SNCA and Parkinson disease: We found that pathologic α-synuclein activates the mammalian target of rapamycin complex 1 (mTORC1), leading to enhanced mRNA translation, protein synthesis, and concomitant neurodegeneration in PD, with the genetic and pharmacologic inhibition of mTOR and protein synthesis in α-synuclein transgenic models rescuing dopamine neuron loss, behavioral deficits, and aberrant biochemical signaling, i.e., reduced protein synthesis is neuroprotective in pathologic α-synuclein models.