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. 2024 Mar 14;13(6):511. doi: 10.3390/cells13060511

Figure 1.

Figure 1

Schematic diagram shows neuroimmune response, neuroinflammation, neurodegeneration and neuronal loss in AD. AD pathogenesis involves neuroimmune response and is associated with the formation of APs and NFTs leading to chronic neuroinflammation, BBB disruption, synaptic loss and neuronal damage in the brain. Chronic activation of astrocytes and microglia release several proinflammatory cytokines, chemokines and neurotoxic mediators (ROS, NO) that further activate glial cells and neurons and induce neuronal death. Molecules released from dying neurons such as DAMPs, S100β, etc. further activate glial cells. Inflammatory cytokines and chemokines from the periphery could enter the brain through damaged BBB and increase neuroinflammation and neurodegeneration. Iba1 = Ionized calcium binding adaptor molecule 1; DAMPS = damage-associated molecular patterns; GFAP = Glial fibrillary acidic protein; NO = nitric oxide; P2Y12R = P2Y12 receptor; ROS = reactive oxygen species; TMEM119 = transmembrane protein 119.