Fig. 8From: Hippocampal stem cells promotes synaptic resistance to the dysfunctional impact of amyloid beta oligomers via secreted exosomesHippocampal synaptic vulnerability to Aβo binding is increased in mice with ablated NSC and this increase is rescued by ICV injection of NSC-exo. a) Nestin-δ-HSV-Tk mice were fed vehicle or valganciclovir (VGCV) chow for 4 weeks. At the end of the 4 weeks, mice were euthanized and synaposomes were isolated from the hippocampus (HIPP), mid brain (MidB), frontal cortex (FCX) and parieto-occipital cortex (POCX) and challenged with Fluor 647-Aβ oligomers (2.5 μM) for 30 min. The percent of synaptosomes with bound Aβ was evaluated using flow cytometry. Mice treated with VGCV (with ablated NSC) showed a significant increase in the percent of Aβ positive synaptosomes as compared to vehicle-treated mice (with intact NSC) in the hippocampus, midbrain and frontal cortex. No statistically significant differences were noted in the parieto-occipital cortex. N = 6 mice/group. *p < 0.05 Student’s two-tailed T-test. b) Nestin-δ-HSV-Tk mice were fed vehicle or valganciclovir (VGCV) chow for 4 weeks. At the end of the 4 weeks, fresh hippocampal brain slices were prepared and treated with NSC-exo or MN-exo for 4 h before being challenged with Aβ oligomers (2.5 μM for 30 min). ELISA was used to measure the amount of Aβ bound to synaptosomes. N = 3 mice/group. *p < 0.05; **p < 0.01 one-way ANOVA (F = 7.276) followed by Tukey’s multiple comparisons testBack to article page