Abstract
Gradual changes in steady-state levels of beta amyloid peptides (Aβ) in the brain are considered as initial step in the amyloid cascade hypothesis of Alzheimers disease (AD). Aβ is a product of the secretase cleavage of the amyloid precursor protein and there is evidence that the membrane lipid environment may modulate secretase activity and alters its function. Aβ disturbs membrane properties of artificial and isolated biological membranes and of plasma membranes in living cells. Aβ induced changes in membrane fluidity could be explained by physico-chemical interactions of the peptide with membrane components such as cholesterol, phospholipids and gangliosides. Thus, cell membranes may be the location where the neurotoxic cascade of Aβ is initiated. Perturbation of membranes, binding to lipids and alteration of cellular calcium signaling by Aβ have been reported by several studies and these topics are examined in this review.
Keywords: Amyloid, membrane, membrane fluidity, cholesterol, ganglioside, Alzheimer, calcium, pyrene, diphenylhexatriene
Current Protein & Peptide Science
Title: Lipid Membranes and β-Amyloid: A Harmful Connection
Volume: 11 Issue: 5
Author(s): G.P. Eckert, W.G. Wood and W.E. Muller
Affiliation:
Keywords: Amyloid, membrane, membrane fluidity, cholesterol, ganglioside, Alzheimer, calcium, pyrene, diphenylhexatriene
Abstract: Gradual changes in steady-state levels of beta amyloid peptides (Aβ) in the brain are considered as initial step in the amyloid cascade hypothesis of Alzheimers disease (AD). Aβ is a product of the secretase cleavage of the amyloid precursor protein and there is evidence that the membrane lipid environment may modulate secretase activity and alters its function. Aβ disturbs membrane properties of artificial and isolated biological membranes and of plasma membranes in living cells. Aβ induced changes in membrane fluidity could be explained by physico-chemical interactions of the peptide with membrane components such as cholesterol, phospholipids and gangliosides. Thus, cell membranes may be the location where the neurotoxic cascade of Aβ is initiated. Perturbation of membranes, binding to lipids and alteration of cellular calcium signaling by Aβ have been reported by several studies and these topics are examined in this review.
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Cite this article as:
Eckert G.P., Wood W.G. and Muller W.E., Lipid Membranes and β-Amyloid: A Harmful Connection, Current Protein & Peptide Science 2010; 11 (5) . https://dx.doi.org/10.2174/138920310791330668
DOI https://dx.doi.org/10.2174/138920310791330668 |
Print ISSN 1389-2037 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5550 |
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