Fig. 1

CLU co-localizes with amyloid plaques in mouse models and human AD and is specifically overexpressed in astrocytes. a Extensive CLU immunoreactivity (red) was observed in amyloid deposits (green) in cortex of APP/PS1 animals and brain tissue of an AD individual. Scale bar, 50 μm. b AAV-mediated specific expression of GFP (green) in GFAP-positive astrocytes (red) but not IBA1-positive microglia (red) or NeuN-specific neurons (red) in APP/PS1 animals. Scale bar, 100 μm. c CLU protein levels were assessed in cortex and hippocampus of WT and APP/PS1 mice by enzyme-linked immunosorbent assay (ELISA). Data represent mean ± S.E.M. Cortex: WT^AAV-GFP: N = 6 mice/group (100 ± 3.70), WT^AAV-CLU: N = 6 mice/group (127 ± 11.99), APP/PS1^AAV-GFP: N = 10 mice/group (118 ± 2.98), APP/PS1^AAV-CLU: N = 10 mice/group (150 ± 4.84). Hippocampus: WT^AAV-GFP: N = 6 mice/group (100 ± 3.09), WT^AAV-CLU: N = 6 mice/group (140 ± 13.37), APP/PS1^AAV-GFP: N = 10 mice/group (103 ± 2.96), APP/PS1^AAV-CLU: N = 10 mice/group (135 ± 6.97). Two-way ANOVA with Tukey’s multiple comparisons tests were used, *p < 0.05, **p < 0.01