Thread by @ZdenekVrozina

A Toronto group took the same brain scan used to track Parkinsons - and pointed it at people with long COVID.
Dopamine nerve terminals in the striatum - reduced. Down in the range you’d see in mild-to-moderate Parkinson’s. Lancet family.🧵

The scan is DTBZ PET. It measures VMAT2 - the density of dopamine neuron terminals across three parts of the striatum. One for motivation, one for movement, one for memory.
This is an established Parkinson’s tool. Not something rigged up for COVID.

24 people with long COVID, 24 age matched healthy controls. Lower signal in all three regions. Magnitude comparable to mild-to-moderate PD - and the putamen sits at the level you see in RBD (REM sleep behaviour disorder, most specific early precursor to synucleinopathy). @DavidJoffe64_2

New. They also took people who’d had COVID and recovered, and compared them to people who’d never had it at all.
No difference. p = 0.77.

It’s not had COVID = less dopamine. People who bounced back look like people who were never infected.
The signal isn’t driven by the infection. It’s driven by the unrecovered state.

So what does VMAT2 actually measure? Picture the dopamine system as a delivery network.
VMAT2 = the loading docks where dopamine gets packed into vesicles. The scan counts the docks. Fewer docks usually means a smaller warehouse.

Usually is honesty, not a hedge. A lower number could also mean fewer vesicles per neuron, or less transporter per vesicle - not necessarily neurons lost. The authors say so themselves.

The strongest piece. Symptom maps onto region.
Apathy - ventral striatum. Motor slowing - putamen. Memory decline - caudate.
Not one vague global number - an anatomically specific map. And the lower the signal, the worse that particular symptom.

And it isn’t depression. Zero correlation with the Beck Depression Inventory. The result holds even after dropping the two people with a prior depressive episode.
An objective imaging abnormality, in an illness the system still frames as functional.

The discussion pushes a treatment direction. L-dopa, MAO inhibitors, dopamine augmentation. Sounds reasonable.

Good to know that the senior author filed a patent in 2026 for rasagiline and a tyramine dopamine-precursor approach - specifically for a long COVID indication.

The data don’t collapse because of that. But L-dopa as a long COVID treatment is the authors hypothesis, not this study’s finding.

Not neuron loss (index), not Parkinsons, not progression (a snapshot), and not long COVIDin general - but the neuropsychiatric LC subset the cohort was pre selected for.
Also not just depression, and not a COVID artefact.

Still - another independent line pointing at the same place. RBD (Gong), α-synuclein in vitro, FDG-PET brainstem (Guedj), TSPO inflammation (Visser), and now the dopamine terminals themselves.

HIV taught us a slow neuro-process can run below the clinical threshold that short windows keep missing.
There’s too much signal now to keep operating without prevention.
Avoid the lottery. Most people don't win in the long run.
@szupraha @ZdravkoOnline @adamvojtech86

Karida Liu at al., Loss of vesicular monoamine transporter 2 in striatum of long COVID and relationship to neuropsychiatric symptoms. thelancet.com/journals/ebiom…