Comment on "ApoE-directed therapeutics rapidly clear β-amyloid and reverse deficits in AD mouse models"

Science. 2013 May 24;340(6135):924-c. doi: 10.1126/science.1235809.

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Comment

MeSH terms

  • Alzheimer Disease / drug therapy*
  • Alzheimer Disease / metabolism*
  • Amyloid beta-Peptides / metabolism*
  • Animals
  • Apolipoproteins E / metabolism*
  • Brain / metabolism*
  • Male
  • Tetrahydronaphthalenes / pharmacology*
  • Tetrahydronaphthalenes / therapeutic use*

Substances

  • Amyloid beta-Peptides
  • Apolipoproteins E
  • Tetrahydronaphthalenes