CAMH study links long COVID symptoms to dopamine neuron loss

Researchers at Toronto’s Centre for Addiction and Mental Health (CAMH) have identified biological evidence linking long COVID to the loss of dopamine-releasing neurons in the brain. The study, published in eBioMedicine, utilized positron emission tomography (PET) imaging to measure vesicular monoamine transporter 2 (VMAT2), a protein that serves as a marker for dopamine nerve terminal density.

Comparing 24 adults with long COVID to 24 healthy controls, the study found significantly lower VMAT2 levels across the striatum, a brain region responsible for motivation, movement, and thinking. The reductions, ranging from 16% to 20%, correlated with specific symptoms: lower levels in the ventral striatum were linked to apathy, reductions in the dorsal putamen to slower movement, and lower levels in the dorsal caudate to memory impairment.

While the findings provide a measurable biological signal for symptoms like fatigue and brain fog, researchers noted that the study does not prove dopamine damage causes long COVID, nor does it establish a current treatment. No dopamine-targeting drugs have been proven to treat the condition, though the results may inform future clinical trials.