Abstract
β-Amyloid (Aβ) modification therapies for Alzheimer's disease are being developed that target Aβ production, aggregation and/or degradation. Some of these medications are already in Phase III studies. Therefore, it will be most relevant to be able to quantify the neurobiological target of such therapies directly in vivo in the brain. This could allow a reduction in the required sample size for future clinical trials and will allow a more individually tailored approach once such treatments become clinically available. This article reviews the prevalence of Alzheimer's disease among other dementias, the Aβ cascade, various Aβ positron emission tomography tracers that are being developed, and the potential application of these tracers for Aβ modification therapies.