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Fig. 4 | Molecular Neurodegeneration

Fig. 4

From: Astrocyte-derived clusterin suppresses amyloid formation in vivo

Fig. 4

CLU haploinsufficiency leads to exaggerated deposition of amyloid plaques in APP/PS1 mice. a Representative images of fibrillar amyloid accumulation in 8-month-old APP/PS1; Clu+/+ and APP/PS1; Clu+/− mice. Scale bar, 100 μm. b-c The amount of b fibrillar (Cortex: APP/PS1; Clu+/+ (0.25 ± 0.05) and APP/PS1; Clu+/− (0.40 ± 0.05); Hippocampus: APP/PS1; Clu+/+ (0.21 ± 0.04) and APP/PS1; Clu+/− (0.45 ± 0.05)) and c diffuse amyloid plaques (Cortex: APP/PS1; Clu+/+ (0.89 ± 0.13) and APP/PS1; Clu+/− (1.01 ± 0.09); Hippocampus: APP/PS1; Clu+/+ (0.85 ± 0.14) and APP/PS1; Clu+/− (1.34 ± 0.11)) was analyzed in cortex and hippocampus. N = 7–8 mice/group. For each animal three brain sections were analyzed. Data are presented as mean ± S.E.M. and Student’s t tests were used for each brain region *p < 0.05, **p < 0.01. d The levels of soluble and insoluble Aβ in the cortex of APP/PS1 mice. N = 7–8 mice/group. Data are presented as mean ± S.E.M.: (soluble Aβ40: APP/PS1; Clu+/+ (1 ± 0.19), APP/PS1; Clu+/− (1.039 ± 0.12); soluble Aβ42: APP/PS1; Clu+/+ (1 ± 0.14), APP/PS1; Clu+/− (0.99 ± 0.13)) and insoluble (Aβ40: APP/PS1; Clu+/+ (1 ± 0.15), APP/PS1; Clu+/− (1.38 ± 0.20); Aβ42: APP/PS1; Clu+/+ (1 ± 0.14), APP/PS1; Clu+/− (1.52 ± 0.18)) Data analyzed by Student’s t test *p < 0.05. e Higher amount of neuritic dystrophy (red) was observed around amyloid plaques (blue) in APP/PS1; Clu+/+ mice. Scale bar, 100 μm. f Stereological analysis of Lamp1 labeling in cortex and hippocampus of APP/PS1; Clu+/+ ((0.69 ± 0.05), (0.46 ± 0.11) and APP/PS1; Clu+/− mice (0.95 ± 0.07) (0.79 ± 0.07). N = 7–8 mice/group. Data are presented as mean ± S.E.M. and each brain region was analyzed by Student’s t test *p < 0.05

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