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. 2017 Dec 7;32(2):174–190. doi: 10.1177/0269881117743484

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© The Author(s) 2017

This article is distributed under the terms of the Creative Commons Attribution 4.0 License (http://www.creativecommons.org/licenses/by/4.0/) which permits any use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 3. — Tc1 mice exhibited increased oxidative stress in the cortex. Oxidative stress was assessed 10 days after intracerebroventricular (i.c.v.) amyloid-β [25-35] (Aβ_25-35) injection by measuring reactive oxygen species (ROS) accumulation using dichlorofluorescein (DCF) fluorescence in mouse cortex (a) and hippocampus (b). The number of animals per group is indicated below the columns. Two-way analysis of variance (ANOVA): F_(1,33)=12.5, p<0.01 for the genotype, F_(1,33)=0.467, p>0.05 for the treatment, F_(1,33)=0.049; p>0.05 for the interaction in (a); F_(1,32)=3.62, p>0.05 for the genotype, F_(1,32)=5.51, p<0.05 for the treatment, F_(1,32)=1.61, p>0.05 for the interaction in (b); *p<0.05 vs same genotype scrambled peptide (Sc.Aβ)-treated mice; #p<0.05 vs same treatment wildtype (WT) mice; Bonferroni’s test.