ArticleEuropean biophysics journal : EBJ2006
Cholesterol inhibits the insertion of the Alzheimer's peptide Abeta(25-35) in lipid bilayers.
Article in European biophysics journal : EBJ, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Cholesterol affects the binding of proteins to phosphatidic acid without influencing its ionization properties.Journal of lipid research · 2025Article
- Aggregation Behavior of Amyloid Beta Peptide Depends Upon the Membrane Lipid Composition.The Journal of membrane biology · 2024Review
- Cholesterol as a key player in amyloid β-mediated toxicity in Alzheimer's disease.Frontiers in molecular neuroscience · 2022Review
- Quantitative Measurement of the Affinity of Toxic and Nontoxic Misfolded Protein Oligomers for Lipid Bilayers and of its Modulation by Lipid Composition and Trodusquemine.ACS chemical neuroscience · 2021Article
- Modelling of interactions between Aβ(25-35) peptide and phospholipid bilayers: effects of cholesterol and lipid saturation.RSC advances · 2020Article
- Structure of amyloid βScientific reports · 2019Article
- Interaction of the β amyloid - Aβ(25-35) - peptide with zwitterionic and negatively charged vesicles with and without cholesterol.Chemistry and physics of lipids · 2018Article
- Membrane-Modulating Drugs can Affect the Size of Amyloid-βScientific reports · 2018Article
- Article
- The Position of Aβ22-40 and Aβ1-42 in Anionic Lipid Membranes Containing Cholesterol.Membranes · 2015Article
- The interaction between amyloid-β peptides and anionic lipid membranes containing cholesterol and melatonin.PloS one · 2014Article
- Embedding Aβ42 in heterogeneous membranes depends on cholesterol asymmetries.Biophysical journal · 2013Article
- Membrane cholesterol modulates {beta}-amyloid-dependent tau cleavage by inducing changes in the membrane content and localization of N-methyl-D-aspartic acid receptors.The Journal of biological chemistry · 2011Article
- CHOLESTEROL AND NEURONAL SUSCEPTIBILITY TO BETA-AMYLOID TOXICITY.Cognitive sciences · 2010Article
- Retardation of Abeta fibril formation by phospholipid vesicles depends on membrane phase behavior.Biophysical journal · 2010Article
- Abeta(25-35) attenuated SREBP level in nuclear extracts of serum-deprived human neuroblastoma cells.Neurochemical research · 2009Article
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Authors and funding
3 authors.
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Abstract
The physiological relationship between brain cholesterol content and the action of amyloid beta (Abeta) peptide in Alzheimer's disease (AD) is a highly controversially discussed topic. Evidences for modulations of the Abeta/membrane interaction induced by plasma membrane cholesterol have already been observed. We have recently reported that Abeta(25-35) is capable of inserting in lipid membranes and perturbing their structure. Applying neutron diffraction and selective deuteration, we now demonstrate that cholesterol alters, at the molecular level, the capability of Abeta(25-35) to penetrate into the lipid bilayers; in particular, a molar weight content of 20% of cholesterol hinders the intercalation of monomeric Abeta(25-35) completely. At very low cholesterol content (about 1% molar weight) the location of the C-terminal part of Abeta(25-35) has been unequivocally established in the hydrocarbon region of the membrane, in agreement with our previous results on pure phospholipids membrane. These results link a structural property to a physiological and functional behavior and point to a therapeutical approach to prevent the AD by modulation of membrane properties.
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