Clinical trials of cell transplantation therapy using fetal mesencephalic tissue provided a proof-of-concept for regenerative therapy for the patients with Parkinson‘s disease. Postmortem studies of the patients who received fetal grafts revealed that α-synuclein (α-syn)⁺ Lewy body-like inclusions were emerged in long-term transplantation and may reduce the clinical outcomes even the grafts were well survived in the recipients. Various studies were conducted to reveal that the host derived α-syn are transferred to the grafted neurons to assess the exsert of α-syn⁺ inclusions in the grafts. However, these studies remain the possibility to detect the intrinsic expression of α-syn in the grafted neurons. Here, we demonstrated that the human α-syn preformed fibrils inoculated into the cerebral cortex were transferred to SNCA^-/- human induced pluripotent stem cell-derived midbrain dopaminergic (mDA) neurons grafted into the striatum of rats. Because grafted SNCA^-/- hiPSC-derived mDA neurons lack the intrinsic expression of α-syn protein, the human α-syn-immunoreactivity found in the grafted cells should be derived from the host brain. Our results clearly showed that host-to-graft propagation of α-syn was occurred, and this work contributes to understand the molecular mechanisms to form the α-syn inclusions in the grafted mDA neurons.