However, TLR2 knockout and TLR4 loss-of-function mutant mouse models secreted less neurotoxic proinflammatory mediators IL-1β, IL-6, TNF, and inducible nitric oxide synthase (iNOS) with Aβ stimulation, suggesting that TLR-dependent signaling may contribute to neurotoxicity in AD [84, 85]. This evidence concerns the gene IL6 and Alzheimer disease.