Research Paper Volume 13, Issue 5 pp 7549—7569

Preclinical systematic review of ginsenoside Rg1 for cognitive impairment in Alzheimer’s disease

Possible mechanisms of ginsenoside Rg1 (G-Rg1) in improving cognitive function. Possible mechanisms for Rg1 improving cognitive function are the following. (1) Rg1 could inhibit the pathogenesis of Alzheimer’s disease (AD). G-Rg1 could promote cleavage of amyloid precursor protein (APP), inhibit the hyperphosphorylation of tau and prevent amyloid - β (Aβ) deposition. This would occur by increasing a disintegrin and metallopeptidase domain 10 (ADAM10) expression and decreasing β-secretase β-site APP-cleaving enzyme 1 (BACE1) expression. (2) Rg1 could offer synapse protection. G-Rg1 could increase the levels of ACh, BDNF, and multiple synaptic proteins, such as synapsin 2 (SYN2), complexin 2 (COM2), and synaptosomal-associated protein 25 (SNP25). (3) Rg1 could increase antioxidant activity. G-Rg1 could increase the activity of SOD and GSH-PX, and could decrease the levels of ROS and MDA. (4) Rg1 could increase anti-inflammatory activity. G-Rg1 could inhibit the expression of TNF-α, decrease the levels of IL-1β, IL-6, and IL-18, and decrease the expression of caspase 1 and caspase 5. (5) Rg1 could up-regulate nerve cells. G-Rg1 treatment delays neural stem cell (NSC) senescence and decreases cell apoptosis, and G-Rg1 treatment increases the number of NSCs and new nerve cells; however, the mechanism for this is not yet clear.

Figure 9. Possible mechanisms of ginsenoside Rg1 (G-Rg1) in improving cognitive function. Possible mechanisms for Rg1 improving cognitive function are the following. (1) Rg1 could inhibit the pathogenesis of Alzheimer’s disease (AD). G-Rg1 could promote cleavage of amyloid precursor protein (APP), inhibit the hyperphosphorylation of tau and prevent amyloid - β (Aβ) deposition. This would occur by increasing a disintegrin and metallopeptidase domain 10 (ADAM10) expression and decreasing β-secretase β-site APP-cleaving enzyme 1 (BACE1) expression. (2) Rg1 could offer synapse protection. G-Rg1 could increase the levels of ACh, BDNF, and multiple synaptic proteins, such as synapsin 2 (SYN2), complexin 2 (COM2), and synaptosomal-associated protein 25 (SNP25). (3) Rg1 could increase antioxidant activity. G-Rg1 could increase the activity of SOD and GSH-PX, and could decrease the levels of ROS and MDA. (4) Rg1 could increase anti-inflammatory activity. G-Rg1 could inhibit the expression of TNF-α, decrease the levels of IL-1β, IL-6, and IL-18, and decrease the expression of caspase 1 and caspase 5. (5) Rg1 could up-regulate nerve cells. G-Rg1 treatment delays neural stem cell (NSC) senescence and decreases cell apoptosis, and G-Rg1 treatment increases the number of NSCs and new nerve cells; however, the mechanism for this is not yet clear.