Fig. 3
Histochemical reactivity of GW-23B7 to Alzheimer’s disease (AD), age-matched control, and young control human brains, and to Gerstmann-Sträussler-Scheinker syndrome (GSS) prion disease, as well as recognition of pathological conformers on immunoblots. a Representative immunohistochemical images showing reactivity of GW-23B7 on human AD brains (top panels) compared with age-matched and young human control brains (middle and bottom panels, respectively). Right panels are magnifications of the boxed areas on the left. Scale bars represent 100 μm on the left panels and 50 μm on the right panels. b Fluorescence immunohistochemistry of human AD brains (two top panels) and a GSS brain (bottom panels). Left panels: GW-23B7 (green channel). Middle panels (red channels): Commercial antibodies 4G8/6E10, PHF-1, and anti-glial fibrillary acidic protein (anti-GFAP), top to bottom, respectively. Right panels: Colocalization (indicated by white arrows). Scale bars represent 50 μm. c Electron microscopy of Aβ1–42 peptides fibrilized or polymerized with glutaraldehyde, paired helical filaments (PHFs), and protein kinase A-treated PHFs used on SDS-PAGE gels for immunoblots. d Immunoblots comparing reactivity of aβComAb GW-23B7 with the specific anti-Aβ peptide antibodies 4G8/6E10 to Aβ1–40, Aβ1–40 polymerized, Aβ1–42 fibrilized, and Aβ1–42 polymerized (lanes 1–4, respectively); the PHF-1 specific antibody for hyperphosphorylated tau on PHF and PHF protein kinase A-treated (lanes 5 and 6, respectively); and the 7D9/6D11 antibodies specific for prion protein (PrP) molecules to oligomerized PrP and chronic wasting disease prions (lanes 7 and 8, respectively)