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. Author manuscript; available in PMC: 2016 Aug 1.
Published in final edited form as: J Neurosci Res. 2015 Feb 24;93(8):1258–1266. doi: 10.1002/jnr.23576

Figure 3.

Figure 3

Long-term therapy (one year after injections beginning at 6 months of age) with shCDK5miR prevents βA aggregation in the hippocampus of 3xTgAD mice. a) Immunohistochemistry did not indicate any changes in the extracellular β-amyloid plaques in 18-month-old 3xTgAD mouse hippocampi injected with shCDK5miR compared to shSCRmiR one year after treatment. Magnification, 10X and 40X, scale bars, 100 μm and 20 μm. n=3–4. b) The fluorescence intensity of intracellular βA in the CA1 region of 3xTg-AD mice remained reduced during long-term therapy with shCDK5miR. Representative images of green fluorescence from pAAV.CMV.hrGFP for the shSCR and shCDK5miR treatments are shown. c) The βA40 and βA42 levels were not affected at one year after treatment in the hippocampi of 18-month-old 3xTgAD mice injected with shCDK5miR or shSCRmiR. d) Western blotting of APP, sAPPβ and CTFβ showed an increasing trend during long-term treatment with shCDK5miR in 18-month-old 3xTgAD mice. Tubulin was used as a loading control, and densitometry quantification was performed. n=5, *=p<0.05.