Additional file 3: Figure S3. of Activation of the unfolded protein response and granulovacuolar degeneration are not common features of human prion pathology

Immunohistochemical detection of pIRE1α and pPERK in AD and CJD hippocampus. Immunohistochemical detection for pIRE1α and pPERK was performed on an AD (case #57) and CJD (case #42) brain tissue with identical post-mortem handling and delay. Pictures from the subiculum are shown. Immunohistochemical detection is visualized by DAB (brown staining) and nuclei are counterstained with haematoxylin (blue staining). Bar 50 μm. (TIF 21347 kb

Additional file 2: Figure S2. of Activation of the unfolded protein response and granulovacuolar degeneration are not common features of human prion pathology

Immunohistochemical detection of PrP, pIRE1α, pPERK, and CK1δ in brain tissue of various human prion disease subtypes. Representative pictures of the immunohistochemical detection of PrP (3F4 antibody), pIRE1α, pPERK and CK1δ in frontal cortex sections of human prion disease patients with different disease subtypes, namely GSS (case #10), VPSPr (case #56), sCJD (case #27), panencephalopatic CJD (case #55), PrP-CAA (case #15), FFI (case #18), vCJD (case #21) and iCJD (#24), showing the absence of these UPR activation and GVD markers in the presence of PrP deposition. Immunohistochemical detection is visualized by DAB (brown staining) and nuclei are counterstained with haematoxylin (blue staining). Bar 200 μm. (PDF 2131 kb

Additional file 1: Figure S1. of Activation of the unfolded protein response and granulovacuolar degeneration are not common features of human prion pathology

Semi-quantitative analysis of the Aβ (IC16) and phosphorylated tau (AT8) burden. Representative examples from our cohort showing the amount of Aβ deposits, small phosphorylated tau positive extracellular inclusions and neuritic changes related to prion disease and phosphorylated tau positive tangle-like structures, most often resulting from AD pathology, corresponding to the semi-quantitative scores +, ++ and +++. Aβ images were taken with the 5× objective, tau (positive inclusions/neuritic changes) images with the 10× objective, tau (tangle-like changes) images with the 20× objective. In Table 3 scores for each case are listed. Scores with a/, e.g. +/++, have a burden in-between the classes represented here. Brown staining with DAB, blue staining of the nucleus with haematoxylin. (PDF 1437 kb

Additional file 1: of Contactin-2, a synaptic and axonal protein, is reduced in cerebrospinal fluid and brain tissue in Alzheimer’s disease

Supplementary methods and results. (DOCX 645 kb

Additional file 7: of Proteomics analysis identifies new markers associated with capillary cerebral amyloid angiopathy in Alzheimer’s disease

Figure S6. Protein expression of males versus females. Quantitative data on several CAA selective data was plotted with males represented as triangles and females as dots. No clear relationship between gender and protein abundance was observed. (TIF 24739 kb

Additional file 8: of Proteomics analysis identifies new markers associated with capillary cerebral amyloid angiopathy in Alzheimer’s disease

Figure S7. Immunoreactivity for COL6A2 is equally present in leptomeningeal vessels in control, AD and CAA tissue. (TIF 3794 kb

Additional file 6: of Proteomics analysis identifies new markers associated with capillary cerebral amyloid angiopathy in Alzheimer’s disease

Figure S5. Protein expression of CAA case #5 relative to the experimental groups and individual cases. (A) On the left the expression profile of case #5 compared to the average expression profile of the control group (2nd row), AD group (3rd row) and the CAA group (4th row). Green, expression below the overall mean; red, above the overall mean. The expression profile of case #5 is largely similar to that of the control groups but some proteins show a similar expression as in the AD and/or CAA groups. (B) Expression values (LFQ values) of several CAA specific proteins identified in this study with case #5 indicated as empty triangle pointing down. Case #5 does not differ from the CAA group in these markers. (TIF 1835 kb

Additional file 1: Figure S3. of Increased occurrence of protein kinase CK2 in astrocytes in Alzheimer’s disease pathology

Detection of CK2α/α’ on formalin fixed paraffin embedded tissue. Five-micrometer-thick sections from formalin-fixed paraffin tissue were mounted on superfrost plus tissue slides (Menzel-Gläser, Germany) and dried overnight at 37 °C. Sections were deparaffinised and subsequently immersed in 0.3 % H2O2 in methanol for 30 min to quench endogenous peroxidase activity. Between the subsequent incubation steps, sections were washed extensively with PBS. Sections were treated in 10 mM pH 6.0 sodium citrate buffer heated by autoclave during 10 min for antigen retrieval. Mouse monoclonal anti-CK2α (1:100, Santa Cruz Biotechnology, CA) was diluted in antibody diluent (Immunologic) and incubated overnight at 4 °C. Omission of the primary antibody served as a negative control. Secondary EnVisonTM HRP goat anti-rabbit/mouse antibody (EV-GαMHRP, Dako) incubation was for 30 min at 4 °C. The secondary antibody was detected using 3,3-diaminobenzidine (Dako). Sections were counterstained with haematoxylin for 1 min, dehydrated and mounted using Quick-D mounting medium (BDH Laboratories Supplies, Poole, England). Shown are representative pictures from the temporal cortex of an AD case with Braak 6 for neurofibrillary tangles. Scale bar A 200 μm, B 50 μm. (PDF 208 kb

Additional file 5: of Proteomics analysis identifies new markers associated with capillary cerebral amyloid angiopathy in Alzheimer’s disease

Figure S4. Clustering analysis of experimental groups and individual cases. Clustering analysis and heat maps of the different experimental groups (A) and individual cases (B) based on proteins with a significant difference (ANOVA, p < 0.05) in expression between any of the groups. (TIF 709 kb

Additional file 1: of Proteomics analysis identifies new markers associated with capillary cerebral amyloid angiopathy in Alzheimer’s disease

Figure S1. Coomassie blue staining of the SDS PAGE gels containing the microdissected tissue lysates. (TIF 478 kb