Research Paper Volume 11, Issue 11 pp 3795—3810

Kainic acid Induces production and aggregation of amyloid β-protein and memory deficits by activating inflammasomes in NLRP3- and NF-κB-stimulated pathways

Figure 8. A functional model of KA-induced activity of inflammasome that exacerbates Aβ production, deposition, and memory deficits. KA treatment triggered the activation of inflammasome and caused the phosphorylation of NF-κB, leading to NLRP3 upregulation in microglia cells. Upregulated NLRP3 eventually resulted in the cleavage of APP by enhancing the expression of BACE1. Bay11-7082 inhibited the KA-induced IL-1β activation and Aβ production and deposition via alleviating the activity of inflammasome in neurons, which ultimately improved the cognitive decline of the APP23 mice.