Skip to main content
Fig. 5 | Alzheimer's Research & Therapy

Fig. 5

From: Empagliflozin reduces vascular damage and cognitive impairment in a mixed murine model of Alzheimer’s disease and type 2 diabetes

Fig. 5

Amyloid pathology is reduced by EMP treatment. a SP burden was lower in APP/PS1xdb/db mice when compared with APP/PS1 animals. EMP treatment slightly reduced SP burden in the cortex after TS and 4G8 staining (TS [F(3, 107) = 20.55], 4G8 [F(3, 104) = 11.89]; ††p < 0.01 vs. APP/PS1 and APP/PS1-EMP). While individual SP size was increased in APP/PS-EMP mice (TS [F(3, 5191) = 8.98], 4G8 [F(3, 5039) = 21.11]; ‡‡p < 0.01 vs. APP/PS1-EMP; ††p < 0.01 vs. APP/PS1 and APP/PS1-EMP), EMP treatment reduced SP density (TS [F(3, 107) = 19.74], 4G8 [F(3, 107) = 17.81]; ‡‡p < 0.01 vs. APP/PS1; ††p < 0.01 vs. APP/PS1 and APP/PS1-EMP). To a lesser extent, we observed a similar trend when we analyzed SP burden in the hippocampus (TS [F(3, 49) = 8.01], 4G8 [F(3, 49) = 6.08]; ‡‡p < 0.01 vs. APP/PS1]), SP density (TS [F(3, 50) = 11.57], 4G8 [F(3, 50) = 9.42]; ‡‡p < 0.01 vs. APP/PS1), and individual plaque size (TS [F(3, 643) = 0.975, p = 0.404]; 4G8 [F(3, 638) = 2.39, p = 0.067]) (APP/PS1 n = 5, APP/PS1-EMP n = 5, APP/PS1xdb/db n = 5, APP/PS1xdb/db-EMP n = 5). b Illustrative example of cortical regions stained with TS and 4G8 where reduced SP density can be observed after EMP treatment. Scale bar = 50 μm. c A similar profile was observed in the hippocampus when we measured SP burden, density, and individual SP size (‡‡p < 0.01 vs. APP/PS1) (APP/PS1 n = 5, APP/PS1-EMP n = 5, APP/PS1xdb/db n = 5, APP/PS1xdb/db-EMP n = 5). d EMP treatment reduced soluble Aβ40 levels in the cortex ([F(3, 27) = 4.20, p = 0.015 vs. APP/PS1xdb/db]). While a similar trend was observed in the hippocampus, differences were not statistically significant ([F(3, 26)=0.479, p = 0.7]). No differences were observed for soluble Aβ42 levels in the cortex ([F(3, 27) = 0.832, p = 0.488]) or the hippocampus ([F(3, 26) = 1.02, p = 0.397]). EMP also reduced insoluble Aβ40 levels in the cortex ([F(3, 25) = 5.98, **p = 0.003 vs. the rest of the groups]), while differences did not reach statistical significance for insoluble Aβ40 in the hippocampus ([F(3, 22) = 2.68, p = 0.072]) as well as for insoluble Aβ42 levels (cortex [F(3, 27) = 1.43, p = 0.254]; hippocampus [F(3, 26) = 1.54, p = 0.228]) (APP/PS1 n = 7, APP/PS1-EMP n = 9, APP/PS1xdb/db n = 7, APP/PS1xdb/db-EMP n = 7)

Back to article page