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Fig. 1 | Alzheimer's Research & Therapy

Fig. 1

From: ApoA-I deficiency increases cortical amyloid deposition, cerebral amyloid angiopathy, cortical and hippocampal astrogliosis, and amyloid-associated astrocyte reactivity in APP/PS1 mice

Fig. 1

Loss of apoA-I significantly reduced plasma cholesterol levels. Plasma levels of (a) total cholesterol, (b) HDL-C, and (c) LDL-C were measured with commercially available kits. ApoE protein in (d) soluble and (e) insoluble half-brain homogenates was measured by ELISA. f Apoe mRNA expression was measured in the parietal cerebral cortex by qRT-PCR. Points represent individual mice and bars represent mean values. Circles represent female mice, and squares represent male mice. 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, and ***p < 0.0001. For plasma lipid and brain protein analysis, N = 6–7 mice per genotype; for mRNA analysis N = 7–17 mice per genotype were used. apoA-I, apolipoprotein A-I; TC, total cholesterol; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; HEM, hemizygous apoA-I genotype; KO, knockout apoA-I genotype; WT, wildtype APP/PS1 genotype; APP/PS1, transgenic APP/PS1 genotype; apoE, apolipoprotein E

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