A Canadian group looked at this directly. Positron emission tomography tracked the VMAT2 protein — a transporter that is abundant at the terminals of dopamine cells. In the striatum, patients had noticeably less of the marker than controls. The pattern matched the complaints. Ventral striatum — a drop in motivation. Dorsal putamen — slower movements. Caudate nucleus — memory.
Alongside this sits an older idea about inflammation in those same dopamine regions. The scan by itself doesn’t prove that the virus killed a neuron. It’s possible the terminals have simply quieted down. It’s possible some terminals really are gone. PET can’t distinguish between these scenarios.
There is no treatment with a proven evidence base against long COVID. The authors hint at drugs that boost the dopamine system and are planning trials. For now, that’s a logical next step, not a pharmacy prescription. Still, the fog stops being just “psychosomatics after illness.” In some people, the brain shows a specific deficit in the circuit that is responsible for the energy to act.
Illustration: Sciencedaily.com