NLRP3 and Alzheimer disease: Inhibition of TXNIP/NLRP3 inflammasome signalling, modulation of SIRT1/HMGB1 axis, interference with pro-inflammatory and pro-apoptotic mechanisms, and restoration of mitochondrial functions and autophagy may represent possible effects by which canagliflozin may emerge as a promising agent for management of the features of AD (Figure 15).