TY - JOUR AU - LaClair, Katherine D. AU - Manaye, Kebreten F. AU - Lee, Dexter L. AU - Allard, Joanne S. AU - Savonenko, Alena V. AU - Troncoso, Juan C. AU - Wong, Philip C. PY - 2013 DA - 2013/06/13 TI - Treatment with bexarotene, a compound that increases apolipoprotein-E, provides no cognitive benefit in mutant APP/PS1 mice JO - Molecular Neurodegeneration SP - 18 VL - 8 IS - 1 AB - Though the precise cause(s) of Alzheimer’s disease (AD) remain unknown, there is strong evidence that decreased clearance of β-amyloid (Aβ) from the brain can contribute to the disease. Therapeutic strategies to promote natural Aβ clearance mechanisms, such as the protein apolipoprotein-E (APOE), hold promise for the treatment of AD. The amount of APOE in the brain is regulated by nuclear receptors including retinoid X receptors (RXRs). Drugs that activate RXRs, including bexarotene, can increase APOE and ABCA1 production, and have been shown to decrease the Aβ burden and improve cognition in mouse models of Aβ amyloidosis. Although recent bexarotene studies failed to replicate the rapid clearance of Aβ from brains, behavioral and cognitive effects of this compound remain controversial. SN - 1750-1326 UR - https://doi.org/10.1186/1750-1326-8-18 DO - 10.1186/1750-1326-8-18 ID - LaClair2013 ER -