RHOT1 and Parkinson disease: Moreover, the overexpression of wild-type α-synuclein and/or the PD-associated A53T mutation led to the stabilization of the α-synuclein-Miro1 complex in PD flies and human iPSC-derived neurons, preventing mitochondria to detach from the transport machinery and subsequently leading to a delayed mitochondrial arrest (Figure 6B) (12).