Jeffrey, my comment was really made tongue-in-cheek. However, if you want to be literal, I believe my comment is actually correct.

All of the research you mention is just support of the same basic theory. Essentially, the two kinases, Parkin and Pink1, add a protein called ubiquitin to PARIS, resulting in it's breakdown. PARIS is critical for proteasome-mediated protein clearance (particularly a-syn) and helps protect against the loss of dopamine neurons. The tyrosine kinase Abelson (c-Abl) is known to interact with many genes, and their protein products. Two of those, specifically, are Parkin and Pink1. c-ABL phosphorylates parkin, which inhibits its ligase activity, leads to substrate accumulation, and interferes with its protection against neurotoxicity. Recent analyses from PD patients and animal models of PD show an increase in the level of c-Abl, suggesting that the gene, and it's kinase, may be dysfunctional in PWP. This leads to the theory that reducing c-abl will reduce the breakdown of other kinases, like Parkin and Pink1, allowing them to function normally in protein clearance. The Brahmachari et al. study you noted demonstrated that deletion of the gene encoding c-Abl reduced α-synuclein aggregation and neurobehavioral deficits whereas overexpression of the constitutively active c-Abl accelerated α-synuclein aggregation, neuropathology, and neurobehavioral deficits. This study was a major component of the the research theory in the protocol for both the Georgetown and MJFF et al new trials.

I know this is an over-simplification, but this is the theory that backs all three of the upcoming trials. What other theories are there behind the use of a c-Abl inhibitor as a neuroprotective agent?