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Fig. 4 | Molecular Neurodegeneration

Fig. 4

From: A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques

Fig. 4

Quantification of insoluble and soluble Aβ in micro-dissected hippocampi and cortices. a-d No difference in insoluble Aβ40 and Aβ42 in hippocampus in 4-month-old 5xFAD/ Trem2R47H vs 5xFAD mice. e–h In the soluble fraction, there is no difference in cortical Aβ40 (e), but a trending decrease in Aβ42 level was observed in the cortical fraction of 4-month-old 5xFAD/ Trem2R47H vs 5xFAD animals (f, p = 0.0997). Increases in (g) Aβ40 and (h) Aβ42 are observed in hippocampal fraction of 5xFAD/ Trem2R47H compared to 5xFAD. i-l At 12-months, insoluble cortical (i) Aβ40 and (j) Aβ42 are increased in 5xFAD/Trem2R47H compare to 5xFAD while no difference was observed in hippocampal fraction (k, l). m-p No difference in soluble fraction except for an increase in hippocampal Aβ42 in 5xFAD/Trem2R47H (p). Data are represented as mean ± SEM. Student’s t-test. Statistical significance is denoted by *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. Statistical trends are given by # 0.05 < p < 0.1

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