Figure 7
From: Systemic immune challenges trigger and drive Alzheimer-like neuropathology in mice
Characterization of the inflammation-induced Aβ plaques in 3xTg-AD mice. (A-C) Immunofluorescence staining using anti-Aβ1–16 antibody (red) counterstained with Fluoro-Jade (green) and DAPI (blue) revealed, in addition to the dystrophic neurites (arrows), the presence of degenerating neurons in the core of amyloid deposits in immune-challenged transgenic mice. (D-F) Double-immunofluorescence staining using anti-N-APP (red) and anti-activated caspase-6 (green) confirmed the presence of dystrophic neurites within and around the amyloid deposits. (G-I) Transgene-driven human Aβ aggregates (green, anti-Aβ1–40/42) around the APP/soluble (s)APP (red, anti-N-APP) accumulations in PolyI:C-treated 3xTg-AD mice, in striking similarity to the phenotype seen in human patients with AD (J-L). Note the close association but no colocalization between APP ectodomains and C-terminal, Aβ-containing fragments (G-L). Scale bars = 10 μm.