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. 2011 Jul 19;286(37):32713–32722. doi: 10.1074/jbc.M111.254268

FIGURE 2.

FIGURE 2.

Deletion of CX3CR1 does not affect Aβ levels or APP processing. A, representative Western blot of the metabolic fragments of hAPP. FL-hAPP, full-length hAPP. B, quantification of hAPP fragments (β-CTF and α-CTF) in the cortex of 5–8-month-old hAPP mice with or without CX3CR1. n = 6–11/genotype. C, ELISA measurements of soluble Aβ1-x or Aβ1–42 in the hippocampus of 2–4-month-old hAPP mice with or without CX3CR1. n = 5/genotype. D, representative picture of 3D6-immunoreactive plaques in the hippocampus of 6–7-month-old hAPP mice with or without CX3CR1. E, quantification of plaque load in the hippocampus of 6–7-month-old hAPP mice with or without CX3CR1. n = 8–11/genotype. F, representative Western blot of Aβ dimers and monomers in the hippocampus of 5–8-month-old hAPP/CX3CR1+/+ or hAPP/CX3CR1−/− mice. NTG, non-transgenic. G, quantification of levels of Aβ monomers or dimers in the hippocampus of 5–8-month-old hAPP/CX3CR1+/+ or hAPP/CX3CR1−/− mice. n = 6–7/genotype. Values are means ± S.E. (B, C, E, and G).