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Fig. 3 | Acta Neuropathologica Communications

Fig. 3

From: Co-deposition of SOD1, TDP-43 and p62 proteinopathies in ALS: evidence for multifaceted pathways underlying neurodegeneration

Fig. 3

Altered p62 localization and deposition in the vulnerable ventral spinal cord of ALS cases. a p62 immunostaining revealed nuclear p62 (open arrowheads) in ventral spinal cord motor neurons of one ALS case and all controls. Diffuse cytoplasmic p62 staining (arrows), as well as punctate (dotted arrowheads), globular (single downwards arrowheads) and fibrillar skein-like (double downwards arrowheads) p62-immunopositive inclusions, were also identified in ventral spinal cord motor neurons of all ALS cases and a small proportion of controls. Case numbers (Additional file 1: Table S1) are listed in the top left corner of each panel and scale bars represent 25 µm. Antibody details are listed in Supplementary Table 3. No immunostaining was observed in spinal cord tissue sections processed as above in the absence of primary antibodies (Additional file 1: Figure S1). b The proportion of motor neurons exhibiting diffuse cytoplasmic p62 or cytoplasmic p62 inclusions (collectively termed atypical p62) was higher in ALS cases compared with controls (Kruskal–Wallis H test with Dunn’s multiple comparisons post-hoc tests; SOD1-fALS: p = 0.018; non-SOD1-fALS: p = 0.0006; sALS: p = 0.0002). c In contrast, nuclear p62 immunostaining was absent in all but one ALS case (open red circle), resulting in a significant reduction in the proportion of motor neurons exhibiting nuclear p62 compared with controls (Kruskal–Wallis H test with Dunn’s multiple comparisons post-hoc tests; SOD1-fALS: p = 0.01; non-SOD1-fALS: p = 0.004; sALS: p < 0.0001). Data in b and c represent mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001

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