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 Aβ25–35-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 Aβ25–35, 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 Aβ25–35. 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.

► Akt activated by low-power laser irradiation (LPLI) interacts with and inactivates GSK3β after Aβ exposure.
► LPLI enhances the prosurvival function of β-catenin upon Aβ treatment.
► LPLI attenuates Aβ-induced cell apoptosis through the Akt/GSK3β/β-catenin pathway.
► LPLI has potential therapeutic value in treating Alzheimer disease by targeting GSK3β.