Abstract
A major hallmark of Alzheimer’s disease is the misfolding and aggregation of the amyloid-β (Aβ) peptide into β-sheet-rich fibrils. Emerging evidence now implicates small oligomeric intermediates produced in the earliest stages of fibril assembly as the predominant neurotoxins and oligomer blocking candidates are driving the search for an effective therapeutic. However, it is also widely accepted that many aggregate characterization strategies suffer from an insensitivity to oligomers due to their low abundance and time-dependent heterogeneity.
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