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. 2017 May 5;12:33. doi: 10.1186/s13024-017-0172-1

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© The Author(s). 2017

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 4 — Armanezumab bound to pathological tau in brain tissues from inferior parietal gyrus of AD (a), midfrontal cortices of both Pick’s Disease (b) and Frontotemporal Dementia (c), while no binding was observed in the inferior parietal gyrus of non-AD brain (d). Adjacent brain sections stained with other antibodies against pathological tau such as PHF1 (e-g), AT8 (i-k), AT100 (m-o), N-terminal tau TNT1 (q-s), as well as HT7 anti-total tau (u-w), showed similar patterns of pathological profiles in perikarya and neuritic processes, while no binding was observed in the adjacent sections from the control brain (d, h, l, p, t, x). Original magnification 60X, scale bar =20 um