Representative whole brain sections of APP/PS1 transgenic and wild-type mice at different time points, stained for β-amyloid (red), Iba-1 (green), GFAP (violet), and DAPI counterstain (blue). Scale bar 1mm.
Progressively increasing β-amyloid stain density (fraction of segmented pixels) in different ROIs as a function of age in the disease groups (6, 9, and 12 months) compared to the control group (6 months). P-value from Dunnett’s T3 multiple comparisons test. * p<0.05, ** p<0.01, *** p<0.001, **** p<0.0001; n = 11 (6 month Ctrl), 13 (6 months), 10 (9 months), and 9 (12 months).
We tested our morphology analysis pipeline in a mouse model with progressive AD-like accumulation of amyloid-β deposits. This transgenic mouse line overexpresses mutant human APP and PS1. We assessed an array of disease metrics at 6 ,9, and 12 months-of-age, compared to 6 month-old control mice. This model shows a progressive accumulation of amyloid-β plaques, as shown here in cortical regions and the hippocampus.