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Amyloid beta (Aβ) fibrils are insoluble, fibrous protein aggregates formed by the self-assembly of amyloid beta peptides. These fibrils are a hallmark of Alzheimer's disease, accumulating as plaques in the brain and contributing to neurodegeneration. The formation and accumulation of Aβ fibrils is considered causative in Alzheimer’s pathology. Aβ fibrils display significant polymorphism—different arrangements at quaternary/protofilament levels—which may influence their biological activity and toxicity profiles. Fibrillar surfaces can catalyze the generation of toxic oligomeric species that damage neuronal cells. Amyloid beta interacts with several cell surface receptors on microglia and other cells including Scavenger receptors, Receptor for advanced glycation end products (RAGE), G-protein coupled receptors, Chemokine-like receptors and Toll-like receptors.
Prevention of fibril formation and destabilization of pre-formed fibrils
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