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