Figure 4. Aβ plaques and levels are not affected in denervated areas after 5,7-DHT administration.

A) Although a relative increase of thioflavin S was observed in the cortex from APPswe/PS1dE9 lesioned mice, differences did not reach statistical significance when compared with sham treated mice, using Student t test for independent samples (thioflavin S, p = 0.382), and the same pattern was observed after anti-Aβ immunohystochemistry (4G8, p = 0.525). Similarly, no differences were observed in the hippocampus of denervated mice (Thioflavin S p = 0.665; anti-Aβ p = 0.729). B) Illustrative example of thioflavin S (green) and anti-Aβ (red) staining in the cortex and hippocampus of Sham APPswe/PS1dE9 mice and 5,7-DHT APPswe/PS1dE9 mice. Scale bar: 250 µm. C) Soluble and insoluble Aβ40 and Aβ42 levels were analyzed in the cortex and hippocampus. Since Aβ40 levels were undetectable in wildtype animals, Student t test for independent sample was used to compare Sham and 5,7-DHT APPswe/PS1dE9 mice. One way ANOVA followed by Tuckey b or Tamhane tests was used for the rest of the comparisons, as required. Cortex: Soluble Aβ40 p = 0.924, soluble Aβ42 [F_(3,12) = 10.563, **p = 0.001 vs. sham wildtype and 5,7-DHT wildtype], insoluble Aβ40 p = 0.898, insoluble Aβ42 [F_(3,12) = 365.243, **p = 0.001 vs. vs. sham wildtype and 5,7-DHT wildtype]. Hippocampus: Soluble Aβ40 p = 0.944, soluble Aβ42 [F_(3,12) = 9.215, **p = 0.002 vs. sham wildtype and 5,7-DHT wildtype], insoluble Aβ40 p = 0.804, insoluble Aβ42 [F_(3,12) = 165.855, **p<0.001 vs. sham wildtype and 5,7-DHT wildtype].