Alzheimer's disease (AD) is a progressive and fatal degenerative neurological disorder that affects approximately one-tenth of the population over the age of 65. The pathological hallmarks of the disease include the formation and accumulation in the brain of Aß, a 39-43 amino acid fragment of a much larger precursor, the ß-amyloid precursor protein (ß-APP). There is currently no cure for the disease. Two classes of FDA approved medications, the acetylcholinesterase inhibitors (eg. Aricept) and the N-methyl-D-aspartate receptor antagonist, Memantine alleviate some disease symptoms but they do not alter the course of the disease. Disease modifying approaches to the treatment of AD, which aim to reduce the rate of disease progression, with prevention and/or reversal of pathology, are badly needed. There are currently no anti-amyloid therapies available.Our recent findings may hold promise of a novel therapeutic approach. Earlier this year we published our new and compelling findings in PNAS that show that the production of Aß requires the prior cell:cell interaction between ß-APP and the Presenilins (PS). Why is that important? Because in a mechanism that requires the interaction of two cells, the possibility exists that if you can interfere with this cell:cell interaction, then you may be able to inhibit the production of Aß. We have been able to do just that. By inhibiting the cell:cell interaction between ß-APP and PS, we successfully inhibited Aß production a cell culture model. These results are very promising because they suggest the potential of novel disease-modifying therapeutic approaches to treat AD by inhibiting Aß production in the brain.