EAN 2026 | Body-first and brain-first Parkinson’s disease subtypes: evidence supporting the differentiation

So essentially, that’s an idea that has been probably in the back of the Parkinson’s disease people in the latest years, probably since 2000, because there was evidence that there was obviously a prodromal condition in Parkinson’s disease, and those were very differentiating patients, were patients that have very long prodromal condition that lead finally to PD and other people that emerge directly with the motor symptoms. So the idea that something could come from let’s say from the autonomic side or REM sleep behavior disorder from one side and be more associated with the autonomic dysfunction and coming let’s say from the body following what is the Braak hypothesis that is the original hypothesis on the development of pathology in PD. So following let’s say body-first there may be or olfactory bulb or the gut essentially those are the two many hypotheses but in general the overall autonomic system in the body and then finally get to the brainstem and then to the brain and finally lead to the motor manifestation that we all know. And there are some other people that probably instead have directly an abrupt emergence of these kind of symptoms, of the motor symptoms, that are directly coming from the brain. So the evidence is coming from the first, the clinical observation, I would say, and the association of the different prodromal phases within each other. So they could understand that probably there are different phenotypes leading to the final Parkinson’s disease, let’s say, symptomatology. And then what is in evidence and is new in evidence has been a lot of work from the Braakammer group that is based in Denmark and they have done a lot of different imaging modalities in the gut that was especially allowing to estimate the amount of dysfunction in the gut that was preceding the development then of Parkinson’s disease especially in REM behavioral disease, and also data from neuropathology that could allow the distinction of two independent distributions of alpha-synuclein pathology, one more brain-centered, especially it seemed to be less, more amygdala-centered, and another that really proceeded from the, let’s say up. And in recent studies what for example we have done was essentially to estimate this in different condition prodromals and PD in the in their let’s say clinical condition in the clinical phase of the disease. And staging having different modalities to stage the pathology the pathology at different levels in the clinical phase of the disease and staging, having different modalities to stage the pathology at different levels in the brain and in the brainstem, but doing this in vivo, so not, let’s say, ex vivo in the neuropathology condition. And this allows us to show that effectively there is a difference between people that emerge directly and abruptly with motor symptoms and people that instead have a long prodromal phase accompanied with autonomic or REM sleep behavior dysfunction.

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