Research Paper Volume 8, Issue 11 pp 2713—2733

An antioxidant specifically targeting mitochondria delays progression of Alzheimer’s disease-like pathology

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Figure 2. SkQ1 retards mitochondrial alterations in the hippocampus. (A) Alterations in the ultrastructure of the mitochondrial apparatus of CA1 pyramidal neurons in OXYS rats were attenuated by SkQ1 administration. (B) The area occupied by mitochondria within the hippocampal pyramidal neurons as a percentage of the total neuronal area in 18-month-old Wistar rats, untreated OXYS rats, and SkQ1-treated OXYS rats (n=4). Compared to Wistar rats, the untreated OXYS rats had a considerably smaller mitochondrial area. SkQ1 administration increased the mitochondria-occupied portion of the neuronal area. (C) Immunolabeling for mitochondrial fission mediator Drp1 (green) and mitochondrial fusion mediator Mfn2 (red) and cell nuclei (DAPI, blue) in the CA3 region of the hippocampus. (D) Enzymatic activities of complexes I and IV in the hippocampus of OXYS rats were ~30% lower than those in Wistar rats (p<0.03 and p<0.02, respectively). Enzymatic activity did not change significantly in complex I but increased by ~30% in complex IV (p<0.001) in the hippocampus of SkQ1-treated OXYS rats (n=6). The data are shown as mean ± SEM. Statistical significance (p<0.05) is denoted by the asterisk. The scale bar is 2 µm (A).