Prior directions in drug development for AD have yielded disappointing results in trials, including strategies to (1) decrease the production of amyloidogenic proteins by inhibiting the rate-limiting enzyme responsible for production of the amyloidogenic protein (e.g., inhibition of β and γ secretases that produce Aβ in AD), (2) directly inhibit aggregation, and (3) promote phagocytic clearance of oligomers or amyloid by passive or active immunization or 4-inhibit enzymes that phosphorylate tau. This evidence concerns the gene PPIB and Alzheimer disease.