Calcium ions do not influence the Aβ(25-35) triggered morphological changes of lipid membranes.

We have studied the effect of calcium ions (Ca) at various concentrations on the structure of lipid vesicles in the presence of amyloid-beta peptide Aβ(25-35). In particular, we have investigated the influence of calcium ions on the formation of recently documented bicelle-like structures (BLSs) emerged as a result of Aβ(25-35) triggered membrane disintegration. First, we have shown by using small-angle X-ray and neutron scattering that peptide molecules rigidify the lipid bilayer of gel phase DPPC unilamellar vesicles (ULVs), while addition of the calcium ions to the system hinders this effect of Aβ(25-35).

Arrangement of lipid vesicles and bicelle-like structures formed in the presence of Aβ(25-35) peptide.

Our complementary experimental data and molecular dynamics (MD) simulations results reveal the structure of previously observed lipid bicelle-like structures (BLSs) formed in the presence of amyloid-beta peptide Aβ(25-35) below the main phase transition temperature (T) of saturated phosphatidylcholine lipids and small unilamellar vesicles (SUVs) above this temperature. First, we show by using solid-state P nuclear magnetic resonance (NMR) spectroscopy that our BLSs being in the lipid gel phase demonstrate magnetic alignment along the magnetic field of NMR spectrometer and undergo a transition to SUVs in the lipid fluid phase when heated through the T. Secondly, thanks to the BLS alignment we present their lipid structure.

Cholesterol and melatonin regulated membrane fluidity does not affect the membrane breakage triggered by amyloid-beta peptide.

We have studied by means of small angle neutron scattering and diffraction, and molecular dynamics simulations the effect of lipid membrane fluidity on the amyloid-beta peptide interactions with the membrane. These interactions have been discovered previously to trigger the reorganization of model membranes between unilamellar vesicles and planar membranes (bicelle-like structures) during the lipid phase transition. The morphology changes were taking place in rigid membranes prepared of fully saturated lipids and were proposed to play a role in the onset of amyloid related disorders.

Reflectometry and molecular dynamics study of the impact of cholesterol and melatonin on model lipid membranes.

The effect of melatonin and/or cholesterol on the structural properties of a model lipid bilayer prepared from 1,2-dioleoyl-sn-glycero-3-phosphocholine (DOPC) has been investigated both experimentally and via molecular dynamics (MD) simulations. Neutron reflectometry experiments performed with single supported membranes revealed changes in lipid bilayer thickness upon the introduction of additional components. While the presence of cholesterol led to an increase in membrane thickness, the opposite effect was observed in the case of melatonin.

Investigating the competitive effects of cholesterol and melatonin in model lipid membranes.

We have studied the impact of cholesterol and/or melatonin on the static and dynamical properties of bilayers made of DPPC or DOPC utilizing neutron scattering techniques, Raman spectroscopy and molecular dynamics simulations. While differing in the amplitude of the effect due to cholesterol or melatonin when comparing their interactions with the two lipids, their addition ensued recognizable changes to both types of bilayers. As expected, based on the two-component systems of lipid/cholesterol or lipid/melatonin studied previously, we show the impact of cholesterol and melatonin being opposite and competitive in the case of three-component systems of lipid/cholesterol/melatonin.