Journal: International Journal of Molecular Sciences

Article Title: Fluoxetine Repurposing Mitigates Alzheimer’s Disease Pathology via the GSK3β–CREB–ADAM10 Axis

doi: 10.3390/ijms27062676

Figure Lengend Snippet: Fluoxetine modulates CaMKII-GSK3β-CREB signaling and ADAM10 expression in vitro. ( A ) Schematic diagram of the experimental design. SH-SY5Y cells were seeded and pretreated with fluoxetine (10 μM) for 12 h, followed by treatment with the CaMKII inhibitor 1-NA-PP1 (10 or 20 μM) or the GSK3β inhibitor IX (5 or 10 μM) for 1 h prior to cell harvest. ( B ) Representative Western blot analysis for phosphorylated and total forms of CaMKII (Thr286), GSK3β (Ser9), and CREB (Ser133). ( C ) Quantification of relative phosphorylation levels normalized to the corresponding total protein. ( D ) Representative Western blot analysis of signaling and APP-processing-related proteins following fluoxetine and/or GSK3β inhibitor treatment. ( E ) Quantification of protein expression levels normalized to β-actin (for protein) or to the corresponding total protein (for phosphorylated forms), as indicated. Data are presented as mean ± SEM ( n = 3 independent experiments). Individual data points represent independent biological replicates. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. * p < 0.05, ** p < 0.01 vs. control; # p < 0.05, ## p < 0.01, ### p < 0.001 vs. fluoxetine alone; ns, not significant. Created in BioRender. Son, Y. (2026) https://BioRender.com/s91n646 (accessed on 31 January 2026).

Article Snippet: After 24 h, 10 μM fluoxetine was added to the culture dishes for 12 h. 1-Naphthyl PP1 (1-NA-PP1, HY-13941), a CAMKII inhibitor, and GSK3 inhibitor IX (HY-10580), a GSK3β inhibitor, were purchased from MedChem Express (Princeton, NJ, USA).

Techniques: Expressing, In Vitro, Western Blot, Phospho-proteomics, Control