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In control mice, no plaques with macrophages were observed, while fibrous/fibroatheromatous plaques were present in the aortas extracted from ApoE-KO mice.
In young ApoE−/− mice, no plaques were visible by eye, and Sudan IV staining revealed either no plaque or barely visible tiny areas presumably indicating where plaques would later form.
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In control mice, no plaque areas were seen and ROIs were defined for healthy vessel wall, adventitia, and muscle.
Wild-type mice presented no plaques in any brain region (see squared area in Figure 2(f)).
Although intraneuronal Aβ-positive cells were present in the cortex, hippocampus and amygdala in brain sections of 4- to 10-month-old 3xTgAD mice, no Aβ plaques or hyperphosphorylated tau were detected at these ages, apart from a few scattered Aβ plaques and neurones positive for hyperphosphorylated tau in 10-month-old mice.
In the aortas of the control mice, no atherosclerotic plaques were detected.
Note the presence of atherosclerotic plaques predominantly located at the level of the aortic arch and the supra-aortic vessels of the hyperlipidemic mouse (white arrows); no plaque is apparent in the aorta of the control mouse.
Although the Tg2576 mice showed AD-like pathologies with plaque formation in the brain, there were no plaques observed in their age-matched WT animals.
Despite increased atherosclerotic lesion formation in ApoE/MGL double-knockout (DKO) compared to ApoE−/− mice, plaques from DKO mice have reduced lipid and macrophage content, markedly increased amount of collagen, and a thicker fibrous cap, demonstrating lesion stabilization.
Kathleen, Philadelphia A. Bexarotene is a cancer drug that in mice cleared plaques.
In the brain sections of Tg_sh-CTL mice, amyloid plaques were highly stained by 6E10 antibody in the cortex and hippocampal region (Figure 5A).
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