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. 2020 Sep 11;11:4571. doi: 10.1038/s41467-020-18405-9

Fig. 6. Pre-symptomatic VX-765 treatment does not affect Aβ accumulation and deposition.

Fig. 6

a Representative Aβ micrographs of hippocampal SLM (top panels) and retrosplenial cortex (bottom panels) in vehicle- and VX-765 treated J20 mice as indicated in (b). Scale bar in hippo = 200 μm, cortex = 50 μm. b Quantitative analysis comparing Aβ immunostaining density between vehicle- and VX-765-treated J20 mice in the hippocampal pyramidal cell layer to the SLM and retrosplenial cortex at 4-week (n = 7 mice per group), 12-week (n = 7 mice per group) and 20-week (n = 6 mice per group) WO (cortex 12-week WO, p = 0.0402, two-tailed, unpaired t test). c RIPA-soluble and d FA-soluble total Aβ levels and Aβ42/total Aβ ratio in the hippocampus and cortex (Aβ42/total Aβ hippo 20-week WO, p = 0.0369, two-tailed, unpaired t test). In (c), n = 7 J20 + veh and 8 J20 + VX mice at 4-week WO; n = 6 J20 + veh and 7 J20 + VX mice at 12-week WO; n = 7 mice per group at 20-week WO. In (d), n = 7 J20 + veh and 8 J20 + VX mice at 4-week WO; n = 4 J20 + veh and 5 J20 + VX at 12-week WO; n = 7 mice per group at 20-week WO. e IDE and f Nep western blot quantification in the hippocampus at 4- and 20-week WO. In (e) and (f), n = 7 mice per group at 4-week WO and n = 8 WT + veh, 7 J20 + veh, 7 J20 + VX mice at 20-week WO. Data represents mean and s.e.m. *p < 0.05.