AKT1 and Alzheimer disease: Using an Aβ25-35-treated HT22 cell model to establish an AD model, it has been found that GA-A can change the effects of Aβ25-35 in inhibiting cell viability, promoting apoptosis, and senescence, and it has been hypothesized that GA-A delays the senescence of AD cells through the modulation of immune-inflammatory mechanisms via the JAK-PI3K-AKT-mTOR signaling pathway [78].