Abstract
Repetitive transcranial magnetic stimulation (rTMS) is a noninvasive and painless technique that has been applied for the treatments of diverse neurodegenerative disorders. In the current study, its anti-Alzheimer's disease (AD) effect was assessed and the mechanism driving the effect was explored. The AD symptoms were induced via the intracranial injection of Aβ 1-42 in mice and then treated with rTMS of 1 Hz or 10 Hz. The anti-AD effect of rTMS was assessed by Morris water maze (MWM), histological staining and western blotting. The results showed that rTMS administrations of both frequencies improved the cognitive function and suppressed neuron apoptosis in AD mice. Moreover, the treatment also increased the brain BDNF, NGF, and doublecortin levels, which represented the increased viability of neurons by rTMS. The injection of Aβ 1-42 also increased the expressions of p-GSK-3β, p-Tau, and p-β-catenin and suppressed the level of total β-catenin. After the treatments of rTMS, the level of β-catenin was restored, indicating the activation of β-catenin signaling. In conclusion, the findings outlined in the current study demonstrated that the anti-AD effect of rTMS was associated with the activation of β-catenin, which would promote the survival of neurons.