The blood-derived immune cells, sera, and brain regions of PD patients with SNCA defect have also shown overexpression of α-syn and their association with cellular activation and increased generation of pro-inflammatory mediators (e.g., IFNγ, TNFα, IL-1β, IL-4, IL-5, IL-6, IL-18, and CCL2) as well as their link to neuronal cell damage (Table 4B). The gene discussed is CCL2; the disease is Parkinson disease.