Abstract: Objective To explore the relationship between central nervous system (CNS) inflammation and Parkinson disease (PD) caused by different causes. Methods Two modeling methods were selected: a 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) chronic model and a A53T-α-synuclein gene mutation model. Immunofluorescence staining was used to observe the activation of microglia in the substantia nigra (SN), ventral tegmental area (VTA) and hippocampus (Hipp). Results The number of activated microglia in the SN, VTA and Hipp in the two model groups significantly increased. Conclusions Both the chronic MPTP model and the A53T-α-synuclein gene mutation model can cause inflammatory state in CNS for a long-term.