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To better understand the consequences attributable to a sole BEC injury and to unravel the mechanisms underlying bile duct repair through BEC proliferation after acute injury, we developed a mouse model of inducible BEC death by overexpressing human CD59 (hCD59) on BECs (biliary-specific hCD59-transgenic mice, referred to hereafter as ihCD59 BEC-TG mice)

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This existing knowledge facilitates rational dose selection for AD trials and reduces uncertainties regarding drug-drug interactions a particularly salient consideration given that AD patients frequently receive cholinesterase inhibitors, memantine, and medications for comorbid conditions (Schneider, 2011)