Journal article

Publication year: 2010

Pages: 319-325

Journal: Current Protein & Peptide Science

Volume number: 11

Issue number: 5

ISSN: 1389-2037

DOI Link: https://doi.org/10.2174/138920310791330668

Publisher: Bentham Science Publishers

Abstract: 
Gradual changes in steady-state levels of beta amyloid peptides (A beta) in the brain are considered as initial step in the amyloid cascade hypothesis of Alzheimer's disease (AD). A beta 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. A beta disturbs membrane properties of artificial and isolated biological membranes and of plasma membranes in living cells. A beta 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 A beta is initiated. Perturbation of membranes, binding to lipids and alteration of cellular calcium signaling by A beta have been reported by several studies and these topics are examined in this review.

Harvard Citation style: Eckert, G., Wood, W. and Müller, W. (2010) Lipid Membranes and beta-Amyloid: A Harmful Connection, Current Protein & Peptide Science, 11(5), pp. 319-325. https://doi.org/10.2174/138920310791330668

APA Citation style: Eckert, G., Wood, W., & Müller, W. (2010). Lipid Membranes and beta-Amyloid: A Harmful Connection. Current Protein & Peptide Science. 11(5), 319-325. https://doi.org/10.2174/138920310791330668