Research Paper Volume 13, Issue 14 pp 18033—18050

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

class="figure-viewer-img"

Figure 2. The endogenous release of Aβ sustained neuronal survival, lactate release and ATP levels in the presence of oligomycin. Experiments were performed as represented in the drawing (A). In the presence of oligomycin (Oligo, 5 μg/ml), blockade of Aβ production by γ-secretase inhibitor IX (γ-Sec Inh, 100 nM) worsened neuronal survival (B), reduced lactate release (C) and ATP content (D). The addition of synthetic Aβ42 monomers (mAβ, 100 nM) prevented the effects of γ-Sec Inh (BD). Both in (B and C) bars represent the means ± SEM of 4 determinations. P < 0.001 vs. *glucose (Gluc), or #Gluc ± Oligo in the absence of γ-Sec Inh, or **Gluc ± Oligo in the presence of γ-Sec Inh; one-way ANOVA with post hoc Fisher LSD multiple comparison method. In (D) bars represent the means ± SEM of 3–4 determinations. *P < 0.05 vs. 2-DG or Gluc ± Oligo in the presence of γ-Sec Inh; one-way ANOVA with post hoc Fisher LSD multiple comparison method.