Apolipoprotein E (APOE) is indirectly involved in the proteolytic degradation of amyloid-β, and allelic variation in the APOE gene is the leading genetic risk factor for Alzheimer disease (AD). As APOE expression is transcriptionally regulated by retinoid X receptors (RXRs), Cramer et al. investigated the oral RXR agonist bexarotene in AD mice. The resultant increase in APOE levels was accompanied by increased clearance of amyloid-β, rapid reduction in plaque volume and improvements in functional deficits associated with AD. Bexarotene is already approved as an anticancer drug.
ORIGINAL RESEARCH PAPER
Cramer, P. E. et al. ApoE-directed therapeutics rapidly clear β-amyloid and reverse deficits in AD mouse models. Science 335, 1503–1506 (2012)
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Targeting apolipoprotein E improves AD phenotype in mice. Nat Rev Neurol 8, 242 (2012). https://doi.org/10.1038/nrneurol.2012.75
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DOI: https://doi.org/10.1038/nrneurol.2012.75
