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. 2019 Dec 23;116(52):26230–26238. doi: 10.1073/pnas.1903671116

Fig. 2.

Fig. 2.

AT8 pTau and amyloid pathology in aged rhesus monkeys (26 to 38 y). (A) AT8 label is first seen in layer II cell islands in the ERC in a 26-y-old monkey. (B) In an older monkey (33 y), AT8 labeling is more extensive in layer II and now extends to deeper layers. (C and D) Higher-magnification view of neurofibrillary tangles in layer II (C) and layer V (D) from a 38-y-old monkey. (E–G) High-magnification view of AT8-labeled (red arrrowheads) paired helical filaments from an aged monkey (E and G) or human (F). Note the same width (10 nm) and helical frequency (80 nm). Black arrows in G show the abrupt ends of each filament. (H) A degenerating dendrite (Den) from an AT8-labeled neuron in aged monkey layer II ERC. The dendrite is devoid of normal organelles and is filled with autophagic vacuoles similar to those in LOAD. (I) An Aβ-labeled (magenta arrowheads) amyloid plaque from layer V ERC in an aged monkey. Reprinted from ref. 7, with permission from Elsevier. (Scale bars: A and B, 100 μm; C and D, 10 μm; E–G, 40 nm; H, 500 nm; I, 20 μm.)