This paper will be a review of current and ongoing literature surrounding how the aggregation of amyloid-β can induce cognitive impairment, neuronal loss, and the overall pathogenesis of Alzheimer’s disease through its interactions with glutamate receptors, microglia, tau proteins, and lipid rafts. Through these mechanisms of action, amyloid-β can induce synaptic dysfunction, neuroinflammation, neurotoxicity, impaired synaptic plasticity, and other issues that worsen AD- associated neurodegeneration. Multiple preclinical studies have been conducted to better understand these mechanisms as potential targets for therapeutic intervention. Unfortunately, when tested in clinical trials, drugs targeting amyloid-β have consistently failed. However, there are still futures for various ongoing clinical trials targeted at dissolving soluble and insoluble amyloid- β deposits, reducing the production of amyloid-β, and preventing amyloid-β aggregation, specifically: passive vaccination, monoclonal antibodies, and γ-secretase inhibitors. Monoclonal antibodies, in particular, have proven to be most promising. This paper reviews some of the most novel and recent findings and their implications for the future of the field. This paper will also evaluate the most promising forms of therapeutic intervention that have been and are currently being investigated, as well as limitations and future prospects of targeting amyloid-β to slow the progression of Alzheimer’s disease.