Correction: Photobiomodulation mitigates blood–brain barrier disruption in APP/PS1 mouse model of Alzheimer’s disease by activating the AMPK pathway

Correction: Alz Res Therapy 17, 141 (2025)

https://doi.org/10.1186/s13195-025-01787-7

Following publication of the original article [1], an error was identified in Fig. 9 of the published version. Specifically, Figs. 9F and 9G were mistakenly used, resulting in an inaccurate representation of the corresponding experimental data.

Fig. 9.

PBM Enhances Inflammation-Induced Mitochondrial Function in bEnd.3 Cells by Activating AMPK. A Flow cytometry assessment of ROS levels in bEnd.3 cells following AMPK activation/inhibition by AICAR/Compound C with quantitative analysis. B-D ELISA analysis of SOD, Bax, and Bcl-2 secretion in the supernatant of bEnd.3 cells following AMPK activation/inhibition by AICAR/Compound C. E–F Fluo-4 detection of Ca2+ production in bEnd.3 cells and quantitative analysis following AMPK activation/inhibition by AICAR/Compound C (scale bar: 100 μm). G JC-1 assessment of mitochondrial membrane potential in bEnd.3 cells following AMPK activation/inhibition by AICAR/Compound C, with JC-1 aggregates (red) and JC-1 monomers (green) (scale bar: 100 μm). H ATP production in bEnd.3 cells. I ELISA measurement of CCO secretion in the supernatant of bEnd.3 cells. Data are presented as Mean ± SEM (n = 3 per group). Comparisons show statistical significance relative to the Control + p-AMPK group: *p < 0.05, **p < 0.01, ***p < 0.001, relative to the Control + ko-AMPK group: #p < 0.05, ##p < 0.01, ###p < 0.001, and relative to the p-AMPK group, ▲p < 0.05, ▲▲p < 0.01, ▲▲▲p < 0.001

To maintain the accuracy and integrity of the published work, we have corrected Fig. 9. Furthermore, the fluorescence intensity in Fig. 9E has been re-quantified, and the corrected Fig. 9 is provided below.

Fig. 9.

PBM Enhances Inflammation-Induced Mitochondrial Function in bEnd.3 Cells by Activating AMPK. A Flow cytometry assessment of ROS levels in bEnd.3 cells following AMPK activation/inhibition by AICAR/Compound C with quantitative analysis. B-D ELISA analysis of SOD, Bax, and Bcl-2 secretion in the supernatant of bEnd.3 cells following AMPK activation/inhibition by AICAR/Compound C. E–F Fluo-4 detection of Ca2+ production in bEnd.3 cells and quantitative analysis following AMPK activation/inhibition by AICAR/Compound C (scale bar: 100 μm). G JC-1 assessment of mitochondrial membrane potential in bEnd.3 cells following AMPK activation/inhibition by AICAR/Compound C, with JC-1 aggregates (red) and JC-1 monomers (green) (scale bar: 100 μm). H ATP production in bEnd.3 cells. I ELISA measurement of CCO secretion in the supernatant of bEnd.3 cells. Data are presented as Mean ± SEM (n = 3 per group). Comparisons show statistical significance relative to the Control + p-AMPK group: *p < 0.05, **p < 0.01, ***p < 0.001, relative to the Control + ko-AMPK group: #p < 0.05, ##p < 0.01, ###p < 0.001, and relative to the p-AMPK group, ▲p < 0.05, ▲▲p < 0.01, ▲▲▲p < 0.001

The original article [1] has been updated.

The corrected Fig. 9:

The original version of Fig. 9: