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Results: 4

1.
Figure 2

Figure 2. From: Clinical and neuropathologic heterogeneity of c9FTD/ALS associated with hexanucleotide repeat expansion in C9ORF72.

Ubiquitin immunohistochemistry of cerebellum of c9FTD/ALS shows many NCI in internal granular cell layer in FTLD-TDP (a) and fewer in ALS (b). Insets show higher magnification of NCI. (bar = 30 μm for a & b and 90 μm for insets)

Melissa E. Murray, et al. Acta Neuropathol. ;122(6):673-690.
2.
Figure 4

Figure 4. From: Clinical and neuropathologic heterogeneity of c9FTD/ALS associated with hexanucleotide repeat expansion in C9ORF72.

Phospho-TDP-43 immunohistochemistry of c9FTD/ALS shows unusual neuritic and synaptic pathology. Fine neurites in CA1 of hippocampus (a); Synaptic-like TDP-43 grains in CA3 of hippocampus (b), superficial cortical layer (c) and globus pallidus (d). (bar = 30 μm for a, b, c & d)

Melissa E. Murray, et al. Acta Neuropathol. ;122(6):673-690.
3.
Figure 1

Figure 1. From: Clinical and neuropathologic heterogeneity of c9FTD/ALS associated with hexanucleotide repeat expansion in C9ORF72.

Macroscopic findings in c9FTD/ALS (Case 1: a, b & c; Case 9: d, e & f; Case 14: g, h & i)). ALS case with mild peri-Rolandic cortical atrophy (a, arrow), but no ventricular enlargement on a coronal section at level of the subthalamic nucleus (b) and no gross hippocampal atrophy (c). FTLD-MND case (Mackenzie Type 3) with moderate peri-Rolandic cortical atrophy (arrow) and moderate frontal-predominant atrophy (d). Enlargement of the frontal, but not temporal horn of the lateral ventricle can be seen on a coronal section at level of the subthalamic nucleus (e) and mild hippocampal atrophy of the subiculum (f). FTLD-TDP case (Mackenzie Type 1) with no peri-Rolandic atrophy (arrow), but moderate frontal and temporal atrophy (g), as well as enlargement of both frontal and temporal horns of the lateral ventricle on a coronal section at level of the subthalamic nucleus (h). Hippocampal sclerosis was severe and correlates with atrophy in CA1 and the subiculum (arrow) (i).

Melissa E. Murray, et al. Acta Neuropathol. ;122(6):673-690.
4.
Figure 3

Figure 3. From: Clinical and neuropathologic heterogeneity of c9FTD/ALS associated with hexanucleotide repeat expansion in C9ORF72.

Phospho-TDP-43 immunohistochemistry of c9FTD/ALS cases with range of TDP-43 pathology. (a) ALS cortex has many GCI in lower cortical layers. (b) Type 1 cases have many NCI and DN in the superficial cortical layers, with lentiform NII (upper left inset) and dense, globular PV astrocytic inclusions (lower right inset). (c) Type 2 cases have large thick dystrophic neurites in lower (in this figure) and upper cortical layers, with dense round Pick body like NCI in the hippocampal dentate fascia (upper left inset) (d) Type 3 cases have many granular or pre-inclusion type NCI with sparse or absent DN in cortex and hippocampal dentate fascia (upper left inset). (bar = 30 μm for a, b, c & d and 90 μm for insets)

Melissa E. Murray, et al. Acta Neuropathol. ;122(6):673-690.

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