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Fig. 4 | Acta Neuropathologica Communications

Fig. 4

From: Intracellular dynamics of Ataxin-2 in the human brains with normal and frontotemporal lobar degeneration with TDP-43 inclusions

Fig. 4

Comparison of ATXN2 localization in the neuronal cytoplasm in control and FTLD-TDP brains. af The confocal microscopic images of neuronal cytoplasmic ATXN2 and organelle marker proteins or ATXN2’s related proteins from a FTLD-TDP patient’s brain were obtained as were those of controls. Representative fluorescent double-stained images from the upper layer of the cerebral temporal cortex, including merged images with DAPI staining and two-dimensional scatterplots, are presented. The localization of ATXN2 in the neuronal cytoplasm did not differ from that in the controls shown in Fig. 3. Note that the LAMP1-immunoreactivity was strikingly decreased (d). f In the double-fluorescent images using the rabbit polyclonal anti-ATXN2 antibody and the mouse monoclonal phosphorylation-independent anti-TDP-43 antibody, asterisks indicate that ATXN2 did not appear in TDP-43 positive dystrophic neurites. Pseudo coloring was used for each channel. gj Colocalization coefficient values for the upper layer of the temporal cortex (g, i) and hippocampal CA1 (h, j) were obtained from normal controls and FTLD-TDP patients. The mean values of Pearson’s correlation coefficients above threshold (PCC) (g, h) and Manders’ colocalization coefficients above threshold (tM) (i, j) are plotted. ATXN2 and Calnexin did not show significant PCC rates but moderate tM rates, indicating their fractional overlapping. RPS6 and PABP1 showed both significant PCC rates and high tM rates with ATXN2, indicating their linear relation and strong overlapping. LAMP1, GLG1, and TDP-43 showed the most insignificant PCC rates and the lowest tM rates with ATXN2. Those coefficients were not very different between the controls and FTLD-TDP cases

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