Figure 5
ROS production induced by the Alzheimer disease-related peptide, Aβ, is diminished by MAO-A inhibition. HT-22 cells were treated with Aβ(1–40) (30 μM, 48 h). The effect of Aβ(1–40) on (A) free intracellular Ca2+, assessed using FLUO-3AM fluorescence, and on the production of ROS, assessed using the H2O2-binding DCF fluorogen. (B) Hoechst staining of primary hippocampal cell cultures was used to determine the proportion of cells exhibiting chromatin condensation (an indication of apoptotic cell death: arrows) in Aβ(1–42)-treated cultures. In both HT-22 cultures (A) and primary neuronal cultures (B), the effect of Aβ was reversed by pretreatment with the specific MAO-A inhibitor, clorgyline (CLG; 100 μM, 1 h). (C) Number of primary hippocampal cells (expressed as a percentage of control) that exhibit chromatin condensation following treatment with Aβ and/or CLG (groups shown in B). ***: P < 0.001 vs. control. ##: P < 0.01 between the indicated groups. Data are presented as mean ± SD.