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• W3038006089 abstract "Pathogenesis of Alzheimer’s disease (AD), the most common type of dementia, involves misfolding and aggregation of the extracellular amyloid-β (Aβ) protein where the intermediate oligomers, formed during the aggregation progression cascade, are considered the prime toxic species. Here, we identify an active peptide fragment from a medicinal plant-derived (Aristolochia indica) fibrinolytic enzyme having anti-amyloidogenic effects against Aβ fibrillation and toxicity. Liquid chromatography with tandem mass spectrometry (LC-MS/MS), followed by computational analysis of the peptide pool generated by proteolytic digestion of the enzyme, identifies two peptide sequences with predictive high-propensity binding to Aβ42. Microscopic visualizations in conjunction with biochemical and biophysical assessments suggest that the synthetic version of one of the peptides (termed here Pactive, GFLLHQK) arrests Aβ molecules in off-pathway oligomers that can no longer participate in the cytotoxic fibrillation pathway. In contrast, the other peptide (termed P1) aggravates the fibrillation process. Further investigations confirm the strong binding affinity of Pactive with both Aβ42 monomers and toxic oligomers by biolayer interferometric assays. We have also shown that, mechanistically, Pactive binding induces conformational alterations in the Aβ molecule along with modification of Aβ hydrophobicity, one of the key players in aggregation. Importantly, the biostability of Pactive in human blood serum and its nontoxic nature make it a promising therapeutic candidate against Alzheimer’s, for which no disease-modifying treatments are available to date." @default.
• W3038006089 created "2020-07-02" @default.
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• W3038006089 date "2020-06-25" @default.
• W3038006089 modified "2023-10-14" @default.
• W3038006089 title "Heptameric Peptide Interferes with Amyloid-β Aggregation by Structural Reorganization of the Toxic Oligomers" @default.
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• W3038006089 doi "https://doi.org/10.1021/acsomega.0c01730" @default.
• W3038006089 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7346273" @default.
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• W3038006089 hasPublicationYear "2020" @default.
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