We illustrate that neuroinflammatory reactions in PD models can be induced by various factors including MPTP, α-syn, 6-OHDA, and pKr-2, while other mechanisms, such as TLR2, NLRP3, IL-1β, TNF-α, NF-κB pathway, HMBG1, ROS production, CD36, Fyn, mast cells, ASK1, Lcn-2, TG2, CCL2, IL-33, TLR4, mPGES-1, and PGE2, contribute to the establishment and progression of the pathogenetic mechanisms in these models. This evidence concerns the gene CD36 and Parkinson disease.