Skip to main content
Figure 3 | Molecular Neurodegeneration

Figure 3

From: MyD88-adaptor protein acts as a preventive mechanism for memory deficits in a mouse model of Alzheimer's disease

Figure 3

Amyloid plaque load and soluble Aβ levels in the brain of APP swe /PS1 in a context of partial MyD88 deficiency. Deposition of Aβ plaques is significantly more abundant in 6 and 9 month-old APPswe/PS1 compared to APPswe/PS1-Myd88+/- mice (a). Aβ immunoreactivity in cortex and hippocampus is shown in brain sections of 9 month-old APPswe/PS1 and APPswe/PS1-Myd88+/- mice. Percentage of area covered by plaques was quantified for mice of 3, 6 and 9 month-old, respectively. n = 9-10. (Two-way ANOVA was performed revealing a significant interaction between factors age and genotype. The comparison of genotype for each age was performed by Student's t-test). To detect soluble Aβ, western blot analysis on 10-20% Tris-Tricine denaturing polyacrylamide gels of extracellular (b), intracellular (c) and membrane-associated (d) enriched proteins of 6 month-old mice were assessed using monoclonal 6E10 antibody to reveal the different species. Most of Aβ oligomers were significantly higher in the brains of APPswe/PS1-MyD88+/- (AM) mice than that of APPswe/PS1 (A) in all protein fractions. Bands depicted here were cut from the same membrane for each protein fraction. Values are expressed as optical densities (OD) in arbitrary units (a.u.) of Aβ normalized with β-actin. n = 4-7; Student's t-test; * P < 0.05, ** P < 0.01, *** P < 0.001. Error bars: SEM. Scale bar = 500 μm

Back to article page