Accumulation of Amyloid beta (A-beta) peptides, particular A-beta (aa1-42), is thought to be one of the main causes of neurodegeneration in Alzheimer’s disease (AD). A-beta levels are determined by both the rates of production and clearance of the peptides. Proteolytic degradation of A-beta is one of the main methods by which A-beta is cleared from the brain, and it is thought that impaired degradation of A-beta may play an important role in the pathogenesis of AD. A diverse array of proteases has been shown to work jointly with each other and with other clearance mechanisms to eliminate A-beta. A-beta degrading enzymes are located in multiple cell types, such as astrocytes, microglia, and brain vascular endothelial cells, as well as in the extracellular space. In addition, many of these enzymes can cleave A-beta at more than one site. Research has shown that both genetic and environmental factors, such as mutations and oxidative damage, can cause decreased activity of these A-beta degrading enzymes, thus, resulting in aberrant A-beta catabolism. R&D Systems offers a range of research tools needed for investigating enzymatic degradation of A-beta peptides.