We hypothesize that this increase in p-rpS6 may reflect a compensatory response of the neuron to the modest ongoing α-syn insult, similar to previous reports of a compensatory increase in TH and markers of dopaminergic transmission in early synucleinopathy preclinical models, early-stage PD and non-symptomatic Leucine-rich repeat kinase 2 (LRRK2) mutation carriers71–73. This evidence concerns the gene LRRK2 and synucleinopathy.