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Comment on “ApoE-Directed Therapeutics Rapidly Clear β- Amyloid and Reverse Deficits in AD Mouse Models” by Ina Tesseur, Adrian C. Lo, Anouk Roberfroid,

Published byLinette Freeman Modified over 8 years ago

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Presentation on theme: "Comment on “ApoE-Directed Therapeutics Rapidly Clear β- Amyloid and Reverse Deficits in AD Mouse Models” by Ina Tesseur, Adrian C. Lo, Anouk Roberfroid,"— Presentation transcript:

1 Comment on “ApoE-Directed Therapeutics Rapidly Clear β- Amyloid and Reverse Deficits in AD Mouse Models” by Ina Tesseur, Adrian C. Lo, Anouk Roberfroid, Sofie Dietvorst, Bianca Van Broeck, Marianne Borgers, Harrie Gijsen, Diederik Moechars, Marc Mercken, John Kemp, Rudi D’Hooge, and Bart De Strooper Science Volume 340(6135):924-924 May 24, 2013 Published by AAAS

2 Fig. 1 Soluble brain and CSF Aβ levels are not significantly reduced by bexarotene in wild-type CD1 mice and beagle dogs.(A) Soluble Aβx-37, Aβx-38, Aβx-40, and Aβx-42 levels (enzyme-linked immunosorbent assay) in whole-brain homogenate of wild-type CD1 mice treated with one dose of oral bexarotene (100 mg/kg; 20% Captisol; N = 6 mice) for 7, 24, 49, and 72 hours, and vehicle (N = 6 mice). Ina Tesseur et al. Science 2013;340:924 Published by AAAS

3 Fig. 2 Aβ levels and deposition are not reduced by chronic bexarotene treatment of hAPP/PS1 mice.(A) Representative pictures of cortical sections of control (vehicle) and bexarotene-treated (100 mg/kg per day; 20% Captisol) 10-month-old hAPP/PS1 transgenic mice (N = 9 per group) stained with horseradish peroxidase (HRP)–labeled antibody 6E10 to Aβ and tyramide- fluorescein (green) and 4′,6-diamidino-2-phenylindole (DAPI) (blue). Ina Tesseur et al. Science 2013;340:924 Published by AAAS

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