Fig. 7
Blocking of Nogo/NgR pathway enhanced microglial recruitment toward Aβ and CD36 expression in APP/PS1 mice. To determine the effects of the Nogo/NgR pathway on adhesion and migration of microglia to Aβ fibrils in vivo, NEP1-40 was intracerebroventricularly administered to APP/PS1 mice for 2 months using continuous an Alzet mini-pump. a, b Mice brain sections were processed for anti-Aβ and anti-Iba1 immunofluorescence as indicated. Bar = 50 μM. b Ten randomly chosen plaque areas in the cortex and hippocampus were evaluated for Iba1/Aβ colocalization per animal. Values were reported as the mean ± SD, as a percentage of values determined in vehicle group (control, 100%). ***p < 0.01, when compared with the vehicle group, n = 4–5. c, d After microglia from 3-month-old mice were treated with BSA (0.01% in PBS), fAβ1–42 (10 μM), Nogo-P4 (100 μg/ml), or Nogo-P4 (100 μg/ml) + fAβ1–42 (10 μM) for 24 h, expression of CD36 was measured by Western blot. Values were reported as the mean ± SD, as a percentage of values determined in BSA group (control, 100%). **p < 0.01; ***p < 0.01, when compared with the BSA group; #p < 0.05, when compared with the fAβ1–42 group, n = 3. e, f NEP1-40 was intracerebroventricularly administered to APP/PS1 mice for 2 months. Homogenates from brain tissue of APP/PS1 transgenic mice were subjected to Western blot analysis with markers of CD36. Values were reported as the mean ± SD, as a percentage of values determined in vehicle group (control, 100%). ***p < 0.01, when compared with the vehicle group, n = 4–5