Fig. 5

Trem2 H157Y reduces amyloid pathologies in Founder 2-linage mice at 8.5 months of age. A-B. Aβ40 (A) and Aβ42 (B) were quantified by ELISA and normalized to WT mice in cortical guanidine lysates (GND) for each genotype. C-D. Aβ42 oligomers were quantified by ELISA and normalized to WT mice in cortical TBS (C) and TBSX (D) lysates. E. Representative images of amyloid staining are shown for each genotype. Scale, 400 µm. F-K. Cortical (F–H) and hippocampal (I-K) amyloid plaque area percentages (F, I), densities (G, J) and sizes (H, K) are quantified and normalized to WT mice for each genotype. L. Representative images of dystrophic neurite staining (LAMP1⁺) are shown for each genotype. Scale, 400 µm. M–N. Cortical (M) and Hippocampal (N) LAMP1⁺ area percentages were quantified and normalized to WT mice for each genotype. O. Representative images of IBA1 immunostaining are shown for each genotype. Scale, 400 µm. P-Q. Cortical (P) and hippocampal (Q) IBA1 + area percentages were quantified for each genotype. R-S. Cortical (R) and hippocampal (S) CD68⁺ area percentages were quantified and normalized to WT mice for each genotype. T. Representative images of CD68 immunostaining are shown for each genotype. Scale, 400 µm. U. Representative images of TREM2 immunostaining are shown for each genotype. Scale, 400 µm. V-W. Cortical (V) and hippocampal (W) CD68⁺ area percentages were quantified and normalized to WT mice for each genotype. X. Representative images of GFAP immunostaining are shown for each genotype. Scale, 400 µm. Y–Z. Cortical (Y) and hippocampal (Z) GFAP⁺ area percentages were quantified and normalized to WT for each genotype. A-Z. N = 8–13 mice per genotype, at 8.5 months of age, mixed sex. Data are presented as Mean ± SEM. Kruskal–Wallis tests with uncorrected Dun’s multiple comparisons were used. N.S., not significant. * p < 0.05. **p < 0.01. ****p < 0.0001