TABLE 2.
Pyroptosis in AD.
| Works | Key molecules | Summary |
| Tan et al. (2014) | Aβ, NLRP1, IL-1β | Aβ deposition increased NLRP1. Inhibiting NLRP1 decreased caspase-1 and IL-1β. |
| Wu et al. (2013) | Aβ, NLRP3, IL-1β | In Microglial, IL-1β was activated through Aβ/caspase-1/NLRP3 pathway. |
| Yap et al. (2019) | Aβ | Aβ deposition activated inflammasome, and then cleaved caspase-1 triggering pyroptosis. |
| Venegas et al. (2017) | Aβ | ASC bound to Aβ, resulting in the formation of Aβ oligomers and aggregates. |
| Li J. et al. (2020) | Aβ, GSDMD | Inhibiting NLRP3 reduced pyroptosis and decreased NLRP3, caspase-1, GSDMD. |
| Han et al. (2020) | Aβ, GSDMD | Aβ1-42 induced pyroptosis through NlRP3/caspase-1/GSDMD signaling pathway. |
| Heneka et al. (2013) | Aβ, GSDMD | Aβ deposition induced NLRP3 inflammasome. NLRP3 reduction decreased caspase-1 and GSDMD. |
| Li et al. (2021) | GSDMD | Guanidine reduced hippocampal neuron damage by inhibiting GSDMD mediated pyroptosis. |
| Lei et al. (2021) | Caspase-8, GSDME | Hippocampal injured through caspase-8/GSDME pyroptosis pathway. |
| Liu (2020) | GSDME | Hippocampal CA3 region was found neuronal degeneration and cell death with increased GSDME positive cells. |
| Feng et al. (2021) | Tau protein, IL-1β | IL-1β induced microglial phagocytic activity loss, and tau protein hyperphosphorylation. |
| Ising et al. (2019) | Tau protein, NLRP3 | NLRP3 induced tau protein hyperphosphorylation and aggregation. |
| Li Y. et al. (2020) | Tau protein, caspase-1 | Injecting caspase-1 inhibitor or lithium chloride suppressed tau protein hyperphosphorylation and pyroptosis. |
| Saresella et al. (2016) | NLRP1, IL-1β, IL-18 | NLRP1/caspase-1/ILs pathway activated in AD brain. |
| Ojala et al. (2009) | Inflammatory cytokines | IL-1, IL-1β and IL-18 expression was increased in AD brain. |