Effects of β-amyloid peptides on the fluidity of membranes from frontal and parietal lobes of human brain. High potencies of Aβ1-42 and Aβ1-43

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Abstract
β-amyloid peptide (Aβ) and several Aβ-fragments decrease the fluidity of human cortex membranes in a concentration dependent fashion. The effect of Aβ on membrane fluidity increases with peptide length, is most pronounced for Afil-43 and can be seen at concentrations as low as 100 nmol/l. While the fragment Aβ25-3′5 is active, scrambled peptide (Aβ35-25) when investigated under similar conditions shows no effects on membrane fluidity. The effect of Aβ peptides on fluidity of the phospholipid bilayer is more pronounced in the hydrocarbon core (labeled with the fluorescence probe 1,6-diphenylhexa-l,3,5-triene) than in the region of the hydrophilic heads (labeled with the fluorescence probe l-[4 '-(trimethylamino)phenyl]-6-phenylhexa-1,3,5-triene). It is suggested that the effect of Aft on neuronal membranes is probably a major initial mechanism in a cascade of events finally leading to neurotoxicity and cell death in Alzheimer's disease.