Paula,

I understand that; sorry, my post wasn't very clear in reflecting this. I simply question how our bodies make us receptive to the inflammation in the first place. Identifying another possible trigger (beyond endotoxins) in the form of a virus helps in terms of, possibly, eventually halting the disease before it really takes hold. Could we develop a vaccine, for example?

In the end, and I may be wrong, I still think we need to know what makes our brains so warm and inviting a place for PD in the first place? We all may have variable causative factors or triggers, but there has to be something we all commonly have within our brains that puts out the welcome mat to the pathology in the first place. If we look at Braak's visual model of neuronal pathology, we see that neurons either close or open the door to PD, so to speak. Braak's staging, which focuses on the olfactory region as the "birthplace" of Lewy Body Disease and PD, is wholly dependent on Lewy Bodies, but can we use this model in the absence of LBD? Some of us will, upon autopsy, have no evidence of LBD, yet we still exhibit clinical signs of Parkinsonism. How does the viral, inflammatory trigger work in the absence of the Lewy hallmark?

So many more questions arise for me. I'm a person who craves clarity; I always look at the forest instead of the tree. In adding yet another "tree", variable or pathway in the PD etiology, I feel even farther away from seeing a curative or protective treatment develop that will help the vast majority of us. What scares me is that the more I learn, the more I recognize why PD is a "boutique disease" that may in turn respond (beyond the Sinemet tourniquet) to only boutique interventions.

A couple good resources on what we've been discussing:

Parkinson's Disease: New Research (see link above for Google Book)

Olfactory system pathology as a model of Lewy neurodegenerative disease a literature review at PDOnline Research

Laura