A CAMH PET study finds lower dopamine terminal markers across the striatum in long COVID

PET sees a radioligand binding to a target, not the neurons themselves. The target here is what the release calls a well-established marker of the health and integrity of dopamine neurons ^[2]. Lower binding suggests a reduced density of dopamine nerve terminals ^[4]. The release keeps that step as an inference; Jeffrey Meyer, the senior author, put it more firmly. "Our findings provide compelling evidence that long COVID involves the loss of dopamine-releasing neurons," he said ^[9]. Reduced expression of the marker and loss of the terminal itself would both lower the signal. The release did not state the number of participants, the radiotracer or the size of the reduction, only that levels were substantially lower ^[19].

The result that is hard to explain with a general sickness factor is the regional split. Low binding in the ventral striatum went with greater loss of motivation, reductions in the dorsal putamen with slower movement, and lower levels in the caudate putamen with memory difficulties ^[6][7][8]. If deconditioning or illness severity were driving the whole thing, you would expect the striatum to be uniformly low and every symptom to correlate with every region ^[5].

The same group's earlier scans found unusually high brain inflammation in people with long COVID, most pronounced in regions containing large numbers of dopamine-releasing neurons ^[11]. "We know that inflammation can injure dopamine neurons," Meyer said ^[10]. That route is established, and this design cannot show it ran here: the study compares people who already have long COVID against healthy participants ^[2]. The scans fix no order of events.

Scale, as reported, is one estimate used twice. Long COVID is put at about five per cent of the global population and roughly two million people in Canada ^[14]. Two million divided by five per cent implies a national denominator of 40 million ^[18], so the Canadian number follows from applying the same rate. For a single patient, a group difference in binding is not a test; classification needs two distributions that barely overlap, and a real gap between averages can still misclassify half the people who arrive at a fatigue clinic.

Meyer said the results suggest "repurposing medications that augment the function of dopamine-releasing neurons, including dopamine precursors and inhibitors of dopamine metabolism, could be a promising approach" ^[13]. Those drugs raise signalling in a system with fewer terminals. They leave the terminals as they are, and a correlation between marker level and symptom severity does not establish that restoring the signal restores the function. He also said the findings indicate long COVID is "at least in part, a disorder of the brain's dopamine system" ^[12]. There are no evidence-based treatments for the condition at present ^[16], and according to the release, most research has gone to inflammation and immune activity while very few clinical trials have targeted dopamine-releasing neurons directly ^[17].