Fig. 7

Effects of AMFR on AD-like pathologies and synaptic plasticity in APP/PS1 mice. A Viral diffusion in the hippocampus of the APP/PS1-Flag-AAV9-Ctrl and APP/PS1-Flag-AAV9-AMFR groups by immunofluorescence analysis. mCherry (red), nuclei (DAPI, blue), merge (mCherry + DAPI); scale bars represent 2000 μm. Data presented are representative of three separate experiments. B AMFR and APP protein levels in the hippocampus of WT (n = 7), APP/PS1-Flag-AAV9-Ctrl (n = 7), and APP/PS1-Flag-AAV9-AMFR (n = 7) groups. Data are shown as mean ± SEM from three independent experiments (*P < 0.05, **P < 0.01). C-E sAPPβ, Aβ40, and Aβ42 levels in the hippocampus of the three mouse groups by ELISA (n = 7). Data are shown as mean ± SEM from three independent experiments (ns, not significant, *P < 0.05, **P < 0.01). F APP ubiquitination in the hippocampus of the three mouse groups by Co-IP assays (n = 7). The protein levels of APP and AMFR in the tissue lysates were confirmed. Data presented are representative of three separate experiments. G Amyloid plaque deposition (green) in the hippocampus of different groups of mice by immunofluorescence analysis (n = 3). Scale bars represent 500 μm. Data are shown as mean ± SEM from three independent experiments (*P < 0.05, ***P < 0.001). H Representative fEPSP recording traces and normalized slopes of the fEPSP of the three mouse groups before and 60 min after high-frequency stimulation with electrophysiology assays. (n = 5 slices from 5 mice per group). Data are shown as mean ± SEM from three independent experiments. I Quantifications of the average percentage changes in the fEPSP slope 0–60 min after high-frequency stimulation. (n = 5 slices from five mice per group). Data are shown as mean ± SEM from three independent experiments (*P < 0.05)