Figure 7
From: IVIg protects the 3xTg-AD mouse model of Alzheimer’s disease from memory deficit and Aβ pathology
Modulation of the fractalkine pathway by IVIg treatment: correlation with cortical Aβ42/Aβ40 ratios and Aβ*56. Expression of CX3CR1 was evaluated using flow cytometry in the bone marrow of 3xTg-AD mice treated with IVIg from 9 to 12 months. Decreases in the percentage of CX3CR1+ cells in (A) total bone marrow cells and (B) the monocyte population were observed in treated animals (n = 11 to 12). (C) The percentage of CX3CR1+ cells in the bone marrow correlated with soluble and insoluble Aβ42/Aβ40 ratios (in IVIg-treated mice) and Aβ*56 concentrations from the parietotemporal cortex (in control and total animals). Statistical analysis: (A,B) one-way ANOVA with Tukey’s multiple comparison test. *P <0.05. (C) Correlations were determined by simple linear regression analysis. 3xTg-AD, triple-transgenic mouse model of Alzheimer’s disease; ANOVA, analysis of variance; IVIg, human intravenous immunoglobulin.