Effect of packing density of lipid vesicles on the Aβ42 fibril polymorphism

A Kinetic Map of the Influence of Biomimetic Lipid Model Membranes on Aβ42 Aggregation

“…This agrees with previous findings where TEM images of fibrils in the presence of LUVs with complex lipid mixtures showed no morphological changes and only weak association between fibrils and LUVs. 10,16 The lack of strong interactions between LUVs and fibrils suggests that the LUVs facilitate the aggregation via a catalytic mechanism that involves interaction with smaller species rather than fibrils. According to this mechanism, the LUV membranes might promote the aggregation of Aβ 42 by transiently binding small species, thereby facilitating nucleation through locally increased concentrations.…”

A Kinetic Map of the Influence of Biomimetic Lipid Membrane Models on Aβ42Aggregation

“…Furthermore, no or only weak association was found between the Aβ 42 fibrils and the SUVs ( Figure 2 f-j ), in a way which resembles previous findings where TEM images of fibrils in presence of SUVs with complex lipid mixtures showed no morphological changes and only partial interactions between fibrils and SUVs. 10,16…”

“…Furthermore, no or only weak association was found between the Ab 42 fibrils and the SUVs (Figure 2 f-j), in a way which resembles previous findings where TEM images of fibrils in presence of SUVs with complex lipid mixtures showed no morphological changes and only partial interactions between fibrils and SUVs. 10,16 A possible explanation of the lack of strong interactions is that the SUVs facilitate the aggregation via a catalytic mechanism that involves the stabilization of the aggregation intermediates, but not of the reactants and the products of the aggregation reaction. According to this mechanism, the SUVs membranes might promote the aggregation of Ab 42 by transiently binding oligomeric species exposing extended hydrophobic surfaces, while not interacting permanently with the monomeric and the fibrillar forms, which expose fewer hydrophobic regions.…”

“…Indeed, different membrane compositions have been shown to affect the proteolytic processing of APP and the kinetics of Ab aggregation. [8][9][10][11][12][13][14][15][16] Furthermore, cholesterol has been shown to increase the primary nucleation rate of Ab in model cell membranes, 15 an effect that is dependent on the composition of the lipid membranes themselves. It is also known that, while individual lipids can either accelerate or delay the aggregation of Ab according to their physicochemical properties, mixtures of lipids can average out these effect and protect against aggregation aggregation.…”

Interaction of Membrane Vesicles with the Pseudomonas Functional Amyloid Protein FapC Facilitates Amyloid Formation

“…Lipid properties such as charge, headgroup composition and ionic strength affect these interactions and change various aspects of the fibrillation process. For example, the Aβ peptide forms short fibrils in the presence of DOPC vesicles but longer fibrils with vesicles containing negatively charged headgroups like DOPG and DOPS [14]. Of equal importance, these membranes greatly accelerate fibrillation of Aβ and both the fibrillation process and formation of toxic oligomers can lead to membrane disruption [15,16].…”