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. 2015 Mar 5;6(3):1676. doi: 10.1038/cddis.2015.37

Figure 7.

Figure 7

Accumulation of cofilin–actin rod/aggregate structures in APP/PS1 mice resembling those in AD brains and mitigation by RanBP9 reduction. (a-c) Nine-month-old WT, APP/PS1, and APP/PS1;RanBP9+/− littermate brains subjected to immunohistochemistry for cofilin and actin in the anterior cortex and hippocampus using Sudan black to quench background signal. (a) Representative images showing increased cofilin–actin rods in APP/PS1 mice and reduction in APP/PS1;RanBP9+/− mice. (b and c) Quantitation of cofilin–actin rods in the hippocampus and anterior cortex normalized to WT (ANOVA, post-hoc Tukey, **P<0.005, ***P<0.0005, n=4 mice per genotype). Error bars represent S.E.M. in graphs. (d) Representative images of cofilin–actin rods and neuropil threads (phospho-Tau 12E8 antibody) using the same Sudan black quenching immunohistochemical method as in (a) in the entorhinal cortex from a cognitively normal control (NC) and AD. Note the marked accumulation of cofilin–actin rods (green) and neuropil threads (red) in AD but few in NC