Chronic hIVIG treatment decreases TNF-α gene expression and boosts neurogenesis. Frozen tissue samples from frontal cortices of APdE9 and wild-type mice (n = 8-10) in saline and hIVIG groups were examined by quantitative RT-PCR for relative expression levels of TNF-α (A) and IL-1β (B) mRNA (in comparison to expression levels of ribosomal RNA). Genotype and treatments effects were tested using two-way ANOVA. (A) For TNF-α after removal of an outlier in hIVIG treated APdE9 group, significant genotype (***, P < 0.01), and treatment effects (***, P < 0.01) were noticed albeit without any interaction. (B) IL-β showed only genotype differences (*, P < 0.05). (C) Representative images from doublecortin stained hippocampal sections of wild-type and APdE9 transgenic mice treated for 8 months with saline or hIVIG. Scale bar represent 100 μm. (D) The doublecortin data are presented as mean ± SEM (n = 10 mice in each group). After removal of an outlier in the hIVIG treated APdE9 group, significant genotype (***, P < 0.01) and treatment effects (**, P < 0.01) emerged, with no significant interaction. (E) CD45 positive microglia also showed a significant negative correlation with the number of doublecortin positive cells in the dentate gyrus (Spearman r = -0.50, P = 0.02). Spearman correlation coefficient was used here to minimize the effect of two outliers. (F) Saline treated APdE9 mice showed a trend towards positive correlation between CD45 microglia and TNF-α (Pearson r = 0.66; P = 0.05). (G) A significant negative correlation was observed between CD45 microglia and TNF-α expression in hIVIG treated mice (Pearson r = -0.86; P = 0.003). (H) Similarly, relative levels of IL-β expression showed a trend for positive correlation (Pearson r = 0.59; P = 0.09) in saline treated mice, whereas hIVIG treatment (I) brought about a significant inverse correlation (Pearson r = -0.76; P = 0.01) between these two variables.