Research Paper Volume 13, Issue 14 pp 18033—18050

β-amyloid monomers drive up neuronal aerobic glycolysis in response to energy stressors


Figure 4. Inhibition of AMPK by Compound C did not prevent lactate production due to Aβ release. Neurons were glucose-starved for 2 hours before returning to 3 mM glucose. γ-Secretase inhibitor IX (γ-Sec Inh, 100 nM) reduced lactate release both in oligomycin-treated neurons (Oligo, 5 μg/ml for 1 hr) (A) and kainate-treated neurons (KA, 100 μM for 40 min) (B). The addition of synthetic Aβ42 monomers (mAβ, 100 nM) prevented the reduction of lactate release, induced by γ-Sec Inh, both in (A and B). Compound C (10 μM), did not affect significantly the rescuing effect of exogenous Aβ42 monomers in either (A or B). Bars represent the means ± SEM of 4 determinations. In (A) p < 0.001 vs. *control (CTRL) or **Oligo in the absence of γ-Sec Inh, and p < 0.05 vs. #Oligo + γ-Sec Inh. In (B) p < 0.001 vs. *control (CTRL) or **KA in the absence of γ-Sec Inh, and p < 0.001 vs. ***KA + γ-Sec Inh; one-way ANOVA with post hoc Fisher LSD multiple comparison method.