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.
MeSH terms
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Alzheimer Disease / metabolism*
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Alzheimer Disease / pathology
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Amyloid / metabolism*
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Amyloid beta-Peptides / metabolism
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Amyloid beta-Protein Precursor / genetics
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Amyloid beta-Protein Precursor / metabolism
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Animals
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Brain / metabolism
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Brain / pathology
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Cathepsin B / genetics
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Cathepsin B / metabolism*
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Humans
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Hydrolysis
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Mice
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Mice, Knockout
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Mice, Transgenic
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Models, Biological
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Mutation / genetics
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Neurites / metabolism
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Neurites / pathology
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Neurons / metabolism
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Neurons / pathology
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Peptide Fragments / metabolism
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Plaque, Amyloid / metabolism
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Plaque, Amyloid / pathology
Substances
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Amyloid
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Amyloid beta-Peptides
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Amyloid beta-Protein Precursor
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Peptide Fragments
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amyloid beta-protein (1-42)
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Cathepsin B