Skip to main content
. 2007 Oct 25;117(11):3393–3402. doi: 10.1172/JCI31547

Figure 4. Valsartan treatments prevented cognitive impairment and attenuate AD-type neuropathology, in part, by promoting membrane-bound insulin degradation enzyme activity.

Figure 4

(A) APP content in the cortex of valsartan-treated or untreated control Tg2576 mice. Inset: Representative immunoreactive APP (C8 antibody) and β-actin signals. (B) Assessments of cellular α-, β-, and γ-secretase activities in the cerebral cortex of Tg2576 mice in response to valsartan treatment. (C) Assessment of Aβ1–42 and Aβ1–40 peptide content in peripheral blood (serum). (D) Assessments of CM-associated (left panel) and cytosolic (right panel) IDE activity in the cerebral cortex of Tg2576 mice in response to valsartan treatment. Inset: Representative immunoblot signals of membrane and cytosolic IDE protein content from the same samples. (E) Assessments of neprilysin content by Western blotting using a commercial rabbit anti-mouse neprilysin antibody. Inset: Representative neprilysin and actin protein signals from the same blot. (F) Assessment of ECE activity using an Endothelin-1 ELISA System. Values represent group mean ± SEM; n = 7–9 mice per group. *P < 0.05; 1-way ANOVA, followed by Newman-Keuls post-hoc analysis.