Figure 1
From: Models of β-amyloid induced Tau-pathology: the long and “folded” road to understand the mechanism
Amyloid cascade hypothesis in transgenic mice with combined amyloid and Tau pathology (left panel). Hippocampal (HC; CA1) and cortical (Cx) immunohistochemical staining for amyloid plaques (anti-Aβ, WO2), astrocytes (GFAP), microglia (Iba1), P-GSK3 (GSK3pT216/279), P-Tau (anti-pTau, AT-8) and NeuN for cortical/hippocampal atrophy (all images are 20×, except NeuN at 4×) is presented in transgenic mice expressing mutant APP/PS1 and mutant Tau [55]. These mice were generated by crossing mutant APP/PS1 and mutant Tau mice, respectively denoted as F+/T- (5xFAD; [59]) and F-/T+(TauP301S; [60]). Of note, AT-8 staining was optimized to match Gallyas silver staining patterns, hence representing NFTs (data not shown). Main pathological features found in F+/T+ mice (right panel). Immunolabeling with anti-Aβ (WO2), showing no changes in amyloid plaque load in the cortex of F+/T + and F+/T- mice (upper panel, 4× and 20×); Aggravation of Tau-pathology, anti-pTau (AT-8) staining (NFT), in hippocampal CA1 region and cortex of F+/T+ compared to F-/T+ parental strain transgenic mice (middle panel, 20×); anti-neuronal nuclear staining (NeuN) showing decreased cortical and hippocampal area in F+/T+ compared to F-/T- mice (lower panel, 4×).