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Background In our aging society Alzheimer’s Disease (AD) is becoming more and more prevalent while effective symptomatic therapeutics remain limited and no cure is available. ApoE4 is the most important genetic risk factor for AD. Previous results by Cramer et al. [1] showed that Bexarotene treatment reduced Ab in the brain of wild type and AD model mice via an apoE-mediated clearance mechanism. Bexarotene, an RXR agonist, is an FDA approved drug for cutaneous T cell lymphoma and hence a preferred candidate for clinical testing. In this study we attempted to replicate the data by Cramer et al. [1].

Bexarotene treatment does not clear β-Amyloid in an AD mouse model and Beagle dogs