FIGURE 1.

Impact of hAβ_1–42 on mitochondrial respiration and function in the entorhinal cortex. (A1) Bar graphs represent mitochondrial substrate utilization in permeabilized entorhinal tissue previously treated with 1 μM hAβ_1–42 for 3 h vs. control tissue, assessed through high-resolution respirometry (n = 5–6). (A2) Graph showing the acceptor control ratio (ACR) which measures the relative efficiency of phosphorylation and is determined by dividing ADP by glutamate average rates of respiration. hAβ_1–42 treatment significantly reduced the ACR relative to control. (B1) Representative immunoblots of mitochondrial membrane and gatekeeper protein voltage-dependent anion channel 1 (VDAC1) and vinculin (loading control) in entorhinal lysates following incubation in control medium or hAβ_1–42. (B2) Bar graphs showing the normalized protein expression of VDAC1 (n = 6). (C1) Representative immunoblots of mitochondrial complex I to V with total OXPHOS rodent antibody cocktail with vinculin serving as a loading control. (C2) Graphs showing normalized data for all five mitochondrial subunits in hAβ_1–42-treated slices vs. the largest expression in the control group (n = 6) (*p < 0.05; **p < 0.01; ****p < 0.0001).