Alzheimer's disease is characterized by extensive cerebral amyloid deposition. Amyloid
deposits associated with damaged neuropil and blood vessels contain abundant fibrils
formed by the amyloid β-protein (Aβ). Fibrils, both in vitro and in vivo, are neurotoxic. For this
reason, substantial effort has been expended to develop therapeutic approaches to control
Aβ production and amyloidogenesis. Achievement of the latter goal is facilitated by a
rigorous mechanistic understanding of the fibrillogenesis process. Recently, we discovered …