Respectfully, in all three of the hypotheses you present the inhibition of c-Abl are the exact same. What you're trying to postulate is what may cause malfunction in the first place. Maybe its environmental like fever, infection, or other toxin. Maybe it's genetic. Maybe it's some other cause we haven't even thought of yet. Nevertheless, in each of your hypotheses, there are no differences once you get to the point oh inhibiting c-Abl. I would be inclined to agree with you if there was evidence, or even a theory (or hypothesis) that c-Abl inhibition reacted differently with genetically mutated Parkin as opposed to environmentally malformed Parkin (associated with idiopathic PD). But, I am not aware of that, at this time.

I think you really are more focused on the theories of the root cause of PD. That goes way beyond any theory or hypothesis as to why c-abl inhibition may be neuroprotective for people with neurological diseases.