Abstract
β-Amyloid (Aβ) may play an important role in the pathogenesis of Alzheimer's disease. However, a causal relationship between Aβ oligomers and layer-specific neurodegeneration has not been clarified. Here we show up-regulation of calsyntenin (Cst)-3 in cultured neurons treated with Aβ oligomers and in Tg2576 mice. Cst-3 is distributed in large neurons in layers 2-3 and 5 of the cerebral cortex, and accumulated in dystrophic neurites surrounding Aβ-plaques. Overexpression of Cst-3 accelerates neuronal death. These results indicate that up-regulation of Cst-3 in cortical neurons in layers 2-3 and 5 by Aβ oligomers may lead to increase in vulnerability of neurons.
Copyright © 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
MeSH terms
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Alzheimer Disease / metabolism
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Amyloid beta-Peptides / toxicity*
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Amyloid beta-Protein Precursor / biosynthesis
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Amyloid beta-Protein Precursor / genetics
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Animals
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Apoptosis / drug effects
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Calcium-Binding Proteins / genetics
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Calcium-Binding Proteins / metabolism*
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Cell Survival / drug effects
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Cells, Cultured
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Cerebral Cortex / cytology
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Cerebral Cortex / drug effects
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Cerebral Cortex / metabolism*
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Cerebral Cortex / pathology
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Down-Regulation / drug effects
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Embryo, Mammalian
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Humans
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Membrane Proteins / genetics
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Membrane Proteins / metabolism*
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Mice
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Mice, Transgenic
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Neurons / drug effects
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Neurons / metabolism*
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Neurons / pathology
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Peptide Fragments / toxicity*
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RNA, Messenger / metabolism
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Rats
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Recombinant Fusion Proteins / metabolism
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Up-Regulation / drug effects*
Substances
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Amyloid beta-Peptides
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Amyloid beta-Protein Precursor
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CLSTN2 protein, human
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CLSTN3 protein, human
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Calcium-Binding Proteins
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Membrane Proteins
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Peptide Fragments
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RNA, Messenger
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Recombinant Fusion Proteins
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amyloid beta-protein (1-42)