Membrane-disordering effects of beta-amyloid peptides.
beta-Amyloid (Abeta) protein is the major constituent of senile plaques and cerebrovascular deposits characteristic of Alzheimer's disease (AD). The causal relationship between Abeta and AD-specific lesions like neurodegeneration and atrophy is still not known. The present article summarizes our studies indicating that rather low concentrations of Abeta significantly alter the fluidity of cell membranes and subcellular fractions from different tissues and different species including humans, as a possible initial step of its biological effects. Using different fluorescent probes our data show clearly that Abeta peptides specifically disturb the acyl-chain layer of cell membranes in a very distinct fashion. By contrast, membrane properties at the level of the polar heads of the phospholipid bilayer at the interface with membrane proteins are much less affected.
Müller
W E
WE
Department of Pharmacology, Biocenter University of Frankfurt, Marie-Curie Strasse 9, D-60439 Frankfurt, Germany. PharmacolNat@em.uni-frankfurt.de
Kirsch
C
C
Eckert
G P
GP
D000544:Alzheimer Disease / Q000503:physiopathology; D016229:Amyloid beta-Peptides / Q000494:pharmacology*; D000818:Animals; D016880:Anisotropy; D001921:Brain / Q000187:drug effects; D002462:Cell Membrane / Q000187:drug effects*; D002540:Cerebral Cortex / Q000187:drug effects; D006801:Humans; D007425:Intracellular Membranes / Q000187:drug effects*; D008560:Membrane Fluidity / Q000187:drug effects*; D051379:Mice; D008928:Mitochondria / Q000187:drug effects; D051381:Rats
D016229:Amyloid beta-Peptides