AKT1 and Alzheimer disease: Qi et al. found that AOSC ameliorated the cognitive deficits in the Aβ1-42-induced mouse model of AD and that AOSC reduced Aβ1-42 deposition and downregulated the hyperphosphorylation of tau proteins, possibly via the PI3K/Akt/Gsk-3β/CREB pathway, thereby reversing cognitive deficits and neurodegeneration in the mice (Table 6) [98].