In summary, our results demonstrate that TMAS enhances microglial functions to reduce amyloid plaque deposition and enhance synaptic rehabilitation, indicating that the effects of TMAS are superior to those of TUS in a microglial-dependent manner via the PI3K-AKT signaling pathway, providing new insights into the potential of TMAS for the treatment of Alzheimer’s disease. Here, AKT1 is linked to Alzheimer disease.