AD is characterized by accumulation of amyloid plaques and paired helical filaments. Mutations that cause early-onset AD are located in the genes that code for the APP and the enzyme responsible for amyloid production, Presenilin 1/Presenilin 2. These observations have led to the widely-held belief that Aβ has a causative role in the development of AD. However, the distribution of amyloid deposits in the brain does not correlate well with disease progression. These results suggest the possibility that APP metabolites other than Aβ might contribute to AD. It…