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Fig. 6 | Alzheimer's Research & Therapy

Fig. 6

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. 6

Loss of apoA-I increases astrocyte reactivity to Aβ plaques and vascular Aβ deposits. GFAP associated with Aβ plaques in the cortex (a, b) and hippocampus (c, d) was visualized with immunofluorescence and normalized to total area of the region. The association of vascular-specific GFAP (GFAP co-localized with CD31) with CAA was visualized using immunofluorescence and normalized to total cortical CAA area (e, g) and total vascular GFAP area (f, g) in the cortex. Representative images are beside (a, c) or below (e, f) graphs. Points represent individual mice, and bars represent mean values. Circles represent female mice, and squares represent male mice. Yellow closed arrowheads () indicate examples of areas of plaque-associated or CAA-associated GFAP, and white open arrowheads () indicate examples areas of plaque or CAA not associated with GFAP. Arrowheads in (g) indicate areas of CAA and vascular GFAP. Results of Mann-Whitney test (a) and unpaired t test (e) are displayed within graphs as *p < 0.05. For plaque and CAA area associated with GFAP, N = 5–6 mice per genotype were used; for CAA area associated with vascular GFAP, N = 4–5 mice per genotype were used. apoA-I, apolipoprotein A-I; HEM, hemizygous apoA-I genotype; KO, knockout apoA-I genotype; APP/PS1, transgenic APP/PS1 genotype; GFAP, glial fibrillary acidic protein; CD31, cluster of differentiation 31; X-34, amyloid stain; CAA, cerebral amyloid angiopathy

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