In cultured neurons, treatment with Tf was found to correct iron accumulation, and in the MPTP-induced PD mice model, Tf treatment ameliorated iron accumulation and improved iron deficits.270 Our recent report showed that α-synuclein-A53T and iron function as a toxic couple, inducing cell senescence in both mice and cell models of PD, which precedes the loss of nigral dopaminergic neuron.23 Additionally, reducing the iron load through DFO or knockdown of TfR1 significantly improves the phenotypes of cell senescence induced by α-synuclein-A53T (Figs. 4, 5). This evidence concerns the gene TF and Parkinson disease.