Abstract
The role of cathepsin B, a lysosomal protease implicated in amyloid-beta (Abeta1-42) metabolism, in Alzheimer's disease remains controversial. In this issue of Neuron, Mueller-Steiner et al. manipulate the expression of cathepsin B in aged APP transgenic mice, observing that increased expression degrades preformed oligomeric and fibrillar amyloid, while inactivation accelerates beta-amyloidosis.
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