FRCP(C): We are going to start a study with an MAO-B inhibitor. Dopamine precursors could be interesting, but limits on funding allow us to prioritize one direction. I am not advising individuals to initiate either of these options outside of a clinical trial, though, as the clinical trial would be the right way to assess benefit and monitor safety. I've advised another group who are using dopamine-2 agonists for major depressive episodes in a clinical trial to be cognizant of whether the participants have long COVID so they can gather data too.

Pharmacy Times: For pharmacists managing long COVID patients who present with fatigue, apathy, or brain fog, how should this finding change the way we think about symptom management in the meantime, before dopamine-targeted therapies are studied in trials?

Meyer: The plan for us is to complete a pilot clinical trial study within 2 to 3 years and concurrently engage pharmaceutical companies to do further clinical trials. The pilot study would randomly assign participants to treatment or placebo under blinded conditions so neither the investigators nor the study participants would know who had the treatment (only the research pharmacy would know). The pilot trial is intended to be a 2-site study. If funding permits, we would like to offer non-responders to the intervention (which could be the medication or placebo) the opportunity to receive the medication as an optional second step for the study.

Pharmacy Times: You mention a clinical trial targeting dopamine function is launching in the coming months. What will that trial look like, and what's the timeline for health care providers to start seeing evidence that could inform practice?

Meyer: Because we applied for patenting for the medication, there is value for a company, hopefully, to license the patent and complete the required regulatory trials if we have reasonably positive results from the pilot study. The duration for development would depend on the number and quality of trials that the regulatory agency of individual governments requires. Probably the fastest estimate would be 2 years per trial and 3 trials, but there could be an additional trial and a longer duration for each trial. I wish the process could be faster, but we are trying to be as fast as we can while carefully meeting ethical and regulatory requirements. Given the urgent need for treatment of brain-based symptoms of long COVID, government regulatory bodies might consider a lesser number of trials to be required.

REFERENCES

1. Liu YK, Persaud, D, Vieira EL, et al. Loss of vesicular monoamine transporter 2 in striatum of long COVID and relationship to neuropsychiatric symptoms. eBioMedicine. Published online July 10, 2026. doi:10.1016/j.ebiom.2026.106339

2. New study provides first evidence of dopamine system injury in the brain of long COVID patients. News release. Centre for Addiction and Mental Health. July 10, 2026. Accessed July 17, 2026. https://www.eurekalert.org/news-releases/1134884

3. Guedj E, Beckman D. Dopaminergic vulnerability in long COVID: striatal PET imaging at the brain-body interface. eBioMedicine. Published online July 10, 2026. Accessed July 20, 2026. doi:10.1016/j.ebiom.2026.106369

4. Morton W. Brain PET scans reveal neuron loss in long COVID. AuntMinnie. July 14, 2026. Accessed July 17, 2026. https://www.auntminnie.com/clinical-news/molecular-imaging/article/15830001/brain-pet-scans-reveal-neuron-loss-in-long-covid

5. Taylor E. Long COVID associated with injury to dopamine system. Medscape. July 16, 2026. Accessed July 17, 2026. https://www.medscape.com/viewarticle/long-covid-associated-injury-dopamine-system-2026a1000o0u