AQP4 influences the brain-to-eye transport rate and exacerbates brain-derived Aβ-induced retinal damage. (A) Representative confocal images showing the transport of Aβ in the optic nerves and retinas of WT and AQP4 KO mice 7 days after injection. (B) Quantitative analysis of the fluorescence intensity in the retinas 7 days after injection (n = 8). (C) Representative confocal images showing the transport of Aβ within optic nerve meningeal lymphatics of WT and AQP4 KO mice 7 days after injection. (D) Line chart of the fluorescence intensity in the retina lymphatics 7 days after injection (n = 8). (E–G) Optomotor response test in WT + DMSO group, WT + Aβ oligomer group, AQP4 KO + DMSO group, and KO + Aβ oligomer group (n = 10). Quantification of (F) optomotor motion and (G) the duration of head movements for each grating density. (H–J) OCT imaging and HE staining of the retina, with quantitative analysis of retinal thickness (n = 9). (K–N) Representative immunofluorescence staining images of RPE65 (L), TUJ1 (M), and Rhodopsin (N) in retinal sections and corresponding quantitative analysis (n = 4). Representative of three independent experiments. Data are presented as mean ± SEM. Statistical analysis was performed using two-tailed unpaired t tests (B) or two-way ANOVA with post hoc Tukey tests (J and L–N), repeated measures ANOVA with Bonferroni post hoc tests (F, G, and I). *P < 0.05; **P < 0.01; ***P < 0.001, AQP4 KO + DMSO group versus AQP4 KO + Aβ group; #P < 0.05, ##P < 0.01, WT+ Aβ group versus AQP4 KO + Aβ group.