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Alzheimer΄s disease (AD) was first described more than 100 years ago; however, the mechanisms underlying its pathogenesis are still poorly understood. Current theories suggest a pivotal role for the protein amyloid-β (Aβ) and many of the novel treatments for AD focus on Aβ. In this chapter, we discuss evidence that Aβ underpins the cognitive decline as a result of direct and indirect toxicity of the peptide on synapses in the cerebral cortex and hippocampus. Furthermore, we will follow the promise that Aβ immunisation holds to alter the natural history of AD, from its beginnings in animal models to the current research on humans. The success seen in mice in preventing both synapse loss and reducing functional decline is yet to be matched in humans and serious adverse events in patients stopped the initial vaccination approach. Research, however, is continuing in human AD aiming to provide a greater understanding of the mechanisms underlying the immune response and the potential effects of immunisation on preventing or reversing cognitive impairment. [ABSTRACT FROM AUTHOR]