Amyloid-beta accumulation in the brain is a major hallmark of Alzheimer's disease and still up to today the most accepted cause explanation for the onset and development of the disease. Recently, nanoparticles have been shown to be able to sequester amyloid-beta 42 after functionalization. In this study, liposomes were functionalized either with phosphatidic acid, or a modified apolipoprotein E (ApoE)-derived peptide, or with a curcumin derivative to try to reduce the levels of amyloid-beta 42 in cerebrospinal fluid or plasma samples from Alzheimer's disease or Down's syndrome patients. The nanoparticles treated with ApoeE derived peptide and phosphatidic acid showed significant binding to amyloid-beta 42 present in the cerebrospinal fluid. Similar results were obtained in plasma samples. The researchers give evidence that suggests that pre-treated liposomes can be a potential therapeutic approach to reduce the amyloid-beta burden in the brain by eliminating it from the body fluids circulation.
Multifunctional liposomes interact with Abeta in human biological fluids: therapeutic implications for Alzheimer's disease
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