I am still on the learning curve on this one so take this for what it is worth...

The bacterial endotoxin lipopolysaccharide (LPS) plays a critical role in PD. Exposure in the womb sets the stage and further exposure after puberty triggers autoimmune problems through microglial activation. Also, because LPS is a constant presence and because of the prenatal sensitization, it results in a chronic inflammatory state which, in turn, induces the body to produce glucosteroids such as cortisol - a natural anti-inflammatory that becomes destructive itself when chronically present.

LPS is, literally, everywhere. It is the main component of ordinary house dust, for example. It is in our food supply (milk and grain in particular). Our immune system constantly creates a residue of it by killing the bacteria that release it pon their death. There is no getting away from it.

Since it is a constant, the body obviously has to have a way of disarming it as a problem in a normal human. And it does indeed. It uses the lipoproteins such as HDL and LDL in a process that binds the toxin and renders it harmless.

The medical community has made the assumption that those substances are dangerous above a certain level that applies to everyone. I don't think that consideration has been given to the possibility that in some situations our bodies may need those higher levels and in fact may create them.

If that were true then statins may be thwarting the attempts and thus leading to God knows what in PD or ALS.

If you want to delve into this you might start with looking at the work of a team at the NIH headed by a rsearcher named Bin Liu. If you do find connections I would like to know. Good luck.