Fig. 2.

Intranasal administration of oxytocin increases hippocampal oxytocin levels in WT animals (a) does not alter the hippocampal plaque load in APPswePS1dE9 mice treated with oxytocin(b-i). Animals treated with oxytocin show a significant increase of hippocampal oxytocin levels over animals treated with saline (e) (Mann-Whitney test: WT CTL versus WT OXT p = 0.02 n = 8) (a). Aβ plaque load was quantified at 20x magnification in the hippocampus of APPswePS1dE9 mice by immunohistochemically staining Aβ (n = 8). Plaque load was calculated as the percentage of the total hippocampal surface area. Plaque load was not found to be altered within the hippocampus (p = 0.07) after oxytocin administration (Mann-Whitney test) (b). Hippocampal Aβ₄₂ plaque-load by means of an ELISA showed no effect in soluble (c), membrane-associated (d) and insoluble fraction (e) of Aβ₄₂ in AD animals. There was no observable difference in diffuse or dense core plaques or plaque amount between AD CTL and AD OXT (f-g). There are more diffuse plaques compared to dense plaques in AD CTL compared to AD OXT animals (p = 0.04) (h). Representative images of the Aβ-stained hippocampus and cortex for the APPswePS1dE9 control group, the APPswePS1dE9 oxytocin-treated group are shown at 2.5x magnification (j). Bars represent mean±SEM. Aβ, amyloid-β; AD, Alzheimer’s disease; WT, wild type. *p < 0.05.