Comment on “ApoE-Directed Therapeutics Rapidly Clear β-Amyloid and Reverse Deficits in AD Mouse Models” | Zendy

Nicholas F. Fitz | Zendy; Andrea A. Cronican | Zendy; Iliya Lefterov | Zendy; Radosveta Koldamova | Zendy

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Comment on “ApoE-Directed Therapeutics Rapidly Clear β-Amyloid and Reverse Deficits in AD Mouse Models”

Author(s) -

Nicholas F. Fitz,

Andrea A. Cronican,

Iliya Lefterov,

Radosveta Koldamova

Publication year - 2013

Publication title -

science

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 12.556

H-Index - 1186

eISSN - 1095-9203

pISSN - 0036-8075

DOI - 10.1126/science.1235809

Subject(s) - apolipoprotein e , amyloid (mycology) , bexarotene , disease , β amyloid , medicine , alzheimer's disease , neuroscience , endocrinology , pathology , psychology , biology , biochemistry , gene , nuclear receptor , transcription factor

Crameret 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.

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