It is hypothesized that misfolded α-syn may potentiate the observed increase in inflammation seen in PD, as excessive aggregated α-syn can hyperactivate microglia18 and promote neurotoxic effects by enhancing the release of tumor necrosis factor-alpha (TNF-α), interleukin (IL) 1-beta (IL-1β), IL-6, nitric oxide (NO), inducible nitric oxide synthase (iNOS), and reactive oxygen species (ROS). This evidence concerns the gene IL1B and Parkinson disease.