Skip to main content
. 2005 Nov 7;202(9):1163–1169. doi: 10.1084/jem.20051529

Figure 4.

Figure 4.

Figure 4.

Amelioration of late-stage nitrosative/oxidative injury, astrogliosis, microgliosis, and phospho-tau accumulation in AD-transgenic mice by disruption of iNOS alleles. (A) Nitrotyrosine immunoreactivity in the cingulate cortex of iNOS+/+ hAPP0/0 hPS10/0, iNOS+/+ hAPP+/0 hPS1+/0, and iNOS−/− hAPP+/0 hPS1+/0 mice. (B) Nitrotyrosine immunoblot. Brain extract proteins (150 μg) were immobilized on a filter with a slot-blot apparatus and were immunoblotted with anti-nitrotyrosine mAb. (C–F) Reduction of GFAP staining indicative of astrocytosis (C and E) and of CD40 staining indicative of microgliosis (D and F) in the cortex (C and D) and hippocampus (E and F) of iNOS−/− hAPP+/0 hPS1+/0 mice. Statistically significant differences are marked (***P < 0.001; *P < 0.05). (G) Reduction of phospho-tau immunoreactivity around plaques in iNOS−/− hAPP+/0 hPS1+/0 mice. Arrows highlight positive staining. (H) Anti–phospho-tau (p-tau) immunoblot with anti-tubulin as a loading control. Each lane is from a separate mouse of the genotypes indicated. See text for quantitative analysis.