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, which is 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 5% 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. Despite its prevalence, no evidence-based treatments currently exist, largely because the underlying brain pathology remains poorly understood. 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 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 positron emission tomography (PET) with the radiotracer (+)[¹¹C]DTBZ, 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 compared with healthy controls (P < .0001), with reductions ranging from 16% to 20% depending on region; results held when the control group was expanded to 43 participants (P = .0006). Regional reductions correlated with specific symptom domains, as lower ventral striatum binding was associated with greater loss of motivation, dorsal putamen reductions correlated with slower motor performance, and losses in the caudate putamen were linked to 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 long COVID patients, particularly in regions rich in dopamine-releasing neurons. "We know that inflammation can injure dopamine neurons," senior author Jeffrey Meyer, MD, PhD, senior scientist at the Brain Health Imaging Centre, Canada Research Chair, said in a news release. "This study provides direct evidence that the dopamine neuron marker is reduced in the same regions—and that this loss correlates with patients' symptoms."²

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 neuron activity—including dopamine precursors and inhibitors of dopamine metabolism, such as monoamine oxidase-B inhibitors—could represent a promising therapeutic avenue. Notably, disclosures accompanying the study indicate Meyer has a pending patent application involving rasagiline and a tyramine-based dopamine precursor approach specifically for long COVID, filed in January 2026.^1,2,5

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 long COVID patients.²

Looking Ahead

While 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 move forward, pharmacists may play an increasing role in counseling patients on emerging off-label or repurposed therapies, as well as in monitoring for drug interactions and adverse effects associated with dopaminergic agents in a medically complex, often treatment-fatigued patient population.^1-3,5

REFERENCES

1. Liu Y, Persaud, D, Vieira E, et al. Loss of vesicular monoamine transporter 2 in striatum of long COVID and relationship to neuropsychiatric symptoms. eBioMedicine. 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. EurekAlert! News release. 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. 2026.

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. Juluy 16, 2026. Accessed July 17, 2026. https://www.medscape.com/viewarticle/long-covid-associated-injury-dopamine-system-2026a1000o0u