Table 6.
The putative mechanisms of acupuncture on different Alzheimer's disease animal models.
| Model | Acupuncture point | Mechanism |
|---|---|---|
| SAMP8 mice | CV17, CV12, CV6, ST36, SP10 | Regulates brain cell proliferation (34). Reduced neuron loss in hippocampal regions CA3 and DG (35). upregulated the expression of bFGF, EGF, and BDNF (36). improving synaptophysin mRNA and protein levels (37). promoting Hsp84 and Hsp86 expression (38). accelerates synaptophysin production (39). Down-regulating PI3K/PDK1/nPKC/Rac1 signaling pathway (40). |
| GV14, BL23 | increased the levels of p-AMPK (41). upregulated the expression of SIRT1 and PGC-1α (42). downregulation of BACE1(43). | |
| GV20, GV29 | increased CBF in the prefrontal lobe and hippocampus (44). by balancing the gut microbiota (45). enhanced paravascular influx in the glymphatic system inhibited the reactivity of astrocytes and improved AQP4 polarity (46). | |
| GV20, GV29, GV26 | improved the level of glucose metabolism (47). | |
| GV20, BL23 | inhibited the AMPK/eEF2K/eEF2 signaling pathway (48). | |
| GV20, ST36 | downregulated NLRP3/caspase-1 pathway (49). | |
| GV20, BL23, KI3 | inhibited activation of astrocytes and microglia and decreased expression of pro-inflammatory cytokines, TNF-α, and IL-17 (50). | |
| APP/PS1 mice | GV20 | up-regulated the expression of BDNF (51, 52). Induced phosphorylated AMPK and AKT inhibited the phosphorylation level of the mammalian target of mTOR (53). suppressed GFAP and NDRG2 upregulation (54). increased the expression levels of BDNF and proBDNF, p-TrkB was upregulated, and p75NTR was decreased (55). |
| GV20, GV29, GV26 | enhancing glucose metabolism (56, 57). downregulated of BACE1, p-PKA protein (58). inhibited JNK signaling pathway (59). induced AKT (Ser473) and GSK3β (Ser9) phosphorylation, inhibited the phosphorylation of Tau (Ser199 and Ser202) proteins (60). | |
| GV20, BL23 | reduced the expressions of BACE1, and increased the expression of IDE protein (61). | |
| GV20, GV24 | activated AMPK to enhance the process of Aerobic glycolysis (AG), and enhanced glucose metabolism (62). | |
| 5x FAD | KI3 | inhibition of neuroinflammation and increased glucose metabolism (63). upregulation of synaptophysin and postsynaptic density-95 protein (64). |
| GV24, GB13 | activated TFEB via inhibiting the AKT-MAPK1-MTORC1 pathway (65). | |
| GV20, GV24 | activating the medial septal and vertical limb of the diagonal band and dentate gyrus (MS/VDB-DG) cholinergic neural circuit (66). | |
| injecting Aβ1 − 40 Rat Model | GV20, BL23 | activation of PPAR-γ and inhibition of p-p38MAPK expression (67). upregulated the expression of Bcl-2 and downregulated the expression of Bax, downregulated the level of Notch1 and Hes1 mRNA in the hippocampus (68). |
| injecting Aβ1 − 42 Rat Model | GV20, BL23 | downregulated the expression of GSK-3β (69). |
| GV29, LI20 | the activation level of PI3K/AKT signaling and the phosphorylation inactivation of GSK-3β (70). |
Dentate Gyrus (DG), basic fibroblast growth factor (bFGF), epidermal growth factor (EGF), brain-derived neurotrophic factor (BDNF), heat shock protein (Hsp), Phosphatidylinositol 3 Kinase (PI3K), Phosphoinositol-Dependent Kinase 1 (PDK1), Novel Protein Kinase C (nPKC), Sirtuin 1 (SIRT1), proliferator-activated receptor-γ-co-activator-1α (PGC-1α), Beta-secretase 1 (BACE1), Cerebral blood flow (CBF), aquaporin-4 (AQP4), AMP-activated protein kinase (AMPK), eukaryotic elongation factor-2 kinase (eEF2K), eukaryotic elongation factor-2 (eEF2), Nod-like receptor family pyrin domain containing 3 (NLRP3), tumor necrosis factor-α (TNF-α), interleukin-17 (IL-17), thymoma viral proto-oncogene (AKT), glial fibrillary acidic protein (GFAP), N-myc downstream-regulated gene 2 (NDRG2), c-Jun N-terminal kinase(JNK), insulin degrading enzyme (IDE), mitogen-activated protein kinase 1 (MAPK1), mechanistic target of rapamycin kinase complex 1 (MTORC1), glycogen synthase kinase-3β (GSK-3β).