Abstract
Calcium dysregulation, membrane leakage and Aβ amyloid growth are hallmarks of Alzheimer's disease. Here we show that Ca2+ ions inhibit membrane damage due to amyloid channels but enhance membrane disruption associated with fibers growing on the lipid surface. The similarities with IAPP suggest that this may represent a mechanism common to all proteinopathies.
MeSH terms
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Amyloid / antagonists & inhibitors
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Amyloid beta-Peptides / chemistry
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Amyloid beta-Peptides / metabolism*
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Animals
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Calcium / metabolism*
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Cell Membrane / drug effects
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Cell Membrane / metabolism*
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Fluoresceins / pharmacology
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Fluorescent Dyes / pharmacology
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Fura-2 / pharmacology
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Kinetics
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Mice
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Peptide Fragments / chemistry
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Peptide Fragments / metabolism*
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Porosity / drug effects
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Protein Multimerization / drug effects
Substances
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Amyloid
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Amyloid beta-Peptides
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Fluoresceins
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Fluorescent Dyes
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Peptide Fragments
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amyloid beta-protein (1-40)
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6-carboxyfluorescein
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Calcium
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Fura-2