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. 2015 Jul 10;3:43. doi: 10.1186/s40478-015-0216-0

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© Ziskin et al. 2015

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. 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. 2 — Evidence of subependymal and subpial injury. Sections of hippocampal efferent tracts from our patient (a-d) were compared to age-matched control cases (e-h). Luxol fast blue (LFB) stains demonstrate myelin pallor in Ammon’s horn (a, e; LFB; original magnification of 10×), the alveus (b, f; LFB; original magnification of 100×) and fimbria (c, g; LFB; original magnification of 100×) in TTR amyloidosis compared to the age matched hippocampus. Myelin basic protein (MBP) immunostains demonstrated similar myelin pallor in the fimbria (d, h; MBP; original magnification of 100×). i. The superficial insular cortex demonstrated gliosis with eosinophilic bodies (arrows; H&E; original magnification of 100×), similar to those reported in Herrick et al. [14], that were variably GFAP immunoreactive (j; GFAP; original magnification of 100×). Iron stains demonstrated siderosis in the upper cortical layers of the superior temporal gyrus (k; iron stain; original magnification of 200×) and in the Bergmann glia of the atrophied cerebellar vermis (l; iron stain; original magnification of 200×)