Tupelo3, thanks very much for your substantial response.

I used the word "theory" when perhaps I should have been using the word "hypothesis".

Hypothesis No 1:
During bouts of fever or infection, the mitochondria within dopamine neurons release a specific protein, which is transported to the wall of the cell, where it acts as an antigen, signalling T cells to attack the neuron. This process is normally prevented from occurring by the actions of the proteins Parkin and PINK1, except in PWPs, where the c-Abl enzyme interferes with the normal operation of Parkin.

​Hypothesis No 2:
From your text: "... the theory that reducing c-Abl will reduce the breakdown of other kinases, like Parkin and Pink1, allowing them to function normally in protein [e.g. alpha-synuclein] clearance."

Hypothesis No 3:
Within the dopamine neurons of non-PWPs, PINK1 proteins phosphorylate PARIS proteins, and this then enables Parkin proteins to ubiquitinate PARIS proteins, and this then enables PARIS proteins to be degraded by proteasomes. This keeps the number of PARIS proteins in check, thus ensuring that dopamine neurons are not killed by excess amounts of the PARIS protein. However, in PWPs, c-Abl interferes with Parkin, and this stops Parkin from being able to ubiquitinate PARIS.

All three hypotheses have in common the phosphorylation by c-Abl of Parkin. They all support a general "theory" (or broad hypothesis) that inhibition of c-Abl may be neuroprotective.