Tupelo3, I've read your response several times, but I just can't see how you came to understand my post in that way. I'll try to say the same thing once again, but this time in a different way.

From reference [4]: "While the activity of c-Abl is crucial for proper neuronal development, it appears that c-Abl remains relatively quiescent in healthy adult neurons, and there are few known functions of c-Abl in fully differentiated neurons. In recent years, it has been shown that activation of c-Abl in adult brain occurs in the context of human neurodegenerative disease."

From reference [2]: "c-Abl is a nonreceptor tyrosine kinase that is activated by oxidative and cellular stress"

Just from these two statements, it could be hypothesized that the inhibition of c-Abl might be a worthwhile thing to try.

I have simply outlined three different ways by which the inhibition of c-Abl might (hypothetically) result in protection of dopamine neurons.

Granted, hypotheses 1 & 3 have my name on them, but in each case I have only contributed the bit which says that c-Abl prevents Parkin from performing its normal function. The rest of hypothesis 1 and hypothesis 3 is straight from reference [1] and reference [3] respectively.

[1] Matheoud et al. (2016) Parkinson’s Disease-Related Proteins PINK1 and Parkin Repress Mitochondrial Antigen Presentation, Cell 166, 314–327, doi: 10.1016/j.cell.2016.05.039.

[2] Brahmachari et al. (2016) Activation of tyrosine kinase c-Abl contributes to α-synuclein-induced neurodegeneration, J Clin Invest. doi: 10.1172/JCI85456.

[3] Yunjong et al. (2016) PINK1 Primes Parkin-Mediated Ubiquitination of PARIS in Dopaminergic Neuronal Survival, Cell Reports Volume 18, Issue 4, p918–932, doi: 10.1016/j.celrep.2016.12.090.

[4] Schlatterer et al. (2011) c-Abl in Neurodegenerative Disease, J Mol Neurosci. 2011 Nov; 45(3): 445–452, doi: 10.1007/s12031-011-9588-1.