Fig. 5
From: Deletion of Abi3/Gngt2 influences age-progressive amyloid β and tau pathologies in distinctive ways
Loss of Abi3-Gngt2 expression ameliorates Aβ in a gene-dosage manner. a, b Representative immunohistochemical images of total Aβ plaque burden and quantification in 3-month-old APP TG mice with WT (+ / +), heterozygous (+ /−), or KO (−/−) of Abi3-Gngt2 locus. c, d Representative images of thioflavin S-stained cored Aβ plaques and quantitation in 3-month-old APP TG mice with WT (+ / +), heterozygous (+ /−), or KO (−/−) of Abi3-Gngt2 locus. e–h Biochemical levels of formic acid (FA) solubilized and detergent (SDS) soluble Aβ42 and Aβ40 in 3-month-old APP TG mice with WT (+ / +), heterozygous (+ /−), or KO (−/−) of Abi3-Gngt2 locus. i, j Representative immunohistochemical images of total Aβ plaque burden and quantification in 6-month-old APP transgenic mice with WT (+ / +), heterozygous (+ /−), or KO (−/−) of Abi3-Gngt2 locus. k, l Representative images of thioflavin S-stained cored plaques and quantitation in 6-month-old APP TG mice with WT (+ / +), heterozygous (+ /−), or KO (−/−) of Abi3-Gngt2 locus. m–p Biochemical levels of FA solubilized and SDS soluble Aβ42 and Aβ40 in 6-month-old APP TG mice with WT (+ / +), heterozygous (+ /−), or KO (−/.−) of Abi3-Gngt2 locus. N = 6 mice (a–h), 7 mice (i, j, m-p), 6 mice (k, l). Scale bar, 50 µm (a, i); 100 µm (c, k). Clear symbols denote female mice and filled symbols denote male mice (except panel d, k). n = 3 females, 3 males (3 months) and n = 3 females, 4 males (6 months). Data represents mean ± sem. One-way ANOVA; ***p < 0.001; **p < 0.01; *p < 0.05