Rick,

Thanks for starting a debate on this topic: you can't get anything more important for us than the aetiology of PD.

Where I agree with your theory:

I can buy into the importance of neuroinflammation.

I think you're right to say that anti-inflammatories are inversely associated with PD, and inflammatories are positively associated with PD.

I think that your no one cause theory of PD is correct. This leads to a scoring system, a bit of this plus a bit of that, which builds up to something that leads to real damage.

But, all of that is insufficient to show direct causality.

GerryW's question is a good one: many people have exceptionally stressful lives, flu, h.pylori etc., but don't get PD; many people with PD haven't had noticeably stressful lives.

Where I disagree with your theory:

I think what's missing is the role of genetics and the role of alpha-synuclein.

I believe that the true significance of inflammation is that it increases the chance of misfolding, aggregation and clumping of alpha-synuclein. This leads to the death of neurones and the collection of symptoms that we see in PwP.

(I've written this post without references, but references to most of the post's assertations can be found by searching for the string johnt:alpha-synuclein .)

John