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Fig. 3 | Molecular Neurodegeneration

Fig. 3

From: α-Synucleinopathy associated c-Abl activation causes p53-dependent autophagy impairment

Fig. 3

Aberrant accumulation of autophagy markers in TgA53T neurons with αS pathology. a Western blot analysis of LC3-I, LC3-II and p62 in symptomatic TgA53T mice and littermate nTg mice. The graphs (below) show the LC3-II/I ratio and p62 levels derived from the immunoblots. The brain regions analyzed are spinal cord (SPC), brainstem (BST), and cortex (CTX). There is clear increase in the levels of LC3-II and p62 in brain regions (SPC, BST) associated with the αS pathology, while the lack of pathology in CTX is associated with no changes in LC3-II and p62 levels. Values are mean ± SEM; n = 6–8. There was a significant effect (p < 0.001) for species (nTg-Tg), brain location (SPC-BST-CTX) and interaction for both LC3 ratio and p62. ***p < 0.001, *p < 0.05, Two-way ANOVA followed by Bonferroni multiple posttest. b Paraffin sections of brainstem (BST) were double immunofluorescence stained for p62 (green) and pS129αS (red). Arrows show that accumulated p62 is selective localized to the neurons that accumulate pS129αS. Arrowheads show similar p62 accumulation in neurites. Significant accumulation of p62 suggest that autophagosome clearance might be impaired in TgA53T neurons. Scale bar, 10 μm. c, d, e c-Abl activation and p62 accumulation in human PD cases. Levels of phospho-Tyr412 c-Abl (pY412c-Abl), c-Abl and p53 (c) and αS, p62 (d) in pons (c, d), and αS, p62 in cortex (CTX, e) of human postmortem tissue lysates from control (Ctrl) and PD cases were evaluated by Western immunoblot analysis. Bar shows the relative abundance of each protein (Mean ± SEM; n = 3–5). **p < 0.01, *p < 0.05, Student’s t test

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