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Phospho-tau localization in WT and Nfe2l2 −/− mice after AD inoculation is not located in neurons, microglia or astrocytes in the corpus callosum. Double-label immunofluorescence and confocal microscopy for cell-type markers <t>(GFAP,</t> IBA1, NeuN) (green) and AT8 (red) in WT and Nfe2l2 −/− mice inoculated with sarkosyl-insoluble AD fractions into the hippocampus at 3 months of age and analyzed at 6 months (3-month survival). Tau deposits were observed along the corpus callosum (CC) in both genotypes, with no phospho-tau detected in astrocytes (GFAP) (a – h) , microglia (IBA1) (i – p) or neurons (NeuN) (q – x) . However, some nuclei or perineuronal spaces in the CA1 region of WT animals showed positivity, consistent with areas where tau pathology had spread (indicated with white arrows) (q – x) . Nuclei were stained with DAPI (blue). Scale bar = 40 μm.
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Phospho-tau localization in WT and Nfe2l2 −/− mice after AD inoculation is not located in neurons, microglia or astrocytes in the corpus callosum. Double-label immunofluorescence and confocal microscopy for cell-type markers <t>(GFAP,</t> IBA1, NeuN) (green) and AT8 (red) in WT and Nfe2l2 −/− mice inoculated with sarkosyl-insoluble AD fractions into the hippocampus at 3 months of age and analyzed at 6 months (3-month survival). Tau deposits were observed along the corpus callosum (CC) in both genotypes, with no phospho-tau detected in astrocytes (GFAP) (a – h) , microglia (IBA1) (i – p) or neurons (NeuN) (q – x) . However, some nuclei or perineuronal spaces in the CA1 region of WT animals showed positivity, consistent with areas where tau pathology had spread (indicated with white arrows) (q – x) . Nuclei were stained with DAPI (blue). Scale bar = 40 μm.
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Phospho-tau localization in WT and Nfe2l2 −/− mice after AD inoculation is not located in neurons, microglia or astrocytes in the corpus callosum. Double-label immunofluorescence and confocal microscopy for cell-type markers <t>(GFAP,</t> IBA1, NeuN) (green) and AT8 (red) in WT and Nfe2l2 −/− mice inoculated with sarkosyl-insoluble AD fractions into the hippocampus at 3 months of age and analyzed at 6 months (3-month survival). Tau deposits were observed along the corpus callosum (CC) in both genotypes, with no phospho-tau detected in astrocytes (GFAP) (a – h) , microglia (IBA1) (i – p) or neurons (NeuN) (q – x) . However, some nuclei or perineuronal spaces in the CA1 region of WT animals showed positivity, consistent with areas where tau pathology had spread (indicated with white arrows) (q – x) . Nuclei were stained with DAPI (blue). Scale bar = 40 μm.
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Phospho-tau localization in WT and Nfe2l2 −/− mice after AD inoculation is not located in neurons, microglia or astrocytes in the corpus callosum. Double-label immunofluorescence and confocal microscopy for cell-type markers <t>(GFAP,</t> IBA1, NeuN) (green) and AT8 (red) in WT and Nfe2l2 −/− mice inoculated with sarkosyl-insoluble AD fractions into the hippocampus at 3 months of age and analyzed at 6 months (3-month survival). Tau deposits were observed along the corpus callosum (CC) in both genotypes, with no phospho-tau detected in astrocytes (GFAP) (a – h) , microglia (IBA1) (i – p) or neurons (NeuN) (q – x) . However, some nuclei or perineuronal spaces in the CA1 region of WT animals showed positivity, consistent with areas where tau pathology had spread (indicated with white arrows) (q – x) . Nuclei were stained with DAPI (blue). Scale bar = 40 μm.
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Phospho-tau localization in WT and Nfe2l2 −/− mice after AD inoculation is not located in neurons, microglia or astrocytes in the corpus callosum. Double-label immunofluorescence and confocal microscopy for cell-type markers <t>(GFAP,</t> IBA1, NeuN) (green) and AT8 (red) in WT and Nfe2l2 −/− mice inoculated with sarkosyl-insoluble AD fractions into the hippocampus at 3 months of age and analyzed at 6 months (3-month survival). Tau deposits were observed along the corpus callosum (CC) in both genotypes, with no phospho-tau detected in astrocytes (GFAP) (a – h) , microglia (IBA1) (i – p) or neurons (NeuN) (q – x) . However, some nuclei or perineuronal spaces in the CA1 region of WT animals showed positivity, consistent with areas where tau pathology had spread (indicated with white arrows) (q – x) . Nuclei were stained with DAPI (blue). Scale bar = 40 μm.
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Phospho-tau localization in WT and Nfe2l2 −/− mice after AD inoculation is not located in neurons, microglia or astrocytes in the corpus callosum. Double-label immunofluorescence and confocal microscopy for cell-type markers <t>(GFAP,</t> IBA1, NeuN) (green) and AT8 (red) in WT and Nfe2l2 −/− mice inoculated with sarkosyl-insoluble AD fractions into the hippocampus at 3 months of age and analyzed at 6 months (3-month survival). Tau deposits were observed along the corpus callosum (CC) in both genotypes, with no phospho-tau detected in astrocytes (GFAP) (a – h) , microglia (IBA1) (i – p) or neurons (NeuN) (q – x) . However, some nuclei or perineuronal spaces in the CA1 region of WT animals showed positivity, consistent with areas where tau pathology had spread (indicated with white arrows) (q – x) . Nuclei were stained with DAPI (blue). Scale bar = 40 μm.
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Phospho-tau localization in WT and Nfe2l2 −/− mice after AD inoculation is not located in neurons, microglia or astrocytes in the corpus callosum. Double-label immunofluorescence and confocal microscopy for cell-type markers <t>(GFAP,</t> IBA1, NeuN) (green) and AT8 (red) in WT and Nfe2l2 −/− mice inoculated with sarkosyl-insoluble AD fractions into the hippocampus at 3 months of age and analyzed at 6 months (3-month survival). Tau deposits were observed along the corpus callosum (CC) in both genotypes, with no phospho-tau detected in astrocytes (GFAP) (a – h) , microglia (IBA1) (i – p) or neurons (NeuN) (q – x) . However, some nuclei or perineuronal spaces in the CA1 region of WT animals showed positivity, consistent with areas where tau pathology had spread (indicated with white arrows) (q – x) . Nuclei were stained with DAPI (blue). Scale bar = 40 μm.
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Phospho-tau localization in WT and Nfe2l2 −/− mice after AD inoculation is not located in neurons, microglia or astrocytes in the corpus callosum. Double-label immunofluorescence and confocal microscopy for cell-type markers (GFAP, IBA1, NeuN) (green) and AT8 (red) in WT and Nfe2l2 −/− mice inoculated with sarkosyl-insoluble AD fractions into the hippocampus at 3 months of age and analyzed at 6 months (3-month survival). Tau deposits were observed along the corpus callosum (CC) in both genotypes, with no phospho-tau detected in astrocytes (GFAP) (a – h) , microglia (IBA1) (i – p) or neurons (NeuN) (q – x) . However, some nuclei or perineuronal spaces in the CA1 region of WT animals showed positivity, consistent with areas where tau pathology had spread (indicated with white arrows) (q – x) . Nuclei were stained with DAPI (blue). Scale bar = 40 μm.

Journal: Redox Biology

Article Title: NRF2 deficit prevents pathologic Tau seeding and spreading in an induced tauopathy mouse model

doi: 10.1016/j.redox.2026.104068

Figure Lengend Snippet: Phospho-tau localization in WT and Nfe2l2 −/− mice after AD inoculation is not located in neurons, microglia or astrocytes in the corpus callosum. Double-label immunofluorescence and confocal microscopy for cell-type markers (GFAP, IBA1, NeuN) (green) and AT8 (red) in WT and Nfe2l2 −/− mice inoculated with sarkosyl-insoluble AD fractions into the hippocampus at 3 months of age and analyzed at 6 months (3-month survival). Tau deposits were observed along the corpus callosum (CC) in both genotypes, with no phospho-tau detected in astrocytes (GFAP) (a – h) , microglia (IBA1) (i – p) or neurons (NeuN) (q – x) . However, some nuclei or perineuronal spaces in the CA1 region of WT animals showed positivity, consistent with areas where tau pathology had spread (indicated with white arrows) (q – x) . Nuclei were stained with DAPI (blue). Scale bar = 40 μm.

Article Snippet: Glial fibrillary acidic protein , Gfap , Mm01253033_m1.

Techniques: Immunofluorescence, Confocal Microscopy, Staining