| Summary: | The aggregation of amyloid-β (Aβ) into fibrils forms the plaques implicated in the pathology of Alzheimer’s disease, an aggressive cognitive disorder that impairs function of the cerebral cortex. Therefore, discovery of a mechanism by which fibril disaggregation occurs is of vital importance to the medical community. Here, the current knowledge of and methods to measure Aβ aggregation are reviewed, specifically focusing on the formulation of fluorescence assays as well as a review of the use of polyphenolic compounds as disaggregation agents. One such polyphenol is curcumin, a curcuminoid derived from Curcuma longa that has seen some effective results for reducing Aβ aggregation; however, potential intermolecular interaction complications should be considered in analysis, especially in the popular emission assay studies with Thioflavin T as a fluorescent probe. Overall, future work to determine the applicability of curcumin, as well as other polyphenols, on the prevention or disassembly of Aβ fibrils must account for intermolecular interactions by experiment and the employment of computational means to ascertain an accurate degree of potential therapeutic effect.
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