NLRP3 and Alzheimer disease: Moreover, the enhanced activation of the NLRP3 inflammasome, and thus increased IL-1β release, observed in the added presence of anti-α-Syn or anti-Aβ antibodies [28] was also abrogated by CA (Figure 2), implying that this type of therapeutic intervention might offset at least some of the inflammatory side effects of these antibody therapies being developed for AD and PD.