The apolipoprotein E gene is the strongest genetic risk factor for late-onset Alzheimer disease. Figuring out how it drives susceptibility remains a tall order. At a one-day symposium in St. Louis, researchers from across the United States and abroad took stock of the latest on potential mechanisms. Receptors, including ApoE receptor 2, topped the hit parade of ApoE accomplices that might mediate actions of the risky isoform.