Figure 4.

Acute energy inhibition increases BACE1 protein levels in the brains of Tg2576 mice. A-F, Two- to 3-month-old Tg2576 mice were injected with 18 U/kg insulin, 1 g/kg 2DG, 100 mg/kg 3NP, 30 mg/kg KA, or vehicle and were allowed to recover for 4 h (A, B), 2 d (C, D), or 7 d (E, f). A, C, E, Representative immunoblots of brain samples for BACE1 (top panels) and β-actin (bottom panels). B, D, F, BACE1 immunosignals were quantified, normalized against β-actin signals, and expressed as percentages of vehicle controls, as before. Similar to the effects observed in C57/B6 mice, energy-inhibitor treatments in Tg2576 mice caused cerebral BACE1 levels to increase to ∼125-150% of vehicle controls for all recovery times (^*p < 0.05 and ^**p < 0.01, one-way ANOVA with Newman-Keuls multiple-comparison test). Data represent mean ± SEM; n = 6 mice/treatment (A, B), and n = 4 mice/treatment (C-F).