Figure 2.

Chronic tropisetron treatment diminishes Aβ plaque levels in Tg AD mice.

(A) Experimental treatments and timeline. The 5.0–5.5-month-old Tg AD and age-matched WT mice received intraperitoneal injections of tropisetron or normal saline daily for 8 weeks (n = 8–11/group). After cognitive tests, mice were sacrificed and brains were obtained for staining. (B–E) Thioflavin S (Thio-S) staining (B, C) and 6E10 (green, FITC) immunostaining (D, E) showed a significant decrease in Aβ plaque-occupied area in the cortex and hippocampus of tropisetron-treated Tg AD mice relative to Tg-AD controls. Scale bars: 200 μm. (F–I) Representative Aβ bands (F, G) and quantitative results (H, I) showed that chronic tropisetron treatment lessened levels of Aβ plaques in the cortex and hippocampus of Tg AD mice. Data are expressed as mean ± SEM (n = 3/group). *P < 0.05, **P < 0.01, ***P < 0.001 (unpaired Student’s t-test [C, E]; one-way analysis of variance followed by the least significant difference test [H, I]). Aβ: Amyloid beta peptide; AD: Alzheimer’s disease; CTX: cortex; FITC: fluorescein isothiocyanate; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; HIP: hippocampus; NS: normal saline; Tg: transgenic; Trop: tropisetron; WT: wild-type; 6E10: beta amyloid, 1–16.