Table 1: Findings in animal models and clinical studies concerning NLRP3 activity in AD.
| Type of study | Reference | Findings |
| Animal model | Heneka, et al. [37] | NLRP3-/- and Caspase-1-/- mice are resistant to experimentally developed AD |
| Griffin, et al. [28] | IL-1β induces tau protein hyperphosphorylation | |
| Gustin, et al. [42] | Aβ stimuli activate NLRP3 specifically in microglia | |
| Wu, et al. [45] | Aβ protofibrils induce NLRP3 activation and IL-1β accumulation in microglia | |
| Couturier, et al. [38] | ASC-/- mice are resistant to experimentally developed AD | |
| Clinical study | Ojala, et al. [27] | Increase of IL-18 in AD brain |
| Heneka, et al. [37] | Increase of Caspase-1 in AD brain | |
| Griffin, et al. [29] | IL-1β is involved in neuronal damage | |
| Saresella, et al. [30] | NLRP3 is upregulated in monocytes of severe AD patients | |
| Dursun, et al. [31] | IL-1β is significantly increased in serum of early-onset AD patients | |
| Chen, et al. [32] | IL-18 is increased in serum of AD patients |