The issue, as I see it, is whether pathogens continue to play a role once the disease is triggered.

(Note: I use "pathogen" to mean both biological and non-biological agents. I include environmental effects.)

Can epidemiology give an answer?

Suppose you have two identical people whose PD starts at the same time. One goes to live in a high pathogen environment and the other in a low pathogen environment. Then, if the role of the pathogen is solely to trigger the disease, we would expect them to progress at the same rate. Alternatively, if pathogens continue to play a role, we would expect the disease of the person living in the high pathogen environment to progress faster.

We can't get this data experimentally, but we should be able to sift the answer from epidemiological data.

I assume in what follows that the data has been normalized for age, gender, race, socio-economics etc, and that the granularity is such that genetic cluster effects are smoothed out.

We start by noting that if pathogens play a part in the aetiology of PD, the incidence rates of neighbouring areas will be correlated. However, this correlation would not differentiate between the role of pathogens in causing the disease to trigger and their role in the progression.

To separate out these two effects, we focus on disease duration; for PD the time from diagnosis to death. For something that is incurable, disease duration is given by prevalence divided by incidence.

Next, we could again reason that if pathogens continue to play a part, duration statistics for neigbouring areas will be correlated.

Does anyone know of research in this area?

My hope is that soon the Parkinson's community will be organised enough to get a preliminary answer to such questions in one day. YES, ONE DAY!

John