Research Paper Volume 13, Issue 14 pp 18033—18050

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

Inhibition of the PP pathway by 6-aminonicotinamide did not increase significantly oligomycin toxicity. Experiments were performed as represented in the drawing. (A) Following 2 hours of glucose deprivation, neurons were returned to 3 mM glucose (Gluc) in either the absence or the presence of oligomycin (5 μg/ml) to inhibit ATP synthase. (B) Oligomycin induced a 60% neuronal death after 2.5 hours, whereas 2-deoxyglucose (2-DG, 3 mM), which inhibits overall glucose metabolism, virtually killed all neurons. The addition of 6-aminonicotinamide (6-AN, 5 mM) did not potentiate significantly oligomycin toxicity. Neuronal death was quantified by propidium iodide (PI) staining of neurons that had lost membrane integrity and expressed as percentage of 2-DG-induced death. Bars represent the means ± SEM of 4 determinations. *P

Figure 1. Inhibition of the PP pathway by 6-aminonicotinamide did not increase significantly oligomycin toxicity. Experiments were performed as represented in the drawing. (A) Following 2 hours of glucose deprivation, neurons were returned to 3 mM glucose (Gluc) in either the absence or the presence of oligomycin (5 μg/ml) to inhibit ATP synthase. (B) Oligomycin induced a 60% neuronal death after 2.5 hours, whereas 2-deoxyglucose (2-DG, 3 mM), which inhibits overall glucose metabolism, virtually killed all neurons. The addition of 6-aminonicotinamide (6-AN, 5 mM) did not potentiate significantly oligomycin toxicity. Neuronal death was quantified by propidium iodide (PI) staining of neurons that had lost membrane integrity and expressed as percentage of 2-DG-induced death. Bars represent the means ± SEM of 4 determinations. *P < 0.001 vs. 2-DG; one-way ANOVA with post hoc Fisher LSD multiple comparison method.