Fig. 4: Aβ aggregates extracted from 3xTg and Thy1-ApoE4/C/EBPβ Tg mice induce endogenous amyloid-β accumulation in APP/PS1 mice.
From: Thy1-ApoE4/C/EBPβ double transgenic mice act as a sporadic model with Alzheimer’s disease
A Diagram showing in vivo function assay of Aβ aggregates isolated from 3xTg and Thy1-ApoE4/C/EBPβ Tg mice. Aβ aggregates were extracted from cortex and injected into hippocampus of APP/PS1 mouse. After 2 months of injection, the mice were sacrificed for histological analysis in brain. B Representative of Aβ plaque immunostaining images in the hippocampus of APP/PS1 mice inoculated with Aβ aggregates isolated from 3xTg and Thy1-ApoE4/C/EBPβ Tg mice. Scale bar 500 μm. C Relative quantification of Aβ plaque number in B. D Representative of IBA1 (left two panel) and GFAP (right two panel) immunostaining images in hippocampus of APP/PS1 mice inoculation with Aβ aggregates. Scale bar 500 μm for column 1 and 3, 20 μm for column 2 and 4. E Relative quantification of IBA1 and GFAP fluoresce intensity in D. F Schematic drawings representing the distribution of Aβ positive neurons and Aβ plaque in 3xTg and Thy1/ApoE3/C/EBPβ transgenic mice at the age of 2-, 6- and 12-month of age. Note the age-dependent increase in the number of Aβ (4G8) positive neurons in the cortex and hippocampus. CA1: CA1 hippocampal subfield, CA3 CA3 hippocampal subfield, DG dentate gyrus, Ect ectorhinal cortex, M motor cortex, S sensory cortex, Small dots = 5–10 positive neurons (2-month age), medium-size dots = 20–40 positive neurons (6-month age), star = Aβ plaque at different size (12-month age).
