Amyloid-beta protein (A-beta) is the proposed causative agent of Alzheimer's disease (AD). One of the neuropathological hallmarks of AD is the accumulation of senile plaques in the brain. Senile plaques represent extracellular deposits of aggregated A-beta. Prior to its deposition as senile plaques, A-beta oligomerizes to exert pathological actions on neuron function and viability. AD therapies that are in the advanced stages of development mostly target A-beta production, aggregation, or clearance. Although most clinical trials focus on the treatment of symptomatic patients, it has been suggested that earlier intervention or disease prevention would be a more effective strategy. Research studies have investigated receptors that are involved in the uptake of A-beta (i.e. APP, CD36, FPRL, LDL R, LRP1, alpha-2-Macroglobulin, MARCO, SR-A1, and RAGE) and enzymes that are known to degrade A-beta (i.e. ACE, Cystatin C, ECE, Insulysin/IDE, MMPs, and Neprilysin). In fact, a recent report suggested that a combinatorial therapy designed to block A-beta production and enhance A-beta clearance might represent the most effective approach.