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. 2021 Nov 25;48:102198. doi: 10.1016/j.redox.2021.102198

Fig. 6.

Fig. 6

Analysis of astrogliosis in the brain of Nxnl2−/− at 10 months of age using immunohistochemistry and TAU status by 18 months of age using biochemical methods. (A) Immunohistochemical analysis of the expression of glial fibrillary acidic protein (GFAP) in the hippocampus of 10 months aged ♂ mice. The neurons are visualized through the expression of the neuronal marker RNA binding protein fox-1 homolog 3 (RBFOX3/NeuN). (B) TAU aggregation using whole brain extracts after removing of the cerebellum of 18 months aged ♂ mice. The brain extracts of the right are that of human brain from aged-matched healthy and Alzheimer persons scored positive (+) and negative (−) for NFT. (C) TAU expression. On the right brain extracts from Mapt-/- ♂ mouse (C57BL/6-N background) at 18 months aged. (D) TAU expression analyzed by non-reducing gel electrophoresis. (E) TAU phosphorylation using AT100 antibody. On the right brain extracts from Mapt−/− ♂ mouse at 18 months aged. (F) TAU phosphorylation using AT8 antibody. On the right brain extracts from Mapt−/- ♂ mouse at 18 months aged. (G) Loading control using cytoplasmic actin (ACTB) antibody. (H) Quantification of TAU aggregation normalized to TAU expression and to ACTB. (I) Quantification of TAU oligomerization. (J) Quantification of TAU phosphorylation using AT100 antibody normalized to ACTB. (K) Quantification of TAU phosphorylation using AT8 antibody normalized to ACTB. The data are plotted with SEM. The data were analyzed using t-tests.