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Fig. 2 | Journal of Neuroinflammation

Fig. 2

From: Beneficial effects of curtailing immune susceptibility in an Alzheimer’s disease model

Fig. 2

Panel (a): representative pictures of the immunohistochemical detection of Aβ1–42 expression (black arrows), in the spleen of 3xTg-AD treated for 12 months with an anti-TNFSF10 monoclonal antibody (10 μg, i.p. twice a month). Photos A and B: respectively, wild-type mice untreated, or treated with the anti-TNFSF10 antibody. Photos C and D: respectively 3xTg-AD mice untreated or treated with the anti-TNFSF10 antibody. The inserts in photos represent the respective areas magnified. Scale bar = 10 μM. Panel (a’): densitometric count of Aβ1–42 immunopositive cells. *p < 0.05 3xTg-AD mice untreated vs WT treated with vehicle; **p < 0.05 3xTg-AD mice treated with anti-TNFSF10 vs. untreated 3xTg-AD mice (one-way ANOVA, followed by a Duncan’s multiple range test). Vertical bars are means ± S.E.M. WT wild-type (n = 5/group); AD: 3xTg-AD mice (n = 5/group). Panel (b): Western blot analysis of Aβ1–42 in splenic homogenates. Panel (b’): Densitometric analysis of the representative Western blot *p < 0.05 3xTg-AD mice untreated vs WT treated with vehicle; **p < 0.05 3xTg-AD mice treated with anti-TNFSF10 vs. untreated 3xTg-AD mice (one-way ANOVA, followed by a Duncan’s multiple range test). Vertical bars are means ± S.E.M. WT wild-type (n = 5/group); AD: 3xTg-AD mice (n = 5/group)

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