Skip to main content
. 2020 Sep 26;10(25):11794–11819. doi: 10.7150/thno.44152

Figure 6.

Figure 6

Aβ pathology in the cortex, hippocampus, and amygdala of the brain sections from 3×Tg-AD mice in the sham, FUS and FUB group, as well as the WT mice. Coronal sections were stained with anti-Aβ antibody 6E10. (A) Representative immunohistochemical images of the sonicated hemisphere in the FUS/MB group and ipsilateral sides in other three groups. Intraneuronal Aβ immunoreactivity became prominent in the cortex, CA1 and CA3 pyramidal cells (SP) of the hippocampal formation, and the amygdala in sham-treated and FUS-treated 3×Tg-AD mice. Abundant extracellular diffuse Aβ protofibrillar deposits were observed predominantly in the stratum radiatum (SR) of the hippocampus. Reduced Aβ pathology in the cortex, CA1 and CA3 subfield, as well as in the amygdala, could be observed in the FUS/MB-treated 3×Tg-AD mice compared with the sham and FUS-treated group. (B) Quantitative analysis of 6E10-positive areas in the cortex, CA region and amygdala of the ipsilateral hemispheres in the four groups. The 6E10-positive areas in the cortex, CA and amygdala of the sham-treated 3×Tg-AD mice were 3.7% ± 0.9%, 15.0% ± 3.2%, and 14.1% ± 2.5%, which were reduced to 1.2% ± 0.5%, 8.4% ± 2.4%, and 6.1% ± 1.8% after FUS/MB treatment, representing reductions of 67%, 44%, and 57%, respectively. There was no difference between the sham and FUS groups. ***: p < 0.001, vs. WT or sham or FUS. ###: p < 0.001, vs. sham or FUS or FUS/MB.