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Fig. 5 | Molecular Brain

Fig. 5

From: Lentivirus-mediated expression of human secreted amyloid precursor protein-alpha prevents development of memory and plasticity deficits in a mouse model of Alzheimer's disease

Fig. 5

Cellular markers for neuronal and non-neuronal cells. a Western blot analysis of the microglial marker Iba-1 (insoluble fraction), normalised to WT-control, showed an overall group effect (one-way ANOVA F(2,28) = p = 0.041) with a trend toward higher levels in Tg mice (WT-control: 1.0 ± 0.083, n = 12; Tg-control: 1.37 ± 0.299, n = 6), that was even more evident in the Tg-sAPPα group (Tg-sAPPα: 1.39 ± 0.065, n = 13; post-hoc Tukey p = 0.046). b GFAP levels (insoluble fraction) showed a significant overall group effect (F(2,27) = 10.92, p < 0.001), whereby there was significantly higher levels in the Tg-control group compared to the WT-control group (WT-control: 0.998 ± 0.105, n = 13; Tg-control: 1.81 ± 0.284, n = 6, Tukey p = 0.007) and expression of sAPPα did not alter this higher expression level (Tg-sAPPα: 1.86 ± 0.23, n = 11, Tukey p = 0.974). c Neither genotype (WT-control: 1 ± 0.02, n = 13; Tg-control: 1.07 ± 0.674, n = 6) nor sAPPα treatment (Tg-sAPPα: 0.96 ± 0.043, n = 12) affected the presynaptic marker synaptophysin (soluble fraction). d Levels of the postsynaptic marker PSD-95 (insoluble fraction) were also not affected by the APP/PS1 genotype (WT-control: 1.00 ± 0.072, n = 13; Tg-control: 0.82 ± 0.086, n = 5), although the PSD-95 levels tended to be higher for the Tg-sAPPα group compared to Tg-controls (Tg- sAPPα: 1.066 ± 0.082, n = 12, t(17) = − 1.90, p = 0.074. Representative western blots are presented. Note that in the case of Iba-1, its illustration and that of tubulin are from the same blot, but at different exposures. Tubulin was used as the loading control. *p < 0.05, **p < 0.01; synapto: synaptophysin; Lane labels: WT, WT-control; Tg, Tg-control; TgS, Tg-sAPPα

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