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Fig. 4 | Alzheimer's Research & Therapy

Fig. 4

From: Lack of human-like extracellular sortilin neuropathology in transgenic Alzheimer’s disease model mice and macaques

Fig. 4

Representative light microscopic images illustrating a lack of extracellular sortilin pathology in aged monkey neocortex with overt amyloid plaque pathology. Shown are images taken from parallel processed sections from the prefrontal lobe of a 34-year-old rhesus monkey (ah) and from the temporal lobe of a 32-year-old cynomolgus monkey (ip), with framed areas in the low-magnification images enlarged as indicated. Sortilin immunoreactivity in the neocortex is exclusively cellular, largely present in layers II–VI with little labeling in the white matter (WM) (a, e, i, m). β-Amyloid (Aβ) plaques labeled with the 6E10 antibody are present in the middle and lower portions of the cortex in fairly large amounts (b, f, j, n). Clusters of dystrophic neurites show increased β-secretase (BACE1) immunoreactivity relative to background (c, g, k, o) and distributed over the cortex with a laminar pattern similar to that of Aβ plaques. No cellular labeling is visualized by the PHF1 p-tau antibody in the monkey neocortex. The panels shown are derived from corresponding montaged images captured on an automated Olympus Motic microscope across the entire hemispheric area, available online as Additional file 1: Figures S1–S8. Abbreviations are as defined in Fig. 1. Scale bar = 2 mm in (a) applying to (bd, il), equivalent to 500 μm for (eh, mp)

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