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Figure 3 | Acta Neuropathologica Communications

Figure 3

From: Extensive aggregation of α-synuclein and tau in juvenile-onset neuroaxonal dystrophy: an autopsied individual with a novel mutation in the PLA2G6 gene-splicing site

Figure 3

Lewy body (LB) and neurofibrillary tangle (NFT) pathology of the patient. a and inset The substantia nigra contained “brainstem-type” LBs with core and halo (arrows) structures. b and inset In the cingulate gyrus, the neuropil showed spongy changes in the deep layer, and there were “cortical-type” LBs without core and halo structures (arrows). c and d Anti-phosphorylated alpha-synuclein (p-α-synuclein) immunohistochemistry showed abundant LBs in the substantia nigra (c) and cingulate gyrus (d). e and f In the hypothalamus (e) and Ammon’ s horn (f), p-α-synuclein-positive LBs and LNs were strikingly abundant. g and h Electron microscopy of a neuron in the cingulate gyrus showed cortical LBs in a cortical neuron (asterisk), which consisted of granular and filamentous structures. The filaments were arranged at random without a clear central zone density. i - l The pyramidal neuron in the hippocampal cortex contained abundant NFTs and threads that were positive for AT-8 antibody using the Gallyas-Braak method. m-o Confocal microscopy of the amygdala revealed immunoreactivity against p-α-synuclein (m, red), which often co-labeled with AT8 (n, green) in the same neurons (o, merged). Bar (a), (b), (c), and (i) = 100 μm; (d), (e), (m), (n), and (o) = 50 μm; (f) = 250 μm; (g) = 2 μm; (h) = 0.2 μm; (a-inset), (b-inset), (j), (k), and (l) = 20 μm. Hematoxylin and eosin staining (a, b, j), p-α-synuclein immunohistochemistry (c-f), AT8 immunohistochemistry (i, k), and Gallyas-Braak staining (l).

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