Scientists finally find proof of physical damages to the brain after long COVID
It seems like an age ago that we were waving at loved ones through windows, going to the shops on our own while wearing masks, and disinfecting our weekly vegetables while ensuring we stayed six feet apart. But what kind of effect might long COVID have had on our brains?
The COVID-19 pandemic can be traced back to December 19, but even six years later, there's been an influx of interest in the outbreak and its lasting effect. Most notably, former National Institute of Allergy and Infectious Diseases director Dr. Anthony Fauci has been dragged in front of a Republican-led Senate hearing.
With Fauci's diary entries being among the declassified files used as evidence, the Trump administration used the opportunity to share its own accusations that COVID-19 was cooked up in a Chinese lab instead of being a natural outbreak.
While we'll likely never get to the bottom of what actually caused COVID-19, we can continue to study the effects it and the vaccines have had on the human body.
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We previously covered how research suggested those who took the vaccine had a 25% lower risk of death from any cause compared to unvaccinated adults.
Now, a new study published in eBioMedicine looks at the potential effects of long COVID on the brain, and in particular, its apparent impact on dopamine-releasing neurons.
Since the pandemic, long COVID sufferers have complained about health issues like brain fog, a lack of concentration and motivation, and a general feeling of losing pleasure.
The University of Minnesota's Center for Infectious Disease Research and Policy writes that teams from Toronto's Brain Health Imaging Centre and the University of Toronto used positron emission tomography (PET) brain imaging to measure vesicular monoamine transporter 2 (VMAT2) in 24 adults suffering from COVID and persistent neuropsychiatric symptoms, as well as 24 'healthy' control adults. CIDRAP reminds us that VMAT2 is considered a marker of dopamine neuron integrity.
The paper confirmed: "Findings of reduced VMAT2 binding may reflect reduced dopaminergic terminal integrity in long COVID. Loss of dopamine nerve terminals may be contributing to symptom correlates of apathy, motor slowing and memory decline suggesting improved function of dopaminergic synapses as a new therapeutic direction to treat long COVID."
In a news release from the Centre for Addiction and Mental Health, which houses the Brain Health Imaging Centre, senior scientist at the Brain Health Imaging Centre and senior study author, Jeffrey Meyer, MD, PhD, said: "Our findings provide compelling evidence that long COVID involves the loss of dopamine-releasing neurons.
"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."
Those with long COVID are said to have between 16% and 20% lower VMAT2 across three regions in the striatum, with the biggest difference being found in the dorsal putamen.
Considering the dorsal putamen is involved in movement, and the dorsal caudate is associated with memory, it fits with previous theories.
There was the smallest difference in the ventral striatum, which is typically associated with our motivation and reward centers.
In accompanying commentary, Aix Marseille University's Eric Guedj and Helmholtz Munich's Danielle Beckmann say this kind of work moves us from "symptom description to mechanistic stratification." The pair add: "By linking neuropsychiatric symptoms to a presynaptic dopaminergic marker, it reframes part of the long COVID spectrum as a measurable brain-network phenotype."
Still, Guedj and Beckman reiterate that these changes to our brains might not be permanent, with more long-term studies required.
As well as a limited sample size and focusing on long COVID patients who have significant neuropsychiatric symptoms, the findings are limited to association rather than causation.
Meye maintains that long COVID is at least related to our brain's dopamine system, concluding: "This suggests that repurposing medications that augment the function of dopamine-releasing neurons, including dopamine precursors and inhibitors of dopamine metabolism, could be a promising approach."