Fig. 1

Effect of ABX-treatment on sex-specific cerebral amyloidosis of APPPS1-21-CD11br transgenic mice. A Schematic representation of APP/PS1 transgenes and FLAG/EGFP tagged murine Rpl10a under CD11b promoter. I, intervening sequence; II, SV40 polyA. B EGFP expression in brain sections of WT-CD11br, APPPS1-21-CD11br and APPPS1-21 male and female mice. GFP immunostaining co-localized with macrophage/microglial marker, Iba I. C Schematic to represent the treatment regime. Expression of FLAG-EGFP-Rpl10a transgene from cortical RNAs of WT and APPPS1-21-CD11br mice treated with vehicle or ABX by RT-PCR. An amplicon of 0.3 kb corresponding to EGFP in the transgene was detected on 1% agarose gel. APPPS1-21 and non-transgenic mice were used as control. Gapdh was used as a reference gene. D Representative images of Aβ plaque burden in the cortex of vehicle and ABX-treated in 7-wk-old APPPS1-21-CD11br mice using anti-Aβ monoclonal antibody, 3D6 (left). Quantification of plaque burden in vehicle and ABX-treated APPPS1-21-CD11br mice using threshold-limited particle analysis of 3D6 positive staining from six sections per case and expressed relative to the total cortical area of each slice (right, n = 15). E Detection of the expression of human APP and PS1 transgenes in detergent-soluble brain lysates of 7-wk-old male and female APPPS1-21-CD11br mice by Western blot analysis. 6E10, a human APP-specific antibody detected steady-state levels of human full-length APP, soluble APP, -CTF and Aβ peptides. C1/6.1 antibody detected both mouse and human full-length APP and CTFs. The expression of human PS1L166P was confirmed by PS1NT antibody and β-actin was used as loading control. NTG (non-transgenic) and APPPS1-21 served as controls (n = 2)