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Figure 4 | Molecular Neurodegeneration

Figure 4

From: Increased mtDNA mutations with aging promotes amyloid accumulation and brain atrophy in the APP/Ld transgenic mouse model of Alzheimer’s disease

Figure 4

PolgA D257A mutation prevents Aβ-induced IDE elevation. Brain homogenates were prepared from D257A; APP/Ld, D257A, APP/Ld, and wild type mice and 10 μg protein/lane was randomly loaded and subjected to immunoblot analysis for two Aβ degrading enzymes: insulin degrading enzyme (IDE) and neprilysin (NEP). Immunoblot signals were normalized to Ponceau S staining intensities in a given lane. The numbers on immunoblot correspond to a mouse with a specific genotype as denoted in the legend key (box). (A) IDE protein from brain homogenates runs at ~100 kDa. (B) IDE immunosignals from (A) were measured and expressed as percentage of mean wild-type IDE level. Note that IDE levels are reduced slightly in the brains of D257A mice. As previously reported for APP transgenic mice [38, 39], IDE levels are significantly increased in the brains of APP/Ld mice compared to wild-type non-transgenic mice. Most importantly, the D257A mutation completely prevents the Aβ-induced increase in IDE levels in D257A; APP/Ld mice (mean ± SEM; n.s. = not significant; *p < 0.05; ***p < 0.001; One-way ANOVA followed by Newman–Keuls multiple-comparisons post hoc test). (C) NEP protein from brain homogenates runs at ~90 kDa. (D) NEP immunosignals from (C) were measured and expressed as percentage of mean wild-type NEP level. Note that NEP levels are not altered by the D257A mutation, the APP/Ld transgene, or their combination, as compared to wild-type non-transgenic mice.

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