The beta amyloid (Aβ) protein is a key molecule in the pathogenesis of Alzheimer’s disease (AD). The tendency of the Aβ peptide to aggregate, its reported neurotoxicity, and genetic linkage studies, have led to a hypothesis of AD pathogenesis that many AD researchers term the amyloid cascade hypothesis. In this hypothesis, an increased production of Aβ results in neurodegeneration and ultimately dementia through a cascade of events. In the past 15 years, debate amongst AD researchers has arisen as to whether Aβ is a cause or an effect of the pathogenic process. Recent in vitro and in vivo research has consolidated the theory that Aβ is the primary cause, initiating secondary events, culminating in the neuropathological hallmarks associated with AD. This research has led to the development of therapeutic agents, currently in human clinical trials, which target Aβ.