Figure 2.

Illustration of how NLRP3, TREM2, cGAS-STING, and microglial NF-κB contribute to the development of AD. Neuronal death is triggered by Aβ by activating the NLRP3 inflammasome and NF-κB pathway. DAP12 becomes phosphorylated as a result of TREM2’s interaction with it, initiating a signaling cascade. In order to control neuroinflammation, cGAS-STING activates transcription factors for type I interferons and proinflammatory cytokines. Moreover, TLRs are involved in controlling the polarization of macrophages. Extended TLR4 activation increases pro-inflammatory cytokines and chemokines, which in turn exacerbate chronic inflammation.