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. 2010 Nov;177(5):2549–2562. doi: 10.2353/ajpath.2010.100265

Figure 1.

Figure 1

Gene dose-dependent reduction in fibrillar Aβ deposition in the APPPS1 mouse model of AD with CX3CR1 deficiency. Brain sections (30 μm) from APPPS1;Cx3cr1+/+ (A, n = 7), APPPS1;Cx3cr1+/− (B, n = 6), and APPPS1;Cx3cr1−/− (C, n = 7) mice at 4 months of age were stained with Thioflavine S. A series of low-power images (Scale bar = 1 mm) were used to reconstruct the cortex and hippocampus from four sections from each animal. As expected based on the published literature,21 APPPS1;Cx3cr1+/+ animals exhibit abundant fibrillar Aβ deposition throughout the cortex with reduced Aβ deposition in the hippocampus (A). By contrast, age-matched APPPS1;Cx3cr1+/− (B) and APPPS1;Cx3cr1−/− (C) animals exhibited a gene dose-dependent reduction in fibrillar Aβ deposition throughout the cortex and hippocampus. Quantification of Thioflavine S staining in the cortex (D) and hippocampus (E) across all animals revealed a statistically significant decrease in APPPS1 mice with either one or two copies of Cx3cr1 loss of function alleles when compared with age-matched APPPS1;Cx3cr1+/+ controls (*P < 0.001). Notably, there was also a significant difference in Aβ deposition in the cortex between APPPS1;Cx3cr1+/− and APPPS1;Cx3cr1−/− genotypes (P < 0.05). To confirm results obtained using Thioflavine S staining, Western blots of brain extracts from Cx3cr1+/+, APPPS1;Cx3cr1+/+, and APPPS1;Cx3cr1−/− animals were probed with antibodies to human Aβ and GAPDH as a loading control. Consistent with Thioflavine S staining, APPPS1;Cx3cr1−/− brains exhibited lower steady-state Aβ levels when compared with age-matched APPPS1;Cx3cr1+/+ controls (F). Furthermore, ELISAs performed on APPPS1;Cx3cr1+/+ (n = 6) and APPPS1;Cx3cr1−/− brain homogenates (n = 5) revealed reduced Aβ42 levels in CX3CR1-deficient animals (G; *P < 0.05).