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Fig. 9 | Acta Neuropathologica Communications

Fig. 9

From: Characterization of lysosomal proteins Progranulin and Prosaposin and their interactions in Alzheimer’s disease and aged brains: increased levels correlate with neuropathology

Fig. 9

Analysis of PGRN and PSAP colocalization on Aβ plaques in MTG tissue sections. Colocalization of PGRN and PSAP with Aβ in plaques of low plaque, high plaque and Alzheimer’s disease cases. (a-l). Images show representative images of relative patterns of immunoreactivity of PGRN (green), PSAP (red) and their colocalization with Aβ (blue) in low plaque (a-c, j), high plaque (d-f, k) and Alzheimer’s disease (g-i, l) cases. The magnification of the images is constant (scale bar represents 30 μm) to show relative sizes of plaques in these disease groups. (m). Scatter plot showing relative amounts of colocalization of PGRN and PSAP as measured by Pearson’s correlation efficiency calculated using ExColocalization plug-in of Image J software (n = 9 plaques/group). Results show mean values ±S.E.M. Analysis by one-way ANOVA (* p < 0.05, ns; not significant). Value of 1 indicates complete colocalization and value of 0 indicates no colocalization. (n). Area measurements of PGRN/PSAP immunoreactive plaques in LP, HP and AD cases. Three cases/disease group and 6 plaques/case were measured. Results show mean values ±S.E.M. Significant increase in area of PGRN/PSAP associated plaques were detected in AD samples compared to HP and LP cases. Three-dimensional Imaging of PGRN-PSAP interactions in plaques. (o-q). Three-dimensional reconstruction image of merged PGRN and PSAP immunoreactive plaques in LP and AD cases of areas highlighted in panel C (LP) and K (AD) confocal images (panel O). Software modelling using mesh rendering of section of plaque (white boxes) showing close interactions of PGRN and PSAP in both LP and AD cases (yellow areas). Top view mesh rendering (P) and Side view mesh rendering (Q).

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