Based on docking simulations, most interactions were governed by hydrophobic interactions. The hydrophobic nature of these drugs facilitates their ability to cross the blood-brain barrier (BBB), a crucial factor in treating central nervous system (CNS) disorders like Alzheimer's . Hydrophobic drugs can more easily penetrate the BBB due to their ability to dissolve in the lipid-rich barrier environment. Fibril inhibition in Alzheimer's disease is a popular strategy to prevent fibril formation. Aducanumab is the one that directly targets amyloid-beta plaques and inhibits fibril formation by binding to amyloid-beta aggregates. Aducanumab is a monoclonal antibody that binds to aggregated forms of amyloid-beta, promoting their clearance from the brain . By binding to these aggregates, Aducanumab helps reduce the formation and accumulation of amyloid plaques, a hallmark of Alzheimer's disease pathology. Other FDA-approved drugs for Alzheimer's disease primarily focus on symptomatic relief by enhancing cholinergic function or modulating glutamate activity rather than directly inhibiting fibril formation . No drug can bind to the fibril and prevent its formation.