A possible involvement of the NLRP3 inflammasome in the pathogenesis of PD was initially suggested in 2013 by Codolo et al., who demonstrated in vitro that, while both monomeric and fibrillary α-syn increased pro-IL-1β levels via toll-like receptor (TLR)-2 signaling, the fibrillary form of α-syn, alone, stimulated the inflammasome by activating caspase-1, resulting in IL-1β production [71]. Here, IL1B is linked to Parkinson disease.