The gradual accumulation and assembly of beta-amyloid (Abeta) peptide into neuritic plaques is a major pathological hallmark of Alzheimer’s disease (AD). Proteolytic degradation of Abeta is an important clearance mechanism under normal circumstances, and it has been found to be compromised in those afflicted with AD. Here, the extended substrate specificity and Abeta-degrading capacity of kallikrein-7 (KLK7), a protease enzyme that degrades other proteins, was characterized. It was found that treatment of Abeta preparations with KLK7 significantly reduced Abeta mediated toxicity to rat hippocampal neurons Taken together, these results indicate that KLK7 possesses an Abeta degrading activity that could be useful in designing drugs to treat Alzheimer’s Disease.