Research Paper Volume 8, Issue 11 pp 2713—2733

Figure 7. SkQ1 decreases amyloid-β levels and tau hyperphosphorylation and attenuates memory deficits. (A) The increased levels of amyloid-β_1-40 and amyloid-β_1-42 in the hippocampus of untreated OXYS rats (n=8; p<0.05) were attenuated in response to SkQ1 treatment (p<0.05). (B) Immunostaining for amyloid-β_1-42 (Aβ_1-42 in green) in the hippocampus of Wistar rats, untreated OXYS rats, and SkQ1-treated OXYS rats. The DAPI (blue) staining shows cell nuclei. (C and D) The increased levels of Tau, pТ181, pS262, and pS396 in the hippocampus of untreated OXYS rats (n=6; p<0.05) were significantly attenuated (except for pS396) in response to SkQ1 treatment (p<0.05). (E) Compared to Wistar rats, OXYS rats (n=8) showed increased escape latencies on all trial days (p<0.01) and (F) spent less time in the target quadrant on the sixth day (p<0.05). SkQ1 decreased escape latency of OXYS rats on the second trial day (p<0.02) and increased the time spent by OXYS rats in the target northwest quadrant on the sixth day (p<0.02). The scale bar is 5 µm. Aβ: amyloid-β, a.u.: arbitrary units. The data are shown as mean ± SEM. *p<0.05; ^#p<0.05 for effects of SkQ1.