Abstract
Aberrant protein misfolding and aggregation processes are central to the onset and development of multiple neurodegenerative diseases. In particular the aggregation of the amyloid-β peptide (Aβ) plays a key role in Alzheimer’s disease (AD). In the aggregation cascade, cytotoxic protein misfolded oligomers are formed as intermediates in the conversion of soluble monomeric proteins into highly structured fibrils. Targeting the formation or properties of oligomers is therefore a promising therapeutic approach to combat protein misfolded diseases.
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