How effective are the rivastigmine hybrids in inhibiting Aβ1–42 aggregation?

Aβ aggregation is a hallmark of AD, leading to the formation of neurotoxic plaques. Inhibiting Aβ aggregation is a critical strategy for AD treatment.

All rivastigmine hybrids demonstrated significant Aβ1–42 aggregation inhibitory activity, with values ranging from 45% to 82%. The catechol-containing hybrids (4AY5 and 4AY6) showed the highest inhibitory activity, comparable to curcumin (77% inhibition). The presence of free phenolic hydroxyl groups, as in catechol derivatives, contributed to higher inhibitory activity. Structural modifications, such as adding an extra alkene group, also enhanced Aβ aggregation inhibition.