Figure 4

Effects of exenatide on brain COX and LDH in PS1-KI and 3xTg-AD mice. (a) Bar graphs show mitochondrial COX activity in 12-month-old treated and untreated PS1-KI and 3xTg-AD mice. Exenatide had no effects on the mitochondrial respiration of PS1-KI and 3xTg-AD mice. Of note, treated and untreated 3xTg-AD mice showed significantly increased COX activity when compared with PS1-KI mice (untreated PS1-KI versus untreated 3xTg-AD mice, P=0.014; untreated PS1-KI versus treated 3xTg-AD mice, P=0.003; treated PS1-KI versus untreated 3xTg-AD mice, P=0.062; treated PS1-KI versus treated 3xTg-AD mice, P=0.017). COX activity is expressed as nmol_O2/mg_prot/min normalized for brain protein concentration. Data are shown as percentage of mitochondrial COX activity found in untreated PS1-KI mice and presented as mean values±the standard error of the mean (S.E.M.). (b) Forward and (c) reverse brain LDH activities in 12-month-old treated and untreated PS1-KI and 3xTg-AD mice. Exenatide treatment induced significant increase of forward LDH activity in PS1-KI mice (P=0.048). Of note, treated PS1-KI mice showed higher forward LDH activity compared to untreated (P=0.014) and treated (P=0.001) 3xTg-AD mice. LDH activity is expressed as μmol_Substrate/mg_Protein/min normalized for brain protein concentration. Data are shown as percentage of brain LDH activities found in untreated PS1-KI mice and presented as mean values±(S.E.M.). ‘*’ indicates P<0.050