
pmid: 16982408
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.
Mice, Knockout, Neurons, Amyloid, Amyloid beta-Peptides, Neuroscience(all), Hydrolysis, Brain, Mice, Transgenic, Plaque, Amyloid, Models, Biological, Peptide Fragments, Cathepsin B, Amyloid beta-Protein Precursor, Mice, Alzheimer Disease, Mutation, Neurites, Animals, Humans
Mice, Knockout, Neurons, Amyloid, Amyloid beta-Peptides, Neuroscience(all), Hydrolysis, Brain, Mice, Transgenic, Plaque, Amyloid, Models, Biological, Peptide Fragments, Cathepsin B, Amyloid beta-Protein Precursor, Mice, Alzheimer Disease, Mutation, Neurites, Animals, Humans
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