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

Karthikeyan Veeraraghavalu, Can Zhang, Sean Miller, Jasmin K. Hefendehl, Tharinda W. Rajapaksha, Jason Ulrich, Mathias Jucker*, David M. Holtzman, Rudolph E. Tanzi, Robert Vassar, Sangram S. Sisodia

*Corresponding author for this work

Research output: Contribution to journalComment/debate

98 Scopus citations

Abstract

Cramer et al. (Reports, 23 March 2012, p. 1503; published online 9 February 2012) reported that bexarotene rapidly reduces β-amyloid (Aβ) levels and plaque burden in two mouse models of Aβ deposition in Alzheimer's disease (AD). We now report that, although bexarotene reduces soluble Aβ40 levels in one of the mouse models, the drug has no impact on plaque burden in three strains that exhibit Aβ amyloidosis.

Original languageEnglish (US)
Number of pages1
JournalScience
Volume340
Issue number6135
DOIs
StatePublished - Jan 1 2013

ASJC Scopus subject areas

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    Veeraraghavalu, K., Zhang, C., Miller, S., Hefendehl, J. K., Rajapaksha, T. W., Ulrich, J., Jucker, M., Holtzman, D. M., Tanzi, R. E., Vassar, R., & Sisodia, S. S. (2013). Comment on "ApoE-directed therapeutics rapidly clear β-amyloid and reverse deficits in AD mouse models". Science, 340(6135). https://doi.org/10.1126/science.1235505