Photobiomodulation by low-power laser irradiation attenuates Aβ-induced cell apoptosis through the Akt/GSK3β/β-catenin pathway.

Apoptosis induced by amyloid β peptide (Aβ) is thought to associate with the pathogenesis of Alzheimer disease (AD). Accumulating evidence shows that low-power laser irradiation (LPLI) is capable of reducing Aβ-induced apoptosis. However, the underlying mechanisms remain unclear. In this study, we report a novel molecular mechanism by which LPLI attenuates Aβ(25-35)-induced apoptosis through the Akt/GSK3β/β-catenin pathway. We found that Akt activated by LPLI interacted with GSK3β and phosphorylated it on Ser9 in the presence of Aβ(25-35), which resulted in the inhibition of GSK3β. Furthermore, LPLI increased the nuclear translocation of β-catenin and enhanced its T cell factor/lymphocyte enhancer factor-dependent transcriptional activity via the Akt/GSK3β pathway to promote cell survival upon treatment with Aβ(25-35.) Our data demonstrate that LPLI has a prosurvival effect on Aβ-induced apoptosis and may be an effective therapeutic strategy in treating AD by targeting GSK3β.