Fig. 1

Schematic network in AD: a Amyloid precurser protein (APP) sheds Amyloid β peptides. ROS promotes abnormal production of A β [5, 6], which activates GSK-3 [4, 6, 8]. Activated GSK-3 mediates hyperphosphrylation of tau proteins [4, 6], which results in the formation of NFTs [10] and destruction of microtubules [4, 10], leading to neuron death. b Astrocytes are activated by \(A_{\beta }^{o}\) [10, 16] and TNF- α [14, 15], and they produce MCP-1 [17–19], which attracts macrophages into the tissue [17, 19]. NFT activates microglias [10, 13, 15]. Activated proinflammatory microglias and microphages produce TNF- α and other proinflammatory cytokines [20, 22, 23], while anti-inflammatory microglias and macrophages produce IL-10 and other anti-inflammatory cytokines [20, 22, 23]. Dead neurons release A β and NFTs, and soluble A β oligomers activate microglia [11, 12]. Activated astrocytes secrete A β [16]. A β deposit is reduced through endocytosis by microglia and macrophages [12, 20]