Fig. 5

Loss of apoA-I increased the reactivity of astrocytes associated with the cerebrovasculature. a Total GFAP protein levels were measured in soluble half-brain homogenates by ELISA, and values were normalized to total protein concentration in the homogenates. GFAP staining area was visualized by immunofluorescence in cortical (b, c) and hippocampal (d, e) regions, and positive staining area was normalized to total region area. Vascular-specific GFAP expression was visualized using immunofluorescence and observing the association of GFAP with CD31 in cortical (f, g) and hippocampal (h, i) regions, positive co-stained area was normalized to total CD31-positive area. Representative images for immunofluorescent data are below graphs. Points represent individual mice, and bars represent mean values. Circles represent female mice, and squares represent male mice. Yellow arrowheads indicate examples of areas of CD31-associated GFAP in the cortex (g) and hippocampus (i) that are quantified in (f) and (h), respectively. Omnibus analyses of apoA-I and APP/PS1 genotype effects by two-way ANOVA are displayed as exact p values below graphs. Sidak’s multiple comparisons test results are displayed within graphs as *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001. For GFAP ELISA, N = 6–14 mice per genotype were used; for GFAP total and vascular staining, N = 5–6 mice per genotype were used. apoA-I, apolipoprotein A-I; HEM, hemizygous apoA-I genotype; KO, knockout apoA-I genotype; WT, wildtype APP/PS1 genotype; APP/PS1, transgenic APP/PS1 genotype; GFAP, glial fibrillary acidic protein; CD31, cluster of differentiation 31