Over a decade ago the amyloid cascade hypothesis predicted that increased levels of amyloid-β (Aβ) peptide lead to secondary pathologies that ultimately culminate in the onset of Alzheimer disease (AD) [1]. Early support for this hypothesis came from genetic studies linking early-onset AD to mutations in the amyloid precursor protein (APP), from which Aβ is derived, and presenilins 1 and 2, which are interchangeable components of a endoprotease complex that releases Aβ from APP (for review see [2,3]). If, as predicted, overproduction of Aβ initiates the cascade of events leading to disease, then therapeutic strategies that lower Aβ levels should either arrest or reverse the progression from peptide to dementia.