Mage in panel (C corresponds to the boxed area in (B). Scale bars (B,E) = 500 m, (C) = 200 m. Additional file 7: Figure 7. A immunoreactivity (IR) in the dorsal and ventral hippocampus of 15-month-old mice. Representative images of coronal brain sections processed for immunoperoxidase staining using anti-A1?0/42 (AB5076) antibodies. (A-D) Non-transgenic mice and (E-H) 3xTg-AD mice, harboring two transgenes (encoding APPswe and TauP301L, respectively) in a homozygous PS1M146V knock-in background,received a single intravenous injection of (left lane) NaCI or (right lane) PolyI:C (5 mg/kg bodyweight) at 4 months of age. Note that the non-transgenic mice showed an increase in anti-APP/A1?0/42 IR along the dorsal-ventral axis of the hippocampus following a single virallike infection with (B,D) PolyI:C compared with (A,C) NaCI. (E,G) Control treatment of 3xTg-AD mice with NaCI during pre-plaque stage resulted in the typical appearance of A plaques in the ventral subiculum, whereas (F,H) a single exposure to PolyI:C strongly aggravated the A plaque density, covering the entire hippocampus along its septotemporal axis. Scale bars: 500 m. Additional file 8: PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28506461 Figure 8. Summary of the semi-quantitative densitometric analysis of the anti-A and anti-Tau immunoreactivity (IR). Polyriboinosinic-polyribocytidilic acid (PolyI:C; 5 mg/kg body weight) or NaCI in a injection volume of 5 ml/kg was administered intravenously to mice at 4 months of age. Brain tissue was collected at 15 months, and processed for immunoperoxidase staining. Optical-density measurements were performed in the outlined CA1 subfield (including stratum oriens, pyramidale, radiatum), lacunosum moleculare (slm), the molecular and granule cell layer of the dentate gyrus (DG), and the hilus, both in the dorsal and ventral hippocampus. Mean pixel brightness was corrected for non-specific background staining using measurements in the LY317615 cost corpus callosum as reference, indicated as relative optical density (OD). (A) Summary of the changes in APP/A1?0/42 (left) and pTau (right) levels in PolyI:C-treated compared with NaCI-treated 3xTg-AD mice. Arrows show the direction of changes in the different hippocampal subfields. Brackets indicate statistical trends, with P values of 0.06 to 0.09. (B) Summary of the APP/A and pTau measurements in non-transgenic mice, contrasting PolyI:C-treated versus NaCI-treated mice. (C) Graphic representation of the semi-quantitative analysis of (left) the APP/A1?0/42 and (right) pTau immunoreactivity (IR) in the dorsal and ventral hippocampus of non-transgenic and transgenic mice. Values are given as mean ?SEM; n = 4 to 7 per genotype and treatment; *P < 0.05; **P < 0.01, ANOVA and Fisher's least significant difference post-hoc test. Additional file 9: Figure 9. Various forms of human amyloid- plaques all containing significant amounts of N-terminal proteolytic fragments of amyloid precursor protein (APP). (A-I) Immunofluorescence staining using anti-N-APP antibodies (22C11, red), anti-A1?0/42 (AB5076, green), and DAPI (blue) counterstaining of post-mortem brain tissue from an 88-yearold patient with AD. Paraffin sections were pretreated with (A-F) or without (G-I) formic acid (FA), with the latter allowing the detection of significant N-APP-specific immunoreactivity. Note the close association, but no colocalization, between APP ectodomains and C-terminal, Acontaining fragments. Scale bars = 10 m. Additional file 10: Figure 10. Anti-phospho-Tau IR in the dorsal and ven.