Fig. 2: PSEN2 deficiency and PSEN2 N141I knock-in both accelerate AD pathology in an APPKI model. | Nature Communications

Fig. 2: PSEN2 deficiency and PSEN2 N141I knock-in both accelerate AD pathology in an APPKI model.

From: Altered expression of Presenilin2 impacts endolysosomal homeostasis and synapse function in Alzheimer’s disease-relevant brain circuits

Fig. 2

a Coronal hippocampal slices of APPKI, APPxPSEN2KO and APPxFADPSEN2 stained for thioflavin, labelling dense core plaques over time. b Quantification of thioflavin+ area normalized to brain area for hippocampus over time and analyzed using two-way ANOVA using a Dunnett’s correction for multiple testing comparing the different conditions to APPKI. c Dual immunolabelling of Aβ plaques in coronal cortex sections using a fibrillar (fAβ) and monomeric Aβ specific antibody (82e1). d, e Average size (d) and number (e) of thioflavin+ plaques calculated from (a, c). Statistical analysis was through a one-way ANOVA with a Dunnett’s correction for multiple testing compared to APPKI (f). Immunolabelling of 3 month old coronal hippocampal slices of APPKI, APPxPSEN2KO and APPxFADPSEN2 for Aβ/APP-CTF (82e1), LAMP1, full length APP and thioflavin. g Quantification of LAMP1+ area as a percent of total hippocampus area. For (g) a two-way ANOVA analysis with Tukey’s correction for multiple testing compared to APPKI was used. Scale bars and p-values are indicated; number of mice (N) is shown inside the bar and the symbols represent the number of regions analyzed. All graphs are mean ± SEM.

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