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Figure 4 Prevention of onset of behavioral deficits following 3-month treatment of Baxter IG in Dutch APP E693Q transgenic mice Prevention of onset of.

Published byIngrid Håkonsen Modified over 5 years ago

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Presentation on theme: "Figure 4 Prevention of onset of behavioral deficits following 3-month treatment of Baxter IG in Dutch APP E693Q transgenic mice Prevention of onset of."— Presentation transcript:

1 Figure 4 Prevention of onset of behavioral deficits following 3-month treatment of Baxter IG in Dutch APP E693Q transgenic mice Prevention of onset of behavioral deficits following 3-month treatment of Baxter IG in Dutch APP E693Q transgenic mice Five-month-old female Dutch APP E693Q transgenic mice were given weekly subcutaneous injections of either saline (n = 11) or 2 g/kg neat Baxter IG (n = 12), 2 g/kg IG depleted of anti-fibril Aβ antibodies (fibril Aβ-affinity-depleted IG; n = 11), 2 g/kg IG depleted of anti-oligomer Aβ antibodies (oligomer Aβ-affinity-depleted IG; n = 11), or 2 g/kg IG depleted of both anti-oligomer and anti-fibril Aβ antibodies (Aβ-affinity-depleted IG; n = 11) for 3 months. Unlike treatment of saline, fibril Aβ-affinity-depleted IG and Aβ-affinity-depleted IG, treatment of IG prevented onset of behavioral deficits in novel object recognition (A), Y-maze spontaneous alternation (B), and contextual/cued fear conditioning (C) without affecting anxiety-like behavior in the elevated plus maze (C) in Dutch APP E693Q transgenic mice. Treatment of oligomer Aβ-affinity-depleted IG prevented onset of behavioral deficit in novel object recognition (A) in Dutch APP E693Q transgenic mice. *p < 0.05; **p < 0.01; 1-way analysis of variance with Bonferroni post hoc analyses. Data expressed as mean ± SEM. Aβ = β-amyloid; IG = Immune Globulin. Elysse M. Knight et al. Neurol Neuroimmunol Neuroinflamm 2016;3:e237 © 2016 American Academy of Neurology

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