The cognitive decline in Alzheimer’s disease (AD) resulting from neuronal cell death has no cure, identified cause, or early diagnoses. With patient care estimated at >$604 billion/year globally, there is strong motivation to understand the molecular mechanisms underlying AD and the effects of therapeutic drug candidates on disease progression. These mechanistic studies are important for the development of early diagnostics and therapeutic drugs intended to halt or reverse disease progression. Although its mechanism of action remains elusive, the accumulation of Aβ in high concentrations leads to Aβ oligomer and fibril formation, hyperphosphorylation of Tau protein, deficiency in neurotransmitters, production of reactive oxygen species, and calcium dysregulation. This cascade of events lead to weakened cell signaling and neuronal cell death in key areas of the brain. Consequently, Aβ is an excellent molecular target for early diagnostics and drug development. Specifically, drugs that convert Aβ oligomers and fibrils to non-toxic monomers or inhibit its formation for rapid clearance by the brain is of significant interest.