Do lipids change the aggregation of amyloid-beta?
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Lipids play a crucial role in altering the aggregation of amyloid-beta (Aβ) peptides. Various types of lipids such as phosphatidylcholine (PC), cardiolipin (CL), cholesterol (Chol), ceramide (CER), and sphingomyelin (SM) have been shown to impact the aggregation rates and toxicity of Aβ peptides. Lipids like CL, CER, and SM accelerate the aggregation process, while PC inhibits it . Additionally, the presence of lipids like GM1 can influence the aggregation of specific Aβ isoforms, with GM1 inhibiting Aβ40 aggregation but not affecting Aβ42 aggregation. These findings highlight the intricate interplay between lipids and Aβ aggregation, emphasizing the importance of lipid composition in modulating the formation and toxicity of Aβ aggregates in neurodegenerative diseases like Alzheimer's.
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| Papers (4) | Insight |
|---|---|
| Lipid membranes influence the aggregation behavior of amyloid-beta by affecting adsorption, aggregation, and diffusion processes, as observed in the study using TIRFM. | |
6 Citations | Lipids uniquely alter lysozyme aggregation, not amyloid-beta. Cardiolipin, ceramide, and sphingomyelin accelerate, phosphatidylcholine inhibits, and phosphatidylserine has no effect on lysozyme aggregation rates. |
15 Citations | Free gangliosides, like GM1, can alter amyloid-β aggregation. GM1 inhibits Aβ40 aggregation but not Aβ42, forming stable complexes with both isoforms. |
4 Citations | Yes, lipids, such as phosphatidylcholine, cardiolipin, and cholesterol, accelerate the aggregation of amyloid beta 1-42, altering its secondary structure and toxicity. |
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