This looks promising. There is a free-access version of the paper here; JCI -
Activation of tyrosine kinase c-Abl contributes to α-synuclein–induced neurodegeneration.

Abl is a tyrosine protein kinase. What the authors showed is that Abl-mediated phosphorylation of Tyr39 of α-synuclein led to neurodegeneration in a mouse model of PD, probably arising from aggregation of α-synuclein. They also found elevated levels of phosphorylated α-synuclein at Tyr39 in post-mortem examination of people with PD, compared to age-matched controls.