Protein aggregation is facilitated by the generation of partially folded intermediates that lack most of the tertiary interactions, but
retain the complete secondary structure. These partially folded states cross-link each other to form protein aggregates. Protein aggregates in an
advanced stage result in the formation of amyloid fibrils, which have high tensile strength. These amyloid fibrils are associated with a number
of pathologies, especially Alzheimer’s disease, which involves the aggregation of the Aβ peptide. In recent years, much attention has been
paid to the generation of potent therapeutics to reduce Aβ peptide fibrillation. This review summarizes the range of molecules used for this
therapy, showing their potency against Aβ amyloids, and suggests a positive future for the eradication of this dreaded disease.