title: Comment on "ApoE-directed therapeutics rapidly clear β-amyloid and reverse deficits in AD mouse models".
abstract: Cramer et al. (Reports, 23 March 2012, p. 1503; published online 9 February 2012) demonstrated in a mouse model for Alzheimer's disease (AD) that treatment of APP/PS1ΔE9 mice with bexarotene decreased Aβ pathology and ameliorated memory deficits. We confirm the reversal of memory deficits in APP/PS1ΔE9 mice expressing human APOE3 or APOE4 to the levels of their nontransgenic controls and the significant decrease of interstitial fluid Aβ, but not the effects on amyloid deposition.
authors.affiliation: Department of Environmental and Occupational Health, University of Pittsburgh, 100 Technology Drive, Pittsburgh, PA 15219, USA.
authors.forename: Nicholas F
authors.initials: NF
authors.lastname: Fitz
authors.forename: Andrea A
authors.initials: AA
authors.lastname: Cronican
authors.forename: Iliya
authors.initials: I
authors.lastname: Lefterov
authors.forename: Radosveta
authors.initials: R
authors.lastname: Koldamova
mesh_terms: D000544:Alzheimer Disease / Q000188:drug therapy* / Q000378:metabolism*; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D000818:Animals; D001057:Apolipoproteins E / Q000378:metabolism*; D001921:Brain / Q000378:metabolism*; D008297:Male; D013764:Tetrahydronaphthalenes / Q000494:pharmacology* / Q000627:therapeutic use*
chemical_list: D016229:Amyloid beta-Peptides; D001057:Apolipoproteins E; D013764:Tetrahydronaphthalenes