Progressive neurodegeneration in Parkinson's disease is linked to toxic accumulation of α-synuclein aggregates in neurons. Although mutations in the gene encoding α-synuclein are associated with inherited forms of Parkinson's disease, the identification of other factors that contribute to α-synuclein aggregation may lead to more effective approaches for slowing disease advancement. In this month's issue of the JCI, a team led by Ted Dawson and Han Seok Ko at Johns Hopkins School of Medicine determined that activation of a protein called c-Abl exacerbates α-synuclein accumulation and the appearance of behavioral hallmarks of Parkinson's disease in mice. Activating c-Abl accelerated α-synuclein accumulation and the development of motor deficits in mice with Parkinsonian symptoms. In contrast, Parkinsonian mice that lacked c-Abl acquired α-synuclein aggregates and motor deficits more slowly than control mice. These results suggest that c-Abl plays an important role in promoting the α-synuclein accumulation that leads to Parkinson's disease and indicate the potential neuroprotective benefits of therapeutic strategies targeting c-Abl.