On the contrary, a downstream effector of AKT, mTOR, was already significantly phosphorylated in αS Tg animals treated with water compared to Ntg littermates (283.9±42.8 vs 100±22.3), confirming previous data obtained in this and other models of α-synucleinopathy where overexpression of αS was sufficient to activate mTOR33,34. This evidence concerns the gene MTOR and synucleinopathy.